---
_id: '2651'
abstract:
- lang: eng
text: The GABAergic system, a major inhibitory regulator in the central nervous
system, may also play important roles in peripheral nonneuronal tissues and cells.
Recent studies showed that GABAB receptor is expressed in testis and sperm. To
understand the role of the GABAergic system in spermiogenesis, we examined cellular
localization of GABA and GABAB receptor subunits in rat spermatids by immunocytochemistry.
Immunoreactivity for GABA was detected around acrosomal granules of spermatids
during the Golgi and cap phases. GABAB(1) immunoreactivity was observed in the
acrosomal vesicle of spermatids in Golgi phase, and during cap phase, this reactivity
expanded to the entire region of the acrosome covering the nuclear membrane. The
level of reactivity decreased gradually with maturation of spermatids. In contrast,
GABAB(2) immunoreactivity was not observed in spermatids during Golgi phase but
was detected in the equatorial region during cap phase. Both GABA immunoreactivity
and GABAB(2) immunoreactivity were transferred to the residual cytoplasm during
the release of spermatozoa. Electron microscopic immunocytochemistry revealed
that, during cap phase, GABA and GABAB(1) were distributed within the whole acrosomal
vesicle but not in the acrosomal granule. GABAB(2) immunoreactivity was observed
in the narrow space between the inner acrosomal and nuclear membrane and was limited
to the equatorial region of the spermatid head. These results indicate that the
GABAergic system might be involved in regulation of spermiogenesis.
author:
- first_name: Kiyoto
full_name: Kanbara, Kiyoto
last_name: Kanbara
- first_name: Keiko
full_name: Okamoto, Keiko
last_name: Okamoto
- first_name: Sakashi
full_name: Nomura, Sakashi
last_name: Nomura
- first_name: Takeshi
full_name: Kaneko, Takeshi
last_name: Kaneko
- first_name: Ryuichi
full_name: Ryuichi Shigemoto
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Haruhito
full_name: Azuma, Haruhito
last_name: Azuma
- first_name: Yoji
full_name: Katsuoka, Yoji
last_name: Katsuoka
- first_name: Masahiko
full_name: Watanabe, Masahiko
last_name: Watanabe
citation:
ama: Kanbara K, Okamoto K, Nomura S, et al. Cellular localization of GABA and GABAB
receptor subunit proteins during spermiogenesis in rat testis. Journal of Andrology.
2005;26(4):485-493. doi:10.2164/jandrol.04185
apa: Kanbara, K., Okamoto, K., Nomura, S., Kaneko, T., Shigemoto, R., Azuma, H.,
… Watanabe, M. (2005). Cellular localization of GABA and GABAB receptor subunit
proteins during spermiogenesis in rat testis. Journal of Andrology. American
Society of Andrology. https://doi.org/10.2164/jandrol.04185
chicago: Kanbara, Kiyoto, Keiko Okamoto, Sakashi Nomura, Takeshi Kaneko, Ryuichi
Shigemoto, Haruhito Azuma, Yoji Katsuoka, and Masahiko Watanabe. “Cellular Localization
of GABA and GABAB Receptor Subunit Proteins during Spermiogenesis in Rat Testis.”
Journal of Andrology. American Society of Andrology, 2005. https://doi.org/10.2164/jandrol.04185.
ieee: K. Kanbara et al., “Cellular localization of GABA and GABAB receptor
subunit proteins during spermiogenesis in rat testis,” Journal of Andrology,
vol. 26, no. 4. American Society of Andrology, pp. 485–493, 2005.
ista: Kanbara K, Okamoto K, Nomura S, Kaneko T, Shigemoto R, Azuma H, Katsuoka Y,
Watanabe M. 2005. Cellular localization of GABA and GABAB receptor subunit proteins
during spermiogenesis in rat testis. Journal of Andrology. 26(4), 485–493.
mla: Kanbara, Kiyoto, et al. “Cellular Localization of GABA and GABAB Receptor Subunit
Proteins during Spermiogenesis in Rat Testis.” Journal of Andrology, vol.
26, no. 4, American Society of Andrology, 2005, pp. 485–93, doi:10.2164/jandrol.04185.
short: K. Kanbara, K. Okamoto, S. Nomura, T. Kaneko, R. Shigemoto, H. Azuma, Y.
Katsuoka, M. Watanabe, Journal of Andrology 26 (2005) 485–493.
date_created: 2018-12-11T11:58:52Z
date_published: 2005-07-01T00:00:00Z
date_updated: 2021-01-12T06:58:50Z
day: '01'
doi: 10.2164/jandrol.04185
extern: 1
intvolume: ' 26'
issue: '4'
month: '07'
page: 485 - 493
publication: Journal of Andrology
publication_status: published
publisher: American Society of Andrology
publist_id: '4246'
quality_controlled: 0
status: public
title: Cellular localization of GABA and GABAB receptor subunit proteins during spermiogenesis
in rat testis
type: journal_article
volume: 26
year: '2005'
...
---
_id: '2652'
abstract:
- lang: eng
text: We studied neurogliaform neurons in the stratum lacunosum moleculare of the
CA1 hippocampal area. These interneurons have short stellate dendrites and an
extensive axonal arbor mainly located in the stratum lacunosum moleculare. Single-cell
reverse transcription-PCR showed that these neurons were GABAergic and that the
majority expressed mRNA for neuropeptide Y. Most neurogliaform neurons tested
were immunoreactive for α-actinin-2, and many stratum lacunosum moleculare interneurons
coexpressed α-actinin-2 and neuropeptide Y. Neurogliaform neurons received monosynaptic,
DNQX-sensitive excitatory input from the perforant path, and 40 Hz stimulation
of this input evoked EPSCs displaying either depression or initial facilitation,
followed by depression. Paired recordings performed between neurogliaform neurons
showed that 85% of pairs were electrically connected and 70% were also connected
via GABAergic synapses. Injection of sine waveforms into neurons during paired
recordings resulted in transmission of the waveforms through the electrical synapse.
Unitary IPSCs recorded from neurogliaform pairs readily fatigued, had a slow decay,
and had a strong depression of the synaptic response at a 5 Hz stimulation frequency
that was antagonized by the GABA B antagonist (2S)-3-[[(1S)-1-(3,4-dichlorophenyl)ethyl]amino-2-hydroxypropyl](phenylmethyl)
phosphinic acid (CGP55845). The amplitude of the first IPSC during the 5 Hz stimulation
was also increased by CGP55845, suggesting a tonic inhibition of synaptic transmission.
A small unitary GABA B-mediated IPSC could also be detected, providing the first
evidence for such a component between GABAergic interneurons. Electron microscopic
localization of the GABA B1 subunit at neurogliaform synapses revealed the protein
in both presynaptic and postsynaptic membranes. Our data disclose a novel interneuronal
network well suited for modulating the flow of information between the entorhinal
cortex and CA1 hippocampus.
author:
- first_name: Christopher
full_name: Price, Christopher J
last_name: Price
- first_name: Bruno
full_name: Cauli, Bruno
last_name: Cauli
- first_name: Endre
full_name: Kovács, Endre R
last_name: Kovács
- first_name: Ákos
full_name: Kulik, Ákos
last_name: Kulik
- first_name: Bertrand
full_name: Lambolez, Bertrand
last_name: Lambolez
- first_name: Ryuichi
full_name: Ryuichi Shigemoto
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Marco
full_name: Capogna,Marco
last_name: Capogna
citation:
ama: Price C, Cauli B, Kovács E, et al. Neurogliaform neurons form a novel inhibitory
network in the hippocampal CA1 area. Journal of Neuroscience. 2005;25(29):6775-6786.
doi:10.1523/JNEUROSCI.1135-05.2005
apa: Price, C., Cauli, B., Kovács, E., Kulik, Á., Lambolez, B., Shigemoto, R., &
Capogna, M. (2005). Neurogliaform neurons form a novel inhibitory network in the
hippocampal CA1 area. Journal of Neuroscience. Society for Neuroscience.
https://doi.org/10.1523/JNEUROSCI.1135-05.2005
chicago: Price, Christopher, Bruno Cauli, Endre Kovács, Ákos Kulik, Bertrand Lambolez,
Ryuichi Shigemoto, and Marco Capogna. “Neurogliaform Neurons Form a Novel Inhibitory
Network in the Hippocampal CA1 Area.” Journal of Neuroscience. Society
for Neuroscience, 2005. https://doi.org/10.1523/JNEUROSCI.1135-05.2005.
ieee: C. Price et al., “Neurogliaform neurons form a novel inhibitory network
in the hippocampal CA1 area,” Journal of Neuroscience, vol. 25, no. 29.
Society for Neuroscience, pp. 6775–6786, 2005.
ista: Price C, Cauli B, Kovács E, Kulik Á, Lambolez B, Shigemoto R, Capogna M. 2005.
Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area.
Journal of Neuroscience. 25(29), 6775–6786.
mla: Price, Christopher, et al. “Neurogliaform Neurons Form a Novel Inhibitory Network
in the Hippocampal CA1 Area.” Journal of Neuroscience, vol. 25, no. 29,
Society for Neuroscience, 2005, pp. 6775–86, doi:10.1523/JNEUROSCI.1135-05.2005.
short: C. Price, B. Cauli, E. Kovács, Á. Kulik, B. Lambolez, R. Shigemoto, M. Capogna,
Journal of Neuroscience 25 (2005) 6775–6786.
date_created: 2018-12-11T11:58:53Z
date_published: 2005-07-20T00:00:00Z
date_updated: 2021-01-12T06:58:50Z
day: '20'
doi: 10.1523/JNEUROSCI.1135-05.2005
extern: 1
intvolume: ' 25'
issue: '29'
month: '07'
page: 6775 - 6786
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '4245'
quality_controlled: 0
status: public
title: Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1
area
type: journal_article
volume: 25
year: '2005'
...
---
_id: '2653'
abstract:
- lang: eng
text: Synaptic vesicle release occurs at a specialized membrane domain known as
the presynaptic active zone (AZ). Several membrane proteins are involved in the
vesicle release processes such as docking, priming, and exocytotic fusion. Cytomatrix
at the active zone (CAZ) proteins are structural components of the AZ and are
highly concentrated in it. Localization of other release-related proteins including
target soluble N-ethylmaleimide-sensitive-factor attachment protein receptor (t-SNARE)
proteins, however, has not been well demonstrated in the AZ. Here, we used sodium
dodecyl sulfate-digested freeze-fracture replica labeling (SDS-FRL) to analyze
quantitatively the distribution of CAZ and t-SNARE proteins in the hippocampal
CA3 area. The AZ in replicated membrane was identified by immunolabeling for CAZ
proteins (CAZ-associated structural protein [CAST] and Bassoon). Clusters of immunogold
particles for these proteins were found on the P-face of presynaptic terminals
of the mossy fiber and associational/commissural (AJC) fiber. Co-labeling with
CAST revealed distribution of the t-SNARE proteins syntaxin and synaptosomal-associated
protein of 25 kDa (SNAP-25) in the AZ as well as in the extrasynaptic membrane
surrounding the AZ (SZ). Quantitative analysis demonstrated that the density of
immunoparticles for CAST in the AZ was more than 100 times higher than in the
SZ, whereas that for syntaxin and SNAP-25 was not significantly different between
the AZ and SZ in both the A/C and mossy fiber terminals. These results support
the involvement of the t-SNARE proteins in exocytotic fusion in the AZ and the
role of CAST in specialization of the membrane domain for the AZ.
author:
- first_name: Akari
full_name: Hagiwara, Akari
last_name: Hagiwara
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
- first_name: Maki
full_name: Deguchi-Tawarada, Maki
last_name: Deguchi Tawarada
- first_name: Toshihisa
full_name: Ohtsuka, Toshihisa
last_name: Ohtsuka
- first_name: Ryuichi
full_name: Ryuichi Shigemoto
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Hagiwara A, Fukazawa Y, Deguchi Tawarada M, Ohtsuka T, Shigemoto R. Differential
distribution of release-related proteins in the hippocampal CA3 area as revealed
by freeze-fracture replica labeling. Journal of Comparative Neurology.
2005;489(2):195-216. doi:10.1002/cne.20633
apa: Hagiwara, A., Fukazawa, Y., Deguchi Tawarada, M., Ohtsuka, T., & Shigemoto,
R. (2005). Differential distribution of release-related proteins in the hippocampal
CA3 area as revealed by freeze-fracture replica labeling. Journal of Comparative
Neurology. Wiley-Blackwell. https://doi.org/10.1002/cne.20633
chicago: Hagiwara, Akari, Yugo Fukazawa, Maki Deguchi Tawarada, Toshihisa Ohtsuka,
and Ryuichi Shigemoto. “Differential Distribution of Release-Related Proteins
in the Hippocampal CA3 Area as Revealed by Freeze-Fracture Replica Labeling.”
Journal of Comparative Neurology. Wiley-Blackwell, 2005. https://doi.org/10.1002/cne.20633.
ieee: A. Hagiwara, Y. Fukazawa, M. Deguchi Tawarada, T. Ohtsuka, and R. Shigemoto,
“Differential distribution of release-related proteins in the hippocampal CA3
area as revealed by freeze-fracture replica labeling,” Journal of Comparative
Neurology, vol. 489, no. 2. Wiley-Blackwell, pp. 195–216, 2005.
ista: Hagiwara A, Fukazawa Y, Deguchi Tawarada M, Ohtsuka T, Shigemoto R. 2005.
Differential distribution of release-related proteins in the hippocampal CA3 area
as revealed by freeze-fracture replica labeling. Journal of Comparative Neurology.
489(2), 195–216.
mla: Hagiwara, Akari, et al. “Differential Distribution of Release-Related Proteins
in the Hippocampal CA3 Area as Revealed by Freeze-Fracture Replica Labeling.”
Journal of Comparative Neurology, vol. 489, no. 2, Wiley-Blackwell, 2005,
pp. 195–216, doi:10.1002/cne.20633.
short: A. Hagiwara, Y. Fukazawa, M. Deguchi Tawarada, T. Ohtsuka, R. Shigemoto,
Journal of Comparative Neurology 489 (2005) 195–216.
date_created: 2018-12-11T11:58:53Z
date_published: 2005-08-22T00:00:00Z
date_updated: 2021-01-12T06:58:50Z
day: '22'
doi: 10.1002/cne.20633
extern: 1
intvolume: ' 489'
issue: '2'
month: '08'
page: 195 - 216
publication: Journal of Comparative Neurology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '4244'
quality_controlled: 0
status: public
title: Differential distribution of release-related proteins in the hippocampal CA3
area as revealed by freeze-fracture replica labeling
type: journal_article
volume: 489
year: '2005'
...
---
_id: '2654'
abstract:
- lang: eng
text: Presynaptic metabotropic glutamate receptors (mGluRs) show a highly selective
expression and subcellular location in nerve terminals modulating neurotransmitter
release. We have demonstrated that alternatively spliced variants of mGluR8, mGluR8a
and mGluR8b, have an overlapping distribution in the hippocampus, and besides
perforant path terminals, they are expressed in the presynaptic active zone of
boutons making synapses selectively with several types of GABAergic interneurons,
primarily in the stratum oriens. Boutons labeled for mGluR8 formed either type
I or type II synapses, and the latter were GABAergic. Some mGluR8-positive boutons
also expressed mGluR7 or vasoactive intestinal polypeptide. Interneurons strongly
immunopositive for the muscarinic M2 or the mGlu1 receptors were the primary targets
of mGluR8-containing terminals in the stratum oriens, but only neurochemically
distinct subsets were innervated by mGluR8-enriched terminals. The majority of
M2-positive neurons were mGluR8 innervated, but a minority, which expresses somatostatin,
was not. Rare neurons coexpressing calretinin and M2 were consistently targeted
by mGluR8-positive boutons. In vivo recording and labeling of an mGluR8-decorated
and strongly M2-positive interneuron revealed a trilaminar cell with complex spike
bursts during theta oscillations and strong discharge during sharp wave/ripple
events. The trilaminar cell had a large projection from the CA1 area to the subiculum
and a preferential innervation of interneurons in the CA1 area in addition to
pyramidal cell somata and dendrites. The postsynaptic interneuron type-specific
expression of the high-efficacy presynaptic mGluR8 in both putative glutamatergic
and in identified GABAergic terminals predicts a role in adjusting the activity
of interneurons depending on the level of network activity.
author:
- first_name: Francesco
full_name: Ferraguti, Francesco
last_name: Ferraguti
- first_name: Thomas
full_name: Klausberger,Thomas
last_name: Klausberger
- first_name: Philip
full_name: Cobden, Philip M
last_name: Cobden
- first_name: Agnès
full_name: Baude, Agnès
last_name: Baude
- first_name: John
full_name: Roberts, John D
last_name: Roberts
- first_name: Péter
full_name: Szűcs, Péter
last_name: Szűcs
- first_name: Ayae
full_name: Kinoshita, Ayae
last_name: Kinoshita
- first_name: Ryuichi
full_name: Ryuichi Shigemoto
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Péter
full_name: Somogyi, Péter
last_name: Somogyi
- first_name: Yannis
full_name: Dalezios, Yannis
last_name: Dalezios
citation:
ama: Ferraguti F, Klausberger T, Cobden P, et al. Metabotropic glutamate receptor
8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus.
Journal of Neuroscience. 2005;25(45):10520-10536. doi:10.1523/JNEUROSCI.2547-05.2005
apa: Ferraguti, F., Klausberger, T., Cobden, P., Baude, A., Roberts, J., Szűcs,
P., … Dalezios, Y. (2005). Metabotropic glutamate receptor 8-expressing nerve
terminals target subsets of GABAergic neurons in the hippocampus. Journal of
Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.2547-05.2005
chicago: Ferraguti, Francesco, Thomas Klausberger, Philip Cobden, Agnès Baude, John
Roberts, Péter Szűcs, Ayae Kinoshita, Ryuichi Shigemoto, Péter Somogyi, and Yannis
Dalezios. “ Metabotropic Glutamate Receptor 8-Expressing Nerve Terminals Target
Subsets of GABAergic Neurons in the Hippocampus.” Journal of Neuroscience.
Society for Neuroscience, 2005. https://doi.org/10.1523/JNEUROSCI.2547-05.2005.
ieee: F. Ferraguti et al., “ Metabotropic glutamate receptor 8-expressing
nerve terminals target subsets of GABAergic neurons in the hippocampus,” Journal
of Neuroscience, vol. 25, no. 45. Society for Neuroscience, pp. 10520–10536,
2005.
ista: Ferraguti F, Klausberger T, Cobden P, Baude A, Roberts J, Szűcs P, Kinoshita
A, Shigemoto R, Somogyi P, Dalezios Y. 2005. Metabotropic glutamate receptor
8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus.
Journal of Neuroscience. 25(45), 10520–10536.
mla: Ferraguti, Francesco, et al. “ Metabotropic Glutamate Receptor 8-Expressing
Nerve Terminals Target Subsets of GABAergic Neurons in the Hippocampus.” Journal
of Neuroscience, vol. 25, no. 45, Society for Neuroscience, 2005, pp. 10520–36,
doi:10.1523/JNEUROSCI.2547-05.2005.
short: F. Ferraguti, T. Klausberger, P. Cobden, A. Baude, J. Roberts, P. Szűcs,
A. Kinoshita, R. Shigemoto, P. Somogyi, Y. Dalezios, Journal of Neuroscience 25
(2005) 10520–10536.
date_created: 2018-12-11T11:58:53Z
date_published: 2005-11-09T00:00:00Z
date_updated: 2021-01-12T06:58:51Z
day: '09'
doi: 10.1523/JNEUROSCI.2547-05.2005
extern: 1
intvolume: ' 25'
issue: '45'
month: '11'
page: 10520 - 10536
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '4242'
quality_controlled: 0
status: public
title: ' Metabotropic glutamate receptor 8-expressing nerve terminals target subsets
of GABAergic neurons in the hippocampus'
type: journal_article
volume: 25
year: '2005'
...
---
_id: '2655'
abstract:
- lang: eng
text: Input-dependent left-right asymmetry of NMDA receptor ε2 (NR2B) subunit allocation
was discovered in hippocampal Schaffer collateral (Sch) and commissural fiber
pyramidal cell synapses (Kawakami et al., 2003). To investigate whether this asymmetrical
ε2 allocation is also related to the types of the postsynaptic cells, we compared
postembedding immunogold labeling for ε2 in left and right Sch synapses on pyramidal
cells and interneurons. To facilitate the detection of ε2 density difference,
we used ε1 (NR2A) knock-out (KO) mice, which have a simplified NMDA receptor subunit
composition. The labeling density for ε2 but not ζ1 (NR1) and subtype 2/3 glutamate
receptor (GluR2/3) in Sch-CA1 pyramidal cell synapses was significantly different
between the left and right hippocampus with opposite directions in strata oriens
and radiatum; the left to right ratio of ε2 labeling density was 1:1.50 in stratum
oriens and 1.44:1 in stratum radiatum. No significant difference, however, was
detected in CA1 stratum radiatum between the left and right Sch-GluR4-positive
(mostly parvalbumin-positive) and Sch-GluR4-negative interneuron synapses. Consistent
with the anatomical asymmetry, the amplitude ratio of NMDA EPSCs to non-NMDA EPSCs
in pyramidal cells was approximately two times larger in right than left stratum
radiatum and vice versa in stratum oriens of ε1 KO mice. Moreover, the amplitude
of long-term potentiation in the Sch-CA1 synapses of left stratum radiatum was
significantly larger than that in the right corresponding synapses. These results
indicate that the asymmetry of ε2 distribution is target cell specific, resulting
in the left-right difference in NMDA receptor content and plasticity in Sch-CA1
pyramidal cell synapses in ε1 KO mice.
author:
- first_name: Yue
full_name: Wu, Yue
last_name: Wu
- first_name: Ryosuke
full_name: Kawakami, Ryosuke
last_name: Kawakami
- first_name: Yoshiaki
full_name: Shinohara, Yoshiaki
last_name: Shinohara
- first_name: Masahiro
full_name: Fukaya, Masahiro
last_name: Fukaya
- first_name: Kenji
full_name: Sakimura, Kenji
last_name: Sakimura
- first_name: Masayoshi
full_name: Mishina, Masayoshi
last_name: Mishina
- first_name: Masahiko
full_name: Watanabe, Masahiko
last_name: Watanabe
- first_name: Isao
full_name: Ito, Isao
last_name: Ito
- first_name: Ryuichi
full_name: Ryuichi Shigemoto
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Wu Y, Kawakami R, Shinohara Y, et al. Target-cell-specific left-right asymmetry
of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out
mice. Journal of Neuroscience. 2005;25(40):9213-9226. doi:10.1523/JNEUROSCI.2134-05.2005
apa: Wu, Y., Kawakami, R., Shinohara, Y., Fukaya, M., Sakimura, K., Mishina, M.,
… Shigemoto, R. (2005). Target-cell-specific left-right asymmetry of NMDA receptor
content in Schaffer collateral synapses in ε1/NR2A knock-out mice. Journal
of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.2134-05.2005
chicago: Wu, Yue, Ryosuke Kawakami, Yoshiaki Shinohara, Masahiro Fukaya, Kenji Sakimura,
Masayoshi Mishina, Masahiko Watanabe, Isao Ito, and Ryuichi Shigemoto. “Target-Cell-Specific
Left-Right Asymmetry of NMDA Receptor Content in Schaffer Collateral Synapses
in Ε1/NR2A Knock-out Mice.” Journal of Neuroscience. Society for Neuroscience,
2005. https://doi.org/10.1523/JNEUROSCI.2134-05.2005.
ieee: Y. Wu et al., “Target-cell-specific left-right asymmetry of NMDA receptor
content in Schaffer collateral synapses in ε1/NR2A knock-out mice,” Journal
of Neuroscience, vol. 25, no. 40. Society for Neuroscience, pp. 9213–9226,
2005.
ista: Wu Y, Kawakami R, Shinohara Y, Fukaya M, Sakimura K, Mishina M, Watanabe M,
Ito I, Shigemoto R. 2005. Target-cell-specific left-right asymmetry of NMDA receptor
content in Schaffer collateral synapses in ε1/NR2A knock-out mice. Journal of
Neuroscience. 25(40), 9213–9226.
mla: Wu, Yue, et al. “Target-Cell-Specific Left-Right Asymmetry of NMDA Receptor
Content in Schaffer Collateral Synapses in Ε1/NR2A Knock-out Mice.” Journal
of Neuroscience, vol. 25, no. 40, Society for Neuroscience, 2005, pp. 9213–26,
doi:10.1523/JNEUROSCI.2134-05.2005.
short: Y. Wu, R. Kawakami, Y. Shinohara, M. Fukaya, K. Sakimura, M. Mishina, M.
Watanabe, I. Ito, R. Shigemoto, Journal of Neuroscience 25 (2005) 9213–9226.
date_created: 2018-12-11T11:58:54Z
date_published: 2005-10-05T00:00:00Z
date_updated: 2021-01-12T06:58:51Z
day: '05'
doi: 10.1523/JNEUROSCI.2134-05.2005
extern: 1
intvolume: ' 25'
issue: '40'
month: '10'
page: 9213 - 9226
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '4243'
quality_controlled: 0
status: public
title: Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer
collateral synapses in ε1/NR2A knock-out mice
type: journal_article
volume: 25
year: '2005'
...
---
_id: '2656'
abstract:
- lang: eng
text: Previous studies have shown that neurons in the sacral dorsal commissural
nucleus (SDCN) express neurokinin-1 receptor (NK1R) and can be modulated by the
co-release of GABA and glycine (Gly) from single presynaptic terminal. These results
raise the possibility that GABA/Gly-cocontaining terminals might make synaptic
contacts with NK1R-expressing neurons in the SDCN. In order to provide morphological
evidence for this hypothesis, the triple-immunohistochemical studies were performed
in the SDCN. Triple-immunofluorescence histochemical study showed that some axon
terminals in close association with NK1R-immunopositive (NK1R-ip) neurons in the
SDCN were immunopositive for both glutamic acid decarboxylase (GAD) and glycine
transporter 2 (GlyT2). In electron microscopic dual- and triple-immunohistochemistry
for GAD/GlyT2, GAD/NK1R, GlyT2/NK1R, or GAD/GlyT2/NK1R also revealed dually labeled
(GAD/GlyT2-ip) synaptic terminals upon SDCN neurons, as well as GAD- and/or GlyT2-ip
axon terminals in synaptic contact with NK1R-ip SDCN neurons. These results suggested
that some synaptic terminals upon NK1R-expressing SDCN neurons co-released both
GABA and Gly.
author:
- first_name: Yu
full_name: Feng, Yu-Peng
last_name: Feng
- first_name: Yun
full_name: Li, Yun-Qing
last_name: Li
- first_name: Wen
full_name: Wang, Wen
last_name: Wang
- first_name: Sheng
full_name: Wu, Sheng-Xi
last_name: Wu
- first_name: Tao
full_name: Chen, Tao
last_name: Chen
- first_name: Ryuichi
full_name: Ryuichi Shigemoto
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Noboru
full_name: Mizuno, Noboru
last_name: Mizuno
citation:
ama: Feng Y, Li Y, Wang W, et al. Morphological evidence for GABA/glycine-cocontaining
terminals in synaptic contact with neurokinin-1 receptor-expressing neurons in
the sacral dorsal commissural nucleus of the rat. Neuroscience Letters.
2005;388(3):144-148. doi:10.1016/j.neulet.2005.06.068
apa: Feng, Y., Li, Y., Wang, W., Wu, S., Chen, T., Shigemoto, R., & Mizuno,
N. (2005). Morphological evidence for GABA/glycine-cocontaining terminals in synaptic
contact with neurokinin-1 receptor-expressing neurons in the sacral dorsal commissural
nucleus of the rat. Neuroscience Letters. Elsevier. https://doi.org/10.1016/j.neulet.2005.06.068
chicago: Feng, Yu, Yun Li, Wen Wang, Sheng Wu, Tao Chen, Ryuichi Shigemoto, and
Noboru Mizuno. “Morphological Evidence for GABA/Glycine-Cocontaining Terminals
in Synaptic Contact with Neurokinin-1 Receptor-Expressing Neurons in the Sacral
Dorsal Commissural Nucleus of the Rat.” Neuroscience Letters. Elsevier,
2005. https://doi.org/10.1016/j.neulet.2005.06.068.
ieee: Y. Feng et al., “Morphological evidence for GABA/glycine-cocontaining
terminals in synaptic contact with neurokinin-1 receptor-expressing neurons in
the sacral dorsal commissural nucleus of the rat,” Neuroscience Letters,
vol. 388, no. 3. Elsevier, pp. 144–148, 2005.
ista: Feng Y, Li Y, Wang W, Wu S, Chen T, Shigemoto R, Mizuno N. 2005. Morphological
evidence for GABA/glycine-cocontaining terminals in synaptic contact with neurokinin-1
receptor-expressing neurons in the sacral dorsal commissural nucleus of the rat.
Neuroscience Letters. 388(3), 144–148.
mla: Feng, Yu, et al. “Morphological Evidence for GABA/Glycine-Cocontaining Terminals
in Synaptic Contact with Neurokinin-1 Receptor-Expressing Neurons in the Sacral
Dorsal Commissural Nucleus of the Rat.” Neuroscience Letters, vol. 388,
no. 3, Elsevier, 2005, pp. 144–48, doi:10.1016/j.neulet.2005.06.068.
short: Y. Feng, Y. Li, W. Wang, S. Wu, T. Chen, R. Shigemoto, N. Mizuno, Neuroscience
Letters 388 (2005) 144–148.
date_created: 2018-12-11T11:58:54Z
date_published: 2005-11-18T00:00:00Z
date_updated: 2021-01-12T06:58:51Z
day: '18'
doi: 10.1016/j.neulet.2005.06.068
extern: 1
intvolume: ' 388'
issue: '3'
month: '11'
page: 144 - 148
publication: Neuroscience Letters
publication_status: published
publisher: Elsevier
publist_id: '4241'
quality_controlled: 0
status: public
title: Morphological evidence for GABA/glycine-cocontaining terminals in synaptic
contact with neurokinin-1 receptor-expressing neurons in the sacral dorsal commissural
nucleus of the rat
type: journal_article
volume: 388
year: '2005'
...
---
_id: '2658'
abstract:
- lang: eng
text: Enhanced glutamatergic neurotransmission via the subthalamopallidal or subthalamonigral
projection seems crucial for developing parkinsonian motor signs. In the present
study, the possible changes in the expression of metabotropic glutamate receptors
(mGluRs) were examined in the basal ganglia of a primate model for Parkinson's
disease. When the patterns of immunohistochemical localization of mGluRs in monkeys
administered systemically with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)
were analysed in comparison with normal controls, we found that expression of
mGluR1α, but not of other subtypes, was significantly reduced in the internal
and external segments of the globus pallidus and the substantia nigra pars reticulata.
To elucidate the functional role of mGluR1 in the control of pallidal neuron activity,
extracellular unit recordings combined with intrapallidal microinjections of mGluR1-related
agents were then performed in normal and parkinsonian monkeys. In normal awake
conditions, the spontaneous firing rates of neurons in the pallidal complex were
increased by DHPG, a selective agonist of group I mGluRs, whereas they were decreased
by AIDA, a selective antagonist of group I mGluRs, or LY367385, a selective antagonist
of mGluR1. These electrophysiological data strongly indicate that the excitatory
mechanism of pallidal neurons by glutamate is mediated at least partly through
mGluR1. The effects of the mGluR1-related agents on neuronal firing in the internal
pallidal segment became rather obscure after MPTP treatment. Our results suggest
that the specific down-regulation of pallidal and nigral mGluR1 ot in the parkinsonian
state may exert a compensatory action to reverse the overactivity of the subthalamic
nucleus-derived glutamatergic input that is generated in the disease.
author:
- first_name: Katsuyuki
full_name: Kaneda, Katsuyuki
last_name: Kaneda
- first_name: Yoshihisa
full_name: Tachibana, Yoshihisa
last_name: Tachibana
- first_name: Michiko
full_name: Imanishi, Michiko
last_name: Imanishi
- first_name: Hitoshi
full_name: Kita, Hitoshi
last_name: Kita
- first_name: Ryuichi
full_name: Ryuichi Shigemoto
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Atsushi
full_name: Nambu, Atsushi
last_name: Nambu
- first_name: Masahiko
full_name: Takada, Masahiko
last_name: Takada
citation:
ama: Kaneda K, Tachibana Y, Imanishi M, et al. Down-regulation of metabotropic glutamate
receptor 1α in globus pallidus and substantia nigra of parkinsonian monkeys. European
Journal of Neuroscience. 2005;22(12):3241-3254. doi:10.1111/j.1460-9568.2005.04488.x
apa: Kaneda, K., Tachibana, Y., Imanishi, M., Kita, H., Shigemoto, R., Nambu, A.,
& Takada, M. (2005). Down-regulation of metabotropic glutamate receptor 1α
in globus pallidus and substantia nigra of parkinsonian monkeys. European Journal
of Neuroscience. Wiley-Blackwell. https://doi.org/10.1111/j.1460-9568.2005.04488.x
chicago: Kaneda, Katsuyuki, Yoshihisa Tachibana, Michiko Imanishi, Hitoshi Kita,
Ryuichi Shigemoto, Atsushi Nambu, and Masahiko Takada. “Down-Regulation of Metabotropic
Glutamate Receptor 1α in Globus Pallidus and Substantia Nigra of Parkinsonian
Monkeys.” European Journal of Neuroscience. Wiley-Blackwell, 2005. https://doi.org/10.1111/j.1460-9568.2005.04488.x.
ieee: K. Kaneda et al., “Down-regulation of metabotropic glutamate receptor
1α in globus pallidus and substantia nigra of parkinsonian monkeys,” European
Journal of Neuroscience, vol. 22, no. 12. Wiley-Blackwell, pp. 3241–3254,
2005.
ista: Kaneda K, Tachibana Y, Imanishi M, Kita H, Shigemoto R, Nambu A, Takada M.
2005. Down-regulation of metabotropic glutamate receptor 1α in globus pallidus
and substantia nigra of parkinsonian monkeys. European Journal of Neuroscience.
22(12), 3241–3254.
mla: Kaneda, Katsuyuki, et al. “Down-Regulation of Metabotropic Glutamate Receptor
1α in Globus Pallidus and Substantia Nigra of Parkinsonian Monkeys.” European
Journal of Neuroscience, vol. 22, no. 12, Wiley-Blackwell, 2005, pp. 3241–54,
doi:10.1111/j.1460-9568.2005.04488.x.
short: K. Kaneda, Y. Tachibana, M. Imanishi, H. Kita, R. Shigemoto, A. Nambu, M.
Takada, European Journal of Neuroscience 22 (2005) 3241–3254.
date_created: 2018-12-11T11:58:55Z
date_published: 2005-12-01T00:00:00Z
date_updated: 2021-01-12T06:58:52Z
day: '01'
doi: 10.1111/j.1460-9568.2005.04488.x
extern: 1
intvolume: ' 22'
issue: '12'
month: '12'
page: 3241 - 3254
publication: European Journal of Neuroscience
publication_status: published
publisher: Wiley-Blackwell
publist_id: '4240'
quality_controlled: 0
status: public
title: Down-regulation of metabotropic glutamate receptor 1α in globus pallidus and
substantia nigra of parkinsonian monkeys
type: journal_article
volume: 22
year: '2005'
...
---
_id: '2743'
abstract:
- lang: eng
text: We consider the supersymmetric quantum mechanical system which is obtained
by dimensionally reducing d = 6, N = 1 supersymmetric gauge theory with gauge
group U(1) and a single charged hypermultiplet. Using the deformation method and
ideas introduced by Porrati and Rozenberg [1], we present a detailed proof of
the existence of a normalizable ground state for this system.
author:
- first_name: László
full_name: László Erdös
id: 4DBD5372-F248-11E8-B48F-1D18A9856A87
last_name: Erdös
orcid: 0000-0001-5366-9603
- first_name: David
full_name: Hasler, David G
last_name: Hasler
- first_name: Jan
full_name: Solovej, Jan P
last_name: Solovej
citation:
ama: 'Erdös L, Hasler D, Solovej J. Existence of the D0-D4 bound state: A detailed
proof. Annales Henri Poincare. 2005;6(2):247-267. doi:10.1007/s00023-005-0205-0'
apa: 'Erdös, L., Hasler, D., & Solovej, J. (2005). Existence of the D0-D4 bound
state: A detailed proof. Annales Henri Poincare. Birkhäuser. https://doi.org/10.1007/s00023-005-0205-0'
chicago: 'Erdös, László, David Hasler, and Jan Solovej. “Existence of the D0-D4
Bound State: A Detailed Proof.” Annales Henri Poincare. Birkhäuser, 2005.
https://doi.org/10.1007/s00023-005-0205-0.'
ieee: 'L. Erdös, D. Hasler, and J. Solovej, “Existence of the D0-D4 bound state:
A detailed proof,” Annales Henri Poincare, vol. 6, no. 2. Birkhäuser, pp.
247–267, 2005.'
ista: 'Erdös L, Hasler D, Solovej J. 2005. Existence of the D0-D4 bound state: A
detailed proof. Annales Henri Poincare. 6(2), 247–267.'
mla: 'Erdös, László, et al. “Existence of the D0-D4 Bound State: A Detailed Proof.”
Annales Henri Poincare, vol. 6, no. 2, Birkhäuser, 2005, pp. 247–67, doi:10.1007/s00023-005-0205-0.'
short: L. Erdös, D. Hasler, J. Solovej, Annales Henri Poincare 6 (2005) 247–267.
date_created: 2018-12-11T11:59:22Z
date_published: 2005-04-01T00:00:00Z
date_updated: 2021-01-12T06:59:24Z
day: '01'
doi: 10.1007/s00023-005-0205-0
extern: 1
intvolume: ' 6'
issue: '2'
month: '04'
page: 247 - 267
publication: Annales Henri Poincare
publication_status: published
publisher: Birkhäuser
publist_id: '4149'
quality_controlled: 0
status: public
title: 'Existence of the D0-D4 bound state: A detailed proof'
type: journal_article
volume: 6
year: '2005'
...
---
_id: '2744'
abstract:
- lang: eng
text: We study the long time evolution of a quantum particle interacting with a
random potential in the Boltzmann-Grad low density limit. We prove that the phase
space density of the quantum evolution defined through the Husimi function converges
weakly to a linear Boltzmann equation. The Boltzmann collision kernel is given
by the full quantum scattering cross-section of the obstacle potential.
author:
- first_name: David
full_name: Eng, David
last_name: Eng
- first_name: László
full_name: László Erdös
id: 4DBD5372-F248-11E8-B48F-1D18A9856A87
last_name: Erdös
orcid: 0000-0001-5366-9603
citation:
ama: Eng D, Erdös L. The linear Boltzmann equation as the low density limit of a
random Schrödinger equation. Reviews in Mathematical Physics. 2005;17(6):669-743.
doi:10.1142/S0129055X0500242X
apa: Eng, D., & Erdös, L. (2005). The linear Boltzmann equation as the low density
limit of a random Schrödinger equation. Reviews in Mathematical Physics.
World Scientific Publishing. https://doi.org/10.1142/S0129055X0500242X
chicago: Eng, David, and László Erdös. “The Linear Boltzmann Equation as the Low
Density Limit of a Random Schrödinger Equation.” Reviews in Mathematical Physics.
World Scientific Publishing, 2005. https://doi.org/10.1142/S0129055X0500242X.
ieee: D. Eng and L. Erdös, “The linear Boltzmann equation as the low density limit
of a random Schrödinger equation,” Reviews in Mathematical Physics, vol.
17, no. 6. World Scientific Publishing, pp. 669–743, 2005.
ista: Eng D, Erdös L. 2005. The linear Boltzmann equation as the low density limit
of a random Schrödinger equation. Reviews in Mathematical Physics. 17(6), 669–743.
mla: Eng, David, and László Erdös. “The Linear Boltzmann Equation as the Low Density
Limit of a Random Schrödinger Equation.” Reviews in Mathematical Physics,
vol. 17, no. 6, World Scientific Publishing, 2005, pp. 669–743, doi:10.1142/S0129055X0500242X.
short: D. Eng, L. Erdös, Reviews in Mathematical Physics 17 (2005) 669–743.
date_created: 2018-12-11T11:59:22Z
date_published: 2005-07-01T00:00:00Z
date_updated: 2021-01-12T06:59:25Z
day: '01'
doi: 10.1142/S0129055X0500242X
extern: 1
intvolume: ' 17'
issue: '6'
month: '07'
page: 669 - 743
publication: Reviews in Mathematical Physics
publication_status: published
publisher: World Scientific Publishing
publist_id: '4148'
quality_controlled: 0
status: public
title: The linear Boltzmann equation as the low density limit of a random Schrödinger
equation
type: journal_article
volume: 17
year: '2005'
...
---
_id: '2788'
abstract:
- lang: eng
text: We present the results of an experimental investigation into the nature and
structure of turbulent pipe flow at moderate Reynolds numbers. A turbulence regeneration
mechanism is identified which sustains a symmetric traveling wave within the flow.
The periodicity of the mechanism allows comparison to the wavelength of numerically
observed exact traveling wave solutions and close agreement is found. The advection
speed of the upstream turbulence laminar interface in the experimental flow is
observed to form a lower bound on the phase velocities of the exact traveling
wave solutions. Overall our observations suggest that the dynamics of the turbulent
flow at moderate Reynolds numbers are governed by unstable nonlinear traveling
waves.
author:
- first_name: Björn
full_name: Björn Hof
id: 3A374330-F248-11E8-B48F-1D18A9856A87
last_name: Hof
orcid: 0000-0003-2057-2754
- first_name: Casimir
full_name: van Doorne, Casimir W
last_name: Van Doorne
- first_name: Jerry
full_name: Westerweel, Jerry
last_name: Westerweel
- first_name: Frans
full_name: Nieuwstadt, Frans T
last_name: Nieuwstadt
citation:
ama: Hof B, Van Doorne C, Westerweel J, Nieuwstadt F. Turbulence regeneration in
pipe flow at moderate reynolds numbers. Physical Review Letters. 2005;95(21).
doi:10.1103/PhysRevLett.95.214502
apa: Hof, B., Van Doorne, C., Westerweel, J., & Nieuwstadt, F. (2005). Turbulence
regeneration in pipe flow at moderate reynolds numbers. Physical Review Letters.
American Physical Society. https://doi.org/10.1103/PhysRevLett.95.214502
chicago: Hof, Björn, Casimir Van Doorne, Jerry Westerweel, and Frans Nieuwstadt.
“Turbulence Regeneration in Pipe Flow at Moderate Reynolds Numbers.” Physical
Review Letters. American Physical Society, 2005. https://doi.org/10.1103/PhysRevLett.95.214502.
ieee: B. Hof, C. Van Doorne, J. Westerweel, and F. Nieuwstadt, “Turbulence regeneration
in pipe flow at moderate reynolds numbers,” Physical Review Letters, vol.
95, no. 21. American Physical Society, 2005.
ista: Hof B, Van Doorne C, Westerweel J, Nieuwstadt F. 2005. Turbulence regeneration
in pipe flow at moderate reynolds numbers. Physical Review Letters. 95(21).
mla: Hof, Björn, et al. “Turbulence Regeneration in Pipe Flow at Moderate Reynolds
Numbers.” Physical Review Letters, vol. 95, no. 21, American Physical Society,
2005, doi:10.1103/PhysRevLett.95.214502.
short: B. Hof, C. Van Doorne, J. Westerweel, F. Nieuwstadt, Physical Review Letters
95 (2005).
date_created: 2018-12-11T11:59:36Z
date_published: 2005-11-17T00:00:00Z
date_updated: 2021-01-12T06:59:43Z
day: '17'
doi: 10.1103/PhysRevLett.95.214502
extern: 1
intvolume: ' 95'
issue: '21'
month: '11'
publication: Physical Review Letters
publication_status: published
publisher: American Physical Society
publist_id: '4101'
quality_controlled: 0
status: public
title: Turbulence regeneration in pipe flow at moderate reynolds numbers
type: journal_article
volume: 95
year: '2005'
...
---
_id: '2789'
abstract:
- lang: eng
text: Transitional pipe flow is investigated in two different experimental set-ups.
In the first the stability threshold and the initial growth of localized perturbations
are studied. Good agreement is found with an earlier investigation of the transition
threshold. The measurement technique applied in the last part of this study allows
the reconstruction of the streamwise vorticity in a turbulent puff.
author:
- first_name: Björn
full_name: Björn Hof
id: 3A374330-F248-11E8-B48F-1D18A9856A87
last_name: Hof
orcid: 0000-0003-2057-2754
citation:
ama: Hof B. Transition to turbulence in pipe flow. Fluid Mechanics and its Applications.
2005;77:221-231. doi:10.1007/1-4020-4049-0_12
apa: Hof, B. (2005). Transition to turbulence in pipe flow. Fluid Mechanics and
Its Applications. Springer. https://doi.org/10.1007/1-4020-4049-0_12
chicago: Hof, Björn. “Transition to Turbulence in Pipe Flow.” Fluid Mechanics
and Its Applications. Springer, 2005. https://doi.org/10.1007/1-4020-4049-0_12.
ieee: B. Hof, “Transition to turbulence in pipe flow,” Fluid Mechanics and its
Applications, vol. 77. Springer, pp. 221–231, 2005.
ista: Hof B. 2005. Transition to turbulence in pipe flow. Fluid Mechanics and its
Applications. 77, 221–231.
mla: Hof, Björn. “Transition to Turbulence in Pipe Flow.” Fluid Mechanics and
Its Applications, vol. 77, Springer, 2005, pp. 221–31, doi:10.1007/1-4020-4049-0_12.
short: B. Hof, Fluid Mechanics and Its Applications 77 (2005) 221–231.
date_created: 2018-12-11T11:59:36Z
date_published: 2005-09-19T00:00:00Z
date_updated: 2021-01-12T06:59:43Z
day: '19'
doi: 10.1007/1-4020-4049-0_12
extern: 1
intvolume: ' 77'
month: '09'
page: 221 - 231
publication: Fluid Mechanics and its Applications
publication_status: published
publisher: Springer
publist_id: '4100'
quality_controlled: 0
status: public
title: Transition to turbulence in pipe flow
type: journal_article
volume: 77
year: '2005'
...
---
_id: '2790'
abstract:
- lang: eng
text: We present the results of an experimental investigation of the effect of a
magnetic field on the stability of convection in a liquid metal. A rectangular
container of gallium is subjected to a horizontal temperature gradient and a uniform
magnetic field is applied separately in three directions. The magnetic field suppresses
the oscillation most effectively when it is applied in the vertical direction
and is least efficient when applied in the direction of the temperature gradient.
The critical temperature difference required for the onset of oscillations is
found to scale exponentially with the magnitude of the magnetic field for all
three orientations. Comparisons are made with available theory and qualitative
differences are discussed.
author:
- first_name: Björn
full_name: Björn Hof
id: 3A374330-F248-11E8-B48F-1D18A9856A87
last_name: Hof
orcid: 0000-0003-2057-2754
- first_name: Anne
full_name: Juel, Anne
last_name: Juel
- first_name: Tom
full_name: Mullin, Tom P
last_name: Mullin
citation:
ama: Hof B, Juel A, Mullin T. Magnetohydrodynamic damping of oscillations in low-Prandtl-number
convection. Journal of Fluid Mechanics. 2005;545:193-201. doi:10.1017/S0022112005006762
apa: Hof, B., Juel, A., & Mullin, T. (2005). Magnetohydrodynamic damping of
oscillations in low-Prandtl-number convection. Journal of Fluid Mechanics.
Cambridge University Press. https://doi.org/10.1017/S0022112005006762
chicago: Hof, Björn, Anne Juel, and Tom Mullin. “Magnetohydrodynamic Damping of
Oscillations in Low-Prandtl-Number Convection.” Journal of Fluid Mechanics.
Cambridge University Press, 2005. https://doi.org/10.1017/S0022112005006762.
ieee: B. Hof, A. Juel, and T. Mullin, “Magnetohydrodynamic damping of oscillations
in low-Prandtl-number convection,” Journal of Fluid Mechanics, vol. 545.
Cambridge University Press, pp. 193–201, 2005.
ista: Hof B, Juel A, Mullin T. 2005. Magnetohydrodynamic damping of oscillations
in low-Prandtl-number convection. Journal of Fluid Mechanics. 545, 193–201.
mla: Hof, Björn, et al. “Magnetohydrodynamic Damping of Oscillations in Low-Prandtl-Number
Convection.” Journal of Fluid Mechanics, vol. 545, Cambridge University
Press, 2005, pp. 193–201, doi:10.1017/S0022112005006762.
short: B. Hof, A. Juel, T. Mullin, Journal of Fluid Mechanics 545 (2005) 193–201.
date_created: 2018-12-11T11:59:37Z
date_published: 2005-12-25T00:00:00Z
date_updated: 2021-01-12T06:59:44Z
day: '25'
doi: 10.1017/S0022112005006762
extern: 1
intvolume: ' 545'
month: '12'
page: 193 - 201
publication: Journal of Fluid Mechanics
publication_status: published
publisher: Cambridge University Press
publist_id: '4099'
quality_controlled: 0
status: public
title: Magnetohydrodynamic damping of oscillations in low-Prandtl-number convection
type: journal_article
volume: 545
year: '2005'
...
---
_id: '2867'
abstract:
- lang: eng
text: The plant hormone auxin elicits many specific context-dependent developmental
responses. Auxin promotes degradation of Aux/IAA proteins that prevent transcription
factors of the auxin response factor (ARF) family from regulating auxin-responsive
target genes. Aux/IAAs and ARFs are represented by large gene families in Arabidopsis.
Here we show that stabilization of BDL/IAA12 or its sister protein IAA13 prevents
MP/ARF5-dependent embryonic root formation whereas stabilized SHY2/IAA3 interferes
with seedling growth. Although both bdl and shy2-2 proteins inhibited MP/ARF5-dependent
reporter gene activation, shy2-2 was much less efficient than bdl to interfere
with embryonic root initiation when expressed from the BDL promoter. Similarly,
MP was much more efficient than ARF16 in this process. When expressed from the
SHY2 promoter, both shy2-2 and bdl inhibited cell elongation and auxin-induced
gene expression in the seedling hypocotyl. By contrast, gravitropism and auxin-induced
gene expression in the root, which were promoted by functionally redundant NPH4/ARF7
and ARF19 proteins, were inhibited by shy2-2, but not by bdl protein. Our results
suggest that auxin signals are converted into specific responses by matching pairs
of coexpressed ARF and Aux/IAA proteins.
author:
- first_name: Dolf
full_name: Weijers, Dolf
last_name: Weijers
- first_name: Eva
full_name: Eva Benková
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
- first_name: Katja
full_name: Jäger, Katja E
last_name: Jäger
- first_name: Alexandra
full_name: Schlereth, Alexandra
last_name: Schlereth
- first_name: Thorsten
full_name: Hamann, Thorsten
last_name: Hamann
- first_name: Marika
full_name: Kientz, Marika
last_name: Kientz
- first_name: Jill
full_name: Wilmoth, Jill C
last_name: Wilmoth
- first_name: Jason
full_name: Reed, Jason W
last_name: Reed
- first_name: Gerd
full_name: Jürgens, Gerd
last_name: Jürgens
citation:
ama: Weijers D, Benková E, Jäger K, et al. Developmental specificity of auxin response
by pairs of ARF and Aux/IAA transcriptional regulators. EMBO Journal. 2005;24(10):1874-1885.
doi:10.1038/sj.emboj.7600659
apa: Weijers, D., Benková, E., Jäger, K., Schlereth, A., Hamann, T., Kientz, M.,
… Jürgens, G. (2005). Developmental specificity of auxin response by pairs of
ARF and Aux/IAA transcriptional regulators. EMBO Journal. Wiley-Blackwell.
https://doi.org/10.1038/sj.emboj.7600659
chicago: Weijers, Dolf, Eva Benková, Katja Jäger, Alexandra Schlereth, Thorsten
Hamann, Marika Kientz, Jill Wilmoth, Jason Reed, and Gerd Jürgens. “Developmental
Specificity of Auxin Response by Pairs of ARF and Aux/IAA Transcriptional Regulators.”
EMBO Journal. Wiley-Blackwell, 2005. https://doi.org/10.1038/sj.emboj.7600659.
ieee: D. Weijers et al., “Developmental specificity of auxin response by
pairs of ARF and Aux/IAA transcriptional regulators,” EMBO Journal, vol.
24, no. 10. Wiley-Blackwell, pp. 1874–1885, 2005.
ista: Weijers D, Benková E, Jäger K, Schlereth A, Hamann T, Kientz M, Wilmoth J,
Reed J, Jürgens G. 2005. Developmental specificity of auxin response by pairs
of ARF and Aux/IAA transcriptional regulators. EMBO Journal. 24(10), 1874–1885.
mla: Weijers, Dolf, et al. “Developmental Specificity of Auxin Response by Pairs
of ARF and Aux/IAA Transcriptional Regulators.” EMBO Journal, vol. 24,
no. 10, Wiley-Blackwell, 2005, pp. 1874–85, doi:10.1038/sj.emboj.7600659.
short: D. Weijers, E. Benková, K. Jäger, A. Schlereth, T. Hamann, M. Kientz, J.
Wilmoth, J. Reed, G. Jürgens, EMBO Journal 24 (2005) 1874–1885.
date_created: 2018-12-11T12:00:01Z
date_published: 2005-05-18T00:00:00Z
date_updated: 2021-01-12T07:00:22Z
day: '18'
doi: 10.1038/sj.emboj.7600659
extern: 1
intvolume: ' 24'
issue: '10'
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142592/
month: '05'
oa: 1
page: 1874 - 1885
publication: EMBO Journal
publication_status: published
publisher: Wiley-Blackwell
publist_id: '3918'
quality_controlled: 0
status: public
title: Developmental specificity of auxin response by pairs of ARF and Aux/IAA transcriptional
regulators
type: journal_article
volume: 24
year: '2005'
...
---
_id: '2895'
abstract:
- lang: eng
text: One of the fundamental properties of the immune system is its capacity to
avoid autoimmune diseases. The mechanism underlying this process, known as self-tolerance,
is hitherto unresolved but seems to involve the control of clonal expansion of
autoreactive lymphocytes. This article reviews mathematical modeling of self-tolerance,
addressing two specific hypotheses. The first hypothesis posits that self-tolerance
is mediated by tuning of activation thresholds, which makes autoreactive T lymphocytes
reversibly "anergic" and unable to proliferate. The second hypothesis
posits that the proliferation of autoreactive T lymphocytes is instead controlled
by specific regulatory T lymphocytes. Models representing the population dynamics
of autoreactive T lymphocytes according to these two hypotheses were derived.
For each model we identified how cell density affects tolerance, and predicted
the corresponding phase spaces and bifurcations. We show that the simple induction
of proliferative anergy, as modeled here, has a density dependence that is only
partially compatible with adoptive transfers of tolerance, and that the models
of tolerance mediated by specific regulatory T cells are closer to the observations.
acknowledgement: 'The work was financially supported by Fundação para a Ciência e
Tecnologia: grants P/BIA/10094/1998, POCTI/36413/99, and POCTI/MGI/46477/2002;
and fellowships to JF (Praxis/BCC/18972/98), JS (BD/13546/97), KL (SFRH/BPD+/1157/2002),
DM (SFRH/BD/2960/2000) and TP (SFRH/BD/10550/2002).'
author:
- first_name: Jorge
full_name: Carneiro, Jorge
last_name: Carneiro
- first_name: Tiago
full_name: Tiago Paixao
id: 2C5658E6-F248-11E8-B48F-1D18A9856A87
last_name: Paixao
orcid: 0000-0003-2361-3953
- first_name: Dejan
full_name: Milutinovic, Dejan
last_name: Milutinovic
- first_name: João
full_name: Sousa, João
last_name: Sousa
- first_name: Kalet
full_name: Leon, Kalet
last_name: Leon
- first_name: Rui
full_name: Gardner, Rui
last_name: Gardner
- first_name: Jose
full_name: Faro, Jose
last_name: Faro
citation:
ama: 'Carneiro J, Paixao T, Milutinovic D, et al. Immunological self tolerance:
Lessons from mathematical modeling. Journal of Computational and Applied Mathematics.
2005;184(1):77-100. doi:10.1016/j.cam.2004.10.025'
apa: 'Carneiro, J., Paixao, T., Milutinovic, D., Sousa, J., Leon, K., Gardner, R.,
& Faro, J. (2005). Immunological self tolerance: Lessons from mathematical
modeling. Journal of Computational and Applied Mathematics. Elsevier. https://doi.org/10.1016/j.cam.2004.10.025'
chicago: 'Carneiro, Jorge, Tiago Paixao, Dejan Milutinovic, João Sousa, Kalet Leon,
Rui Gardner, and Jose Faro. “Immunological Self Tolerance: Lessons from Mathematical
Modeling.” Journal of Computational and Applied Mathematics. Elsevier,
2005. https://doi.org/10.1016/j.cam.2004.10.025.'
ieee: 'J. Carneiro et al., “Immunological self tolerance: Lessons from mathematical
modeling,” Journal of Computational and Applied Mathematics, vol. 184,
no. 1. Elsevier, pp. 77–100, 2005.'
ista: 'Carneiro J, Paixao T, Milutinovic D, Sousa J, Leon K, Gardner R, Faro J.
2005. Immunological self tolerance: Lessons from mathematical modeling. Journal
of Computational and Applied Mathematics. 184(1), 77–100.'
mla: 'Carneiro, Jorge, et al. “Immunological Self Tolerance: Lessons from Mathematical
Modeling.” Journal of Computational and Applied Mathematics, vol. 184,
no. 1, Elsevier, 2005, pp. 77–100, doi:10.1016/j.cam.2004.10.025.'
short: J. Carneiro, T. Paixao, D. Milutinovic, J. Sousa, K. Leon, R. Gardner, J.
Faro, Journal of Computational and Applied Mathematics 184 (2005) 77–100.
date_created: 2018-12-11T12:00:12Z
date_published: 2005-12-01T00:00:00Z
date_updated: 2021-01-12T07:00:32Z
day: '01'
doi: 10.1016/j.cam.2004.10.025
extern: 1
intvolume: ' 184'
issue: '1'
month: '12'
page: 77 - 100
publication: Journal of Computational and Applied Mathematics
publication_status: published
publisher: Elsevier
publist_id: '3863'
quality_controlled: 0
status: public
title: 'Immunological self tolerance: Lessons from mathematical modeling'
type: journal_article
volume: 184
year: '2005'
...
---
_id: '3000'
abstract:
- lang: eng
text: In plants, cell polarity is an issue more recurring than in other systems,
because plants, due to their adaptive and flexible development, often change cell
polarity postembryonically according to intrinsic cues and demands of the environment.
Recent findings on the directional movement of the plant signalling molecule auxin
provide a unique connection between individual cell polarity and the establishment
of polarity at the tissue, organ, and whole-plant levels. Decisions about the
subcellular polar targeting of PIN auxin transport components determine the direction
of auxin flow between cells and consequently mediate multiple developmental events.
In addition, mutations or chemical interference with PIN-based auxin transport
result in abnormal cell divisions. Thus, the complicated links between cell polarity
establishment, auxin transport, cytoskeleton, and oriented cell divisions now
begin to emerge. Here we review the available literature on the issues of cell
polarity in both plants and animals to extend our understanding on the generation,
maintenance, and transmission of cell polarity in plants.
author:
- first_name: Pankaj
full_name: Dhonukshe, Pankaj
last_name: Dhonukshe
- first_name: Jürgen
full_name: Kleine Vehn, Jürgen
last_name: Kleine Vehn
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: 'Dhonukshe P, Kleine Vehn J, Friml J. Cell polarity, auxin transport and cytoskeleton
mediated division planes: Who comes first? Protoplasma. 2005;226(1-2):67-73.
doi:10.1007/s00709-005-0104-8'
apa: 'Dhonukshe, P., Kleine Vehn, J., & Friml, J. (2005). Cell polarity, auxin
transport and cytoskeleton mediated division planes: Who comes first? Protoplasma.
Springer. https://doi.org/10.1007/s00709-005-0104-8'
chicago: 'Dhonukshe, Pankaj, Jürgen Kleine Vehn, and Jiří Friml. “Cell Polarity,
Auxin Transport and Cytoskeleton Mediated Division Planes: Who Comes First?” Protoplasma.
Springer, 2005. https://doi.org/10.1007/s00709-005-0104-8.'
ieee: 'P. Dhonukshe, J. Kleine Vehn, and J. Friml, “Cell polarity, auxin transport
and cytoskeleton mediated division planes: Who comes first?,” Protoplasma,
vol. 226, no. 1–2. Springer, pp. 67–73, 2005.'
ista: 'Dhonukshe P, Kleine Vehn J, Friml J. 2005. Cell polarity, auxin transport
and cytoskeleton mediated division planes: Who comes first? Protoplasma. 226(1–2),
67–73.'
mla: 'Dhonukshe, Pankaj, et al. “Cell Polarity, Auxin Transport and Cytoskeleton
Mediated Division Planes: Who Comes First?” Protoplasma, vol. 226, no.
1–2, Springer, 2005, pp. 67–73, doi:10.1007/s00709-005-0104-8.'
short: P. Dhonukshe, J. Kleine Vehn, J. Friml, Protoplasma 226 (2005) 67–73.
date_created: 2018-12-11T12:00:47Z
date_published: 2005-10-01T00:00:00Z
date_updated: 2021-01-12T07:40:22Z
day: '01'
doi: 10.1007/s00709-005-0104-8
extern: '1'
intvolume: ' 226'
issue: 1-2
language:
- iso: eng
month: '10'
oa_version: None
page: 67 - 73
publication: Protoplasma
publication_status: published
publisher: Springer
publist_id: '3701'
quality_controlled: '1'
status: public
title: 'Cell polarity, auxin transport and cytoskeleton mediated division planes:
Who comes first?'
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 226
year: '2005'
...
---
_id: '3001'
abstract:
- lang: eng
text: 'One of the mechanisms by which signalling molecules regulate cellular behaviour
is modulating subcellular protein translocation. This mode of regulation is often
based on specialized vesicle trafficking, termed constitutive cycling, which consists
of repeated internalization and recycling of proteins to and from the plasma membrane.
No such mechanism of hormone action has been shown in plants although several
proteins, including the PIN auxin efflux facilitators, exhibit constitutive cycling.
Here we show that a major regulator of plant development, auxin, inhibits endocytosis.
This effect is specific to biologically active auxins and requires activity of
the Calossin-like protein BIG. By inhibiting the internalization step of PIN constitutive
cycling, auxin increases levels of PINs at the plasma membrane. Concomitantly,
auxin promotes its own efflux from cells by a vesicle-trafficking-dependent mechanism.
Furthermore, asymmetric auxin translocation during gravitropism is correlated
with decreased PIN internalization. Our data imply a previously undescribed mode
of plant hormone action: by modulating PIN protein trafficking, auxin regulates
PIN abundance and activity at the cell surface, providing a mechanism for the
feedback regulation of auxin transport.'
author:
- first_name: Tomasz
full_name: Paciorek, Tomasz
last_name: Paciorek
- first_name: Eva
full_name: Zažímalová, Eva
last_name: Zažímalová
- first_name: Nadia
full_name: Ruthardt, Nadia
last_name: Ruthardt
- first_name: Jan
full_name: Petrášek, Jan
last_name: Petrášek
- first_name: York
full_name: Stierhof, York-Dieter
last_name: Stierhof
- first_name: Jürgen
full_name: Kleine-Vehn, Jürgen
last_name: Kleine Vehn
- first_name: David
full_name: Morris, David A
last_name: Morris
- first_name: Neil
full_name: Emans, Neil
last_name: Emans
- first_name: Gerd
full_name: Jürgens, Gerd
last_name: Jürgens
- first_name: Niko
full_name: Geldner, Niko
last_name: Geldner
- first_name: Jirí
full_name: Jirí Friml
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Paciorek T, Zažímalová E, Ruthardt N, et al. Auxin inhibits endocytosis and
promotes its own efflux from cells. Nature. 2005;435(7046):1251-1256. doi:10.1038/nature03633
apa: Paciorek, T., Zažímalová, E., Ruthardt, N., Petrášek, J., Stierhof, Y., Kleine
Vehn, J., … Friml, J. (2005). Auxin inhibits endocytosis and promotes its own
efflux from cells. Nature. Nature Publishing Group. https://doi.org/10.1038/nature03633
chicago: Paciorek, Tomasz, Eva Zažímalová, Nadia Ruthardt, Jan Petrášek, York Stierhof,
Jürgen Kleine Vehn, David Morris, et al. “Auxin Inhibits Endocytosis and Promotes
Its Own Efflux from Cells.” Nature. Nature Publishing Group, 2005. https://doi.org/10.1038/nature03633.
ieee: T. Paciorek et al., “Auxin inhibits endocytosis and promotes its own
efflux from cells,” Nature, vol. 435, no. 7046. Nature Publishing Group,
pp. 1251–1256, 2005.
ista: Paciorek T, Zažímalová E, Ruthardt N, Petrášek J, Stierhof Y, Kleine Vehn
J, Morris D, Emans N, Jürgens G, Geldner N, Friml J. 2005. Auxin inhibits endocytosis
and promotes its own efflux from cells. Nature. 435(7046), 1251–1256.
mla: Paciorek, Tomasz, et al. “Auxin Inhibits Endocytosis and Promotes Its Own Efflux
from Cells.” Nature, vol. 435, no. 7046, Nature Publishing Group, 2005,
pp. 1251–56, doi:10.1038/nature03633.
short: T. Paciorek, E. Zažímalová, N. Ruthardt, J. Petrášek, Y. Stierhof, J. Kleine
Vehn, D. Morris, N. Emans, G. Jürgens, N. Geldner, J. Friml, Nature 435 (2005)
1251–1256.
date_created: 2018-12-11T12:00:47Z
date_published: 2005-06-30T00:00:00Z
date_updated: 2021-01-12T07:40:23Z
day: '30'
doi: 10.1038/nature03633
extern: 1
intvolume: ' 435'
issue: '7046'
month: '06'
page: 1251 - 1256
publication: Nature
publication_status: published
publisher: Nature Publishing Group
publist_id: '3702'
quality_controlled: 0
status: public
title: Auxin inhibits endocytosis and promotes its own efflux from cells
type: journal_article
volume: 435
year: '2005'
...
---
_id: '3003'
abstract:
- lang: eng
text: 'Plant development displays an exceptional plasticity and adaptability that
involves the dynamic, asymmetric distribution of the phytohormone auxin. Polar
auxin flow, which requires polarly localized transport facilitators of the PIN
family, largely contributes to the establishment and maintenance of the auxin
gradients. Functionally overlapping action of PIN proteins mediates multiple developmental
processes, including embryo formation, organ development and tropisms. Here we
show that PIN proteins exhibit synergistic interactions, which involve cross-regulation
of PIN gene expression in pin mutants or plants with inhibited auxin transport.
Auxin itself positively feeds back on PIN gene expression in a tissue-specific
manner through an AUX/IAA-dependent signalling pathway. This regulatory switch
is indicative of a mechanism by which the loss of a specific PIN protein is compensated
for by auxin-dependent ectopic: expression of its homologues. The compensatory
properties of the PIN-dependent transport network might enable the stabilization
of auxin gradients and potentially contribute to the robustness of plant adaptive
development.'
author:
- first_name: Anne
full_name: Vieten, Anne
last_name: Vieten
- first_name: Steffen
full_name: Vanneste, Steffen
last_name: Vanneste
- first_name: Justyna
full_name: Wiśniewska, Justyna
last_name: Wiśniewska
- first_name: Eva
full_name: Eva Benková
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
- first_name: René
full_name: Benjamins, René
last_name: Benjamins
- first_name: Tom
full_name: Beeckman, Tom
last_name: Beeckman
- first_name: Christian
full_name: Luschnig, Christian
last_name: Luschnig
- first_name: Jirí
full_name: Jirí Friml
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Vieten A, Vanneste S, Wiśniewska J, et al. Functional redundancy of PIN proteins
is accompanied by auxin-dependent cross-regulation of PIN expression. Development.
2005;132(20):4521-4531. doi:10.1242/dev.02027
apa: Vieten, A., Vanneste, S., Wiśniewska, J., Benková, E., Benjamins, R., Beeckman,
T., … Friml, J. (2005). Functional redundancy of PIN proteins is accompanied by
auxin-dependent cross-regulation of PIN expression. Development. Company
of Biologists. https://doi.org/10.1242/dev.02027
chicago: Vieten, Anne, Steffen Vanneste, Justyna Wiśniewska, Eva Benková, René Benjamins,
Tom Beeckman, Christian Luschnig, and Jiří Friml. “Functional Redundancy of PIN
Proteins Is Accompanied by Auxin-Dependent Cross-Regulation of PIN Expression.”
Development. Company of Biologists, 2005. https://doi.org/10.1242/dev.02027.
ieee: A. Vieten et al., “Functional redundancy of PIN proteins is accompanied
by auxin-dependent cross-regulation of PIN expression,” Development, vol.
132, no. 20. Company of Biologists, pp. 4521–4531, 2005.
ista: Vieten A, Vanneste S, Wiśniewska J, Benková E, Benjamins R, Beeckman T, Luschnig
C, Friml J. 2005. Functional redundancy of PIN proteins is accompanied by auxin-dependent
cross-regulation of PIN expression. Development. 132(20), 4521–4531.
mla: Vieten, Anne, et al. “Functional Redundancy of PIN Proteins Is Accompanied
by Auxin-Dependent Cross-Regulation of PIN Expression.” Development, vol.
132, no. 20, Company of Biologists, 2005, pp. 4521–31, doi:10.1242/dev.02027.
short: A. Vieten, S. Vanneste, J. Wiśniewska, E. Benková, R. Benjamins, T. Beeckman,
C. Luschnig, J. Friml, Development 132 (2005) 4521–4531.
date_created: 2018-12-11T12:00:48Z
date_published: 2005-10-01T00:00:00Z
date_updated: 2021-01-12T07:40:23Z
day: '01'
doi: 10.1242/dev.02027
extern: 1
intvolume: ' 132'
issue: '20'
month: '10'
page: 4521 - 4531
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '3700'
quality_controlled: 0
status: public
title: Functional redundancy of PIN proteins is accompanied by auxin-dependent cross-regulation
of PIN expression
type: journal_article
volume: 132
year: '2005'
...
---
_id: '3004'
abstract:
- lang: eng
text: Molecular mechanisms of pattern formation in the plant embryo are not well
understood. Recent molecular and cellular studies, in conjunction with earlier
microsurgical, physiological, and genetic work, are now starting to define the
outlines of a model where gradients of the signaling molecule auxin play a central
role in embryo patterning. It is relatively clear how these gradients are established
and interpreted, but how they are maintained is still unresolved. Here, we have
studied the contributions of auxin biosynthesis, conjugation, and transport pathways
to the maintenance of embryonic auxin gradients. Auxin homeostasis in the embryo
was manipulated by region-specific conditional expression of indoleacetic acid-tryptophan
monooxygenase or indoleacetic acid-lysine synthetase, bacterial enzymes for auxin
biosynthesis or conjugation. Neither manipulation of auxin biosynthesis nor of
auxin conjugation interfered with auxin gradients and patterning in the embryo.
This result suggests a compensatory mechanism for buffering auxin gradients in
the embryo. Chemical and genetic inhibition revealed that auxin transport activity,
in particular that of the PIN-FORMED1 (PIN1) and PIN4 proteins, is a major factor
in the maintenance of these gradients.
author:
- first_name: Dolf
full_name: Weijers, Dolf
last_name: Weijers
- first_name: Michael
full_name: Sauer, Michael
last_name: Sauer
- first_name: Olivier
full_name: Meurette, Olivier
last_name: Meurette
- first_name: Jirí
full_name: Jirí Friml
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Karin
full_name: Ljung, Karin
last_name: Ljung
- first_name: Göran
full_name: Sandberg, Göran
last_name: Sandberg
- first_name: Paul
full_name: Hooykaas, Paul
last_name: Hooykaas
- first_name: Remko
full_name: Offringa, Remko
last_name: Offringa
citation:
ama: Weijers D, Sauer M, Meurette O, et al. Maintenance of embryonic auxin distribution
for apical basal patterning by PIN FORMED dependent auxin transport in Arabidopsis.
Plant Cell. 2005;17(9):2517-2526. doi:10.1105/tpc.105.034637
apa: Weijers, D., Sauer, M., Meurette, O., Friml, J., Ljung, K., Sandberg, G., …
Offringa, R. (2005). Maintenance of embryonic auxin distribution for apical basal
patterning by PIN FORMED dependent auxin transport in Arabidopsis. Plant Cell.
American Society of Plant Biologists. https://doi.org/10.1105/tpc.105.034637
chicago: Weijers, Dolf, Michael Sauer, Olivier Meurette, Jiří Friml, Karin Ljung,
Göran Sandberg, Paul Hooykaas, and Remko Offringa. “Maintenance of Embryonic Auxin
Distribution for Apical Basal Patterning by PIN FORMED Dependent Auxin Transport
in Arabidopsis.” Plant Cell. American Society of Plant Biologists, 2005.
https://doi.org/10.1105/tpc.105.034637.
ieee: D. Weijers et al., “Maintenance of embryonic auxin distribution for
apical basal patterning by PIN FORMED dependent auxin transport in Arabidopsis,”
Plant Cell, vol. 17, no. 9. American Society of Plant Biologists, pp. 2517–2526,
2005.
ista: Weijers D, Sauer M, Meurette O, Friml J, Ljung K, Sandberg G, Hooykaas P,
Offringa R. 2005. Maintenance of embryonic auxin distribution for apical basal
patterning by PIN FORMED dependent auxin transport in Arabidopsis. Plant Cell.
17(9), 2517–2526.
mla: Weijers, Dolf, et al. “Maintenance of Embryonic Auxin Distribution for Apical
Basal Patterning by PIN FORMED Dependent Auxin Transport in Arabidopsis.” Plant
Cell, vol. 17, no. 9, American Society of Plant Biologists, 2005, pp. 2517–26,
doi:10.1105/tpc.105.034637.
short: D. Weijers, M. Sauer, O. Meurette, J. Friml, K. Ljung, G. Sandberg, P. Hooykaas,
R. Offringa, Plant Cell 17 (2005) 2517–2526.
date_created: 2018-12-11T12:00:48Z
date_published: 2005-07-01T00:00:00Z
date_updated: 2021-01-12T07:40:24Z
day: '01'
doi: 10.1105/tpc.105.034637
extern: 1
intvolume: ' 17'
issue: '9'
month: '07'
page: 2517 - 2526
publication: Plant Cell
publication_status: published
publisher: American Society of Plant Biologists
publist_id: '3698'
quality_controlled: 0
status: public
title: Maintenance of embryonic auxin distribution for apical basal patterning by
PIN FORMED dependent auxin transport in Arabidopsis
type: journal_article
volume: 17
year: '2005'
...
---
_id: '3141'
abstract:
- lang: eng
text: The two actin-related subunits of the Arp2/3 complex, Arp2 and Arp3, are proposed
to form a pseudo actin dimer that nucleates actin polymerization. However, in
the crystal structure of the inactive complex, they are too far apart to form
such a nucleus. Here, we show using EM that yeast and bovine Arp2/3 complexes
exist in a distribution among open, intermediate and closed conformations. The
crystal structure docks well into the open conformation. The activator WASp binds
at the cleft between Arp2 and Arp3, and all WASp-bound complexes are closed. The
inhibitor coronin binds near the p35 subunit, and all coronin-bound complexes
are open. Activating and loss-of-function mutations in the p35 subunit skew conformational
distribution in opposite directions, closed and open, respectively. We conclude
that WASp stabilizes p35-dependent closure of the complex, holding Arp2 and Arp3
closer together to nucleate an actin filament.
author:
- first_name: Avital
full_name: Rodal, Avital A
last_name: Rodal
- first_name: Olga
full_name: Sokolova, Olga
last_name: Sokolova
- first_name: Deborah
full_name: Robins, Deborah B
last_name: Robins
- first_name: Karen
full_name: Daugherty, Karen M
last_name: Daugherty
- first_name: Simon
full_name: Simon Hippenmeyer
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Howard
full_name: Riezman, Howard
last_name: Riezman
- first_name: Nikolaus
full_name: Grigorieff, Nikolaus
last_name: Grigorieff
- first_name: Bruce
full_name: Goode, Bruce L
last_name: Goode
citation:
ama: Rodal A, Sokolova O, Robins D, et al. Conformational changes in the Arp2 3
complex leading to actin nucleation. Nature Structural and Molecular Biology.
2005;12(1):26-31. doi:10.1038/nsmb870
apa: Rodal, A., Sokolova, O., Robins, D., Daugherty, K., Hippenmeyer, S., Riezman,
H., … Goode, B. (2005). Conformational changes in the Arp2 3 complex leading to
actin nucleation. Nature Structural and Molecular Biology. Nature Publishing
Group. https://doi.org/10.1038/nsmb870
chicago: Rodal, Avital, Olga Sokolova, Deborah Robins, Karen Daugherty, Simon Hippenmeyer,
Howard Riezman, Nikolaus Grigorieff, and Bruce Goode. “Conformational Changes
in the Arp2 3 Complex Leading to Actin Nucleation.” Nature Structural and Molecular
Biology. Nature Publishing Group, 2005. https://doi.org/10.1038/nsmb870.
ieee: A. Rodal et al., “Conformational changes in the Arp2 3 complex leading
to actin nucleation,” Nature Structural and Molecular Biology, vol. 12,
no. 1. Nature Publishing Group, pp. 26–31, 2005.
ista: Rodal A, Sokolova O, Robins D, Daugherty K, Hippenmeyer S, Riezman H, Grigorieff
N, Goode B. 2005. Conformational changes in the Arp2 3 complex leading to actin
nucleation. Nature Structural and Molecular Biology. 12(1), 26–31.
mla: Rodal, Avital, et al. “Conformational Changes in the Arp2 3 Complex Leading
to Actin Nucleation.” Nature Structural and Molecular Biology, vol. 12,
no. 1, Nature Publishing Group, 2005, pp. 26–31, doi:10.1038/nsmb870.
short: A. Rodal, O. Sokolova, D. Robins, K. Daugherty, S. Hippenmeyer, H. Riezman,
N. Grigorieff, B. Goode, Nature Structural and Molecular Biology 12 (2005) 26–31.
date_created: 2018-12-11T12:01:38Z
date_published: 2005-01-01T00:00:00Z
date_updated: 2021-01-12T07:41:21Z
day: '01'
doi: 10.1038/nsmb870
extern: 1
intvolume: ' 12'
issue: '1'
month: '01'
page: 26 - 31
publication: Nature Structural and Molecular Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '3554'
quality_controlled: 0
status: public
title: Conformational changes in the Arp2 3 complex leading to actin nucleation
type: journal_article
volume: 12
year: '2005'
...
---
_id: '3143'
abstract:
- lang: eng
text: Two ETS transcription factors of the Pea3 subfamily are induced in subpopulations
of dorsal root ganglion (DRG) sensory and spinal motor neurons by target-derived
factors. Their expression controls late aspects of neuronal differentiation such
as target invasion and branching. Here, we show that the late onset of ETS gene
expression is an essential requirement for normal sensory neuron differentiation.
We provide genetic evidence in the mouse that precocious ETS expression in DRG
sensory neurons perturbs axonal projections, the acquisition of terminal differentiation
markers, and their dependence on neurotrophic support. Together, our findings
indicate that DRG sensory neurons exhibit a temporal developmental switch that
can be revealed by distinct responses to ETS transcription factor signaling at
sequential steps of neuronal maturation.
author:
- first_name: Simon
full_name: Simon Hippenmeyer
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Eline
full_name: Vrieseling, Eline
last_name: Vrieseling
- first_name: Markus
full_name: Sigrist, Markus
last_name: Sigrist
- first_name: Thomas
full_name: Portmann, Thomas
last_name: Portmann
- first_name: Celia
full_name: Laengle, Celia
last_name: Laengle
- first_name: David
full_name: Ladle, David R
last_name: Ladle
- first_name: Silvia
full_name: Arber, Silvia
last_name: Arber
citation:
ama: Hippenmeyer S, Vrieseling E, Sigrist M, et al. A developmental switch in the
response of DRG neurons to ETS transcription factor signaling. PLoS Biology.
2005;3(5):0878-0890. doi:10.1371/journal.pbio.0030159
apa: Hippenmeyer, S., Vrieseling, E., Sigrist, M., Portmann, T., Laengle, C., Ladle,
D., & Arber, S. (2005). A developmental switch in the response of DRG neurons
to ETS transcription factor signaling. PLoS Biology. Public Library of
Science. https://doi.org/10.1371/journal.pbio.0030159
chicago: Hippenmeyer, Simon, Eline Vrieseling, Markus Sigrist, Thomas Portmann,
Celia Laengle, David Ladle, and Silvia Arber. “A Developmental Switch in the Response
of DRG Neurons to ETS Transcription Factor Signaling.” PLoS Biology. Public
Library of Science, 2005. https://doi.org/10.1371/journal.pbio.0030159.
ieee: S. Hippenmeyer et al., “A developmental switch in the response of DRG
neurons to ETS transcription factor signaling,” PLoS Biology, vol. 3, no.
5. Public Library of Science, pp. 0878–0890, 2005.
ista: Hippenmeyer S, Vrieseling E, Sigrist M, Portmann T, Laengle C, Ladle D, Arber
S. 2005. A developmental switch in the response of DRG neurons to ETS transcription
factor signaling. PLoS Biology. 3(5), 0878–0890.
mla: Hippenmeyer, Simon, et al. “A Developmental Switch in the Response of DRG Neurons
to ETS Transcription Factor Signaling.” PLoS Biology, vol. 3, no. 5, Public
Library of Science, 2005, pp. 0878–90, doi:10.1371/journal.pbio.0030159.
short: S. Hippenmeyer, E. Vrieseling, M. Sigrist, T. Portmann, C. Laengle, D. Ladle,
S. Arber, PLoS Biology 3 (2005) 0878–0890.
date_created: 2018-12-11T12:01:38Z
date_published: 2005-05-01T00:00:00Z
date_updated: 2021-01-12T07:41:21Z
day: '01'
doi: 10.1371/journal.pbio.0030159
extern: 1
intvolume: ' 3'
issue: '5'
license: https://creativecommons.org/licenses/by/4.0/
month: '05'
page: 0878 - 0890
publication: PLoS Biology
publication_status: published
publisher: Public Library of Science
publist_id: '3552'
quality_controlled: 0
status: public
title: A developmental switch in the response of DRG neurons to ETS transcription
factor signaling
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
volume: 3
year: '2005'
...