---
_id: '10712'
abstract:
- lang: eng
text: Solute carriers are increasingly recognized as participating in a plethora
of pathologies, including cancer. We describe here the involvement of the orphan
solute carrier MFSD1 in the regulation of tumor cell migration. Loss of MFSD1
enabled higher levels of metastasis in a mouse model. We identified an increased
migratory potential in MFSD1-/- tumor cells which was mediated by increased focal
adhesion turn-over, reduced stability of mature inactive β1 integrin, and the
resulting increased integrin activation index. We show that MFSD1 promoted recycling
to the cell surface of endocytosed inactive β1 integrin and thereby protected
β1 integrin from proteolytic degradation; this led to dampening of the integrin
activation index. Furthermore, down-regulation of MFSD1 expression was observed
during early steps of tumorigenesis and higher MFSD1 expression levels correlate
with a better cancer patient prognosis. In sum, we describe a requirement for
endolysosomal MFSD1 in efficient β1 integrin recycling to suppress tumor spread.
acknowledged_ssus:
- _id: Bio
acknowledgement: We thank M. Sixt, A. Leithner, and J. Alanko for helpful advice and
the BioImaging Facility at IST Austria for technical support and assistance. We
thank the Siekhaus Lab for the careful review of the manuscript and their input.
MR and DS were funded by the NO Forschungs- und Bildungsges.m.b.H. (LS16-021) and
IST core funding. MD was funded by Deutsche Forschungsgemeinschaft (DA 1785-1).
article_number: '777634'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: Julia
full_name: Bicher, Julia
id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87
last_name: Bicher
- first_name: Merel
full_name: van Gogh, Merel
last_name: van Gogh
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Rita
full_name: Seeböck, Rita
last_name: Seeböck
- first_name: Bozena
full_name: Szulc, Bozena
last_name: Szulc
- first_name: Markus
full_name: Damme, Markus
last_name: Damme
- first_name: Mariusz
full_name: Olczak, Mariusz
last_name: Olczak
- first_name: Lubor
full_name: Borsig, Lubor
last_name: Borsig
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
citation:
ama: Roblek M, Bicher J, van Gogh M, et al. The solute carrier MFSD1 decreases β1
integrin’s activation status and thus tumor metastasis. Frontiers in Oncology.
2022;12. doi:10.3389/fonc.2022.777634
apa: Roblek, M., Bicher, J., van Gogh, M., György, A., Seeböck, R., Szulc, B., …
Siekhaus, D. E. (2022). The solute carrier MFSD1 decreases β1 integrin’s activation
status and thus tumor metastasis. Frontiers in Oncology. Frontiers. https://doi.org/10.3389/fonc.2022.777634
chicago: Roblek, Marko, Julia Bicher, Merel van Gogh, Attila György, Rita Seeböck,
Bozena Szulc, Markus Damme, Mariusz Olczak, Lubor Borsig, and Daria E Siekhaus.
“The Solute Carrier MFSD1 Decreases Β1 Integrin’s Activation Status and Thus Tumor
Metastasis.” Frontiers in Oncology. Frontiers, 2022. https://doi.org/10.3389/fonc.2022.777634.
ieee: M. Roblek et al., “The solute carrier MFSD1 decreases β1 integrin’s
activation status and thus tumor metastasis,” Frontiers in Oncology, vol.
12. Frontiers, 2022.
ista: Roblek M, Bicher J, van Gogh M, György A, Seeböck R, Szulc B, Damme M, Olczak
M, Borsig L, Siekhaus DE. 2022. The solute carrier MFSD1 decreases β1 integrin’s
activation status and thus tumor metastasis. Frontiers in Oncology. 12, 777634.
mla: Roblek, Marko, et al. “The Solute Carrier MFSD1 Decreases Β1 Integrin’s Activation
Status and Thus Tumor Metastasis.” Frontiers in Oncology, vol. 12, 777634,
Frontiers, 2022, doi:10.3389/fonc.2022.777634.
short: M. Roblek, J. Bicher, M. van Gogh, A. György, R. Seeböck, B. Szulc, M. Damme,
M. Olczak, L. Borsig, D.E. Siekhaus, Frontiers in Oncology 12 (2022).
date_created: 2022-02-01T10:33:50Z
date_published: 2022-02-08T00:00:00Z
date_updated: 2023-08-02T14:05:44Z
day: '08'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.3389/fonc.2022.777634
external_id:
isi:
- '000760618800001'
file:
- access_level: open_access
checksum: 63dfecf30c5bbf9408b3512bd603f78c
content_type: application/pdf
creator: cchlebak
date_created: 2022-02-08T13:26:40Z
date_updated: 2022-02-08T13:26:40Z
file_id: '10751'
file_name: 2022_FrontiersOncol_Roblek.pdf
file_size: 6303227
relation: main_file
success: 1
file_date_updated: 2022-02-08T13:26:40Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
project:
- _id: 2637E9C0-B435-11E9-9278-68D0E5697425
grant_number: 'LSC16-021 '
name: Investigating the role of the novel major superfamily facilitator transporter
family member MFSD1 in metastasis
publication: Frontiers in Oncology
publication_identifier:
issn:
- 2234-943X
publication_status: published
publisher: Frontiers
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: confirmation
url: https://ist.ac.at/en/news/suppressing-the-spread-of-tumors/
scopus_import: '1'
status: public
title: The solute carrier MFSD1 decreases β1 integrin’s activation status and thus
tumor metastasis
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
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2022'
...
---
_id: '10918'
abstract:
- lang: eng
text: Cellular metabolism must adapt to changing demands to enable homeostasis.
During immune responses or cancer metastasis, cells leading migration into challenging
environments require an energy boost, but what controls this capacity is unclear.
Here, we study a previously uncharacterized nuclear protein, Atossa (encoded by
CG9005), which supports macrophage invasion into the germband of Drosophila by
controlling cellular metabolism. First, nuclear Atossa increases mRNA levels of
Porthos, a DEAD-box protein, and of two metabolic enzymes, lysine-α-ketoglutarate
reductase (LKR/SDH) and NADPH glyoxylate reductase (GR/HPR), thus enhancing mitochondrial
bioenergetics. Then Porthos supports ribosome assembly and thereby raises the
translational efficiency of a subset of mRNAs, including those affecting mitochondrial
functions, the electron transport chain, and metabolism. Mitochondrial respiration
measurements, metabolomics, and live imaging indicate that Atossa and Porthos
power up OxPhos and energy production to promote the forging of a path into tissues
by leading macrophages. Since many crucial physiological responses require increases
in mitochondrial energy output, this previously undescribed genetic program may
modulate a wide range of cellular behaviors.
acknowledged_ssus:
- _id: Bio
acknowledgement: "We thank the DGRC (NIH grant 2P40OD010949-10A1) for plasmids, the
BDSC (NIH grant P40OD018537) and the VDRC for fly stocks, FlyBase for essential
genomic information, the BDGP in situ database for data (Tomancak et al, 2007),
the IST Austria Bioimaging facility for support, the VBC Core Facilities for RNA
sequencing and analysis, and C. Guet, C. Navarro, C. Desplan, T. Lecuit, I. Miguel-Aliaga,
and Siekhaus group members for comments on the manuscript. The VBCF Metabolomics
Facility is funded by the City of Vienna through the Vienna Business Agency. This
work was supported by the Marie Curie CIG 334077/IRTIM (DES), Austrian Science Fund
(FWF) Lise Meitner Fellowship M2379-B28 (MA and DES), Austrian Science Fund (FWF)
grant ASI_FWF01_P29638S (DES), NIH/NIGMS (R01GM111779-06 (PR), RO1GM135628-01 (PR),
European Research Council (ERC) grant no. 677006 “CMIL” (AB), and Natural Sciences
and Engineering Research Council of Canada\r\n(RGPIN-2019-06766) (TRH). "
article_number: e109049
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Shamsi
full_name: Emtenani, Shamsi
id: 49D32318-F248-11E8-B48F-1D18A9856A87
last_name: Emtenani
orcid: 0000-0001-6981-6938
- first_name: Elliot T
full_name: Martin, Elliot T
last_name: Martin
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Julia
full_name: Bicher, Julia
id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87
last_name: Bicher
- first_name: Jakob-Wendelin
full_name: Genger, Jakob-Wendelin
last_name: Genger
- first_name: Thomas
full_name: Köcher, Thomas
last_name: Köcher
- first_name: Maria
full_name: Akhmanova, Maria
id: 3425EC26-F248-11E8-B48F-1D18A9856A87
last_name: Akhmanova
orcid: 0000-0003-1522-3162
- first_name: Mariana
full_name: Pereira Guarda, Mariana
id: 6de81d9d-e2f2-11eb-945a-af8bc2a60b26
last_name: Pereira Guarda
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: Andreas
full_name: Bergthaler, Andreas
last_name: Bergthaler
- first_name: Thomas R
full_name: Hurd, Thomas R
last_name: Hurd
- first_name: Prashanth
full_name: Rangan, Prashanth
last_name: Rangan
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
citation:
ama: Emtenani S, Martin ET, György A, et al. Macrophage mitochondrial bioenergetics
and tissue invasion are boosted by an Atossa-Porthos axis in Drosophila. The
Embo Journal. 2022;41. doi:10.15252/embj.2021109049
apa: Emtenani, S., Martin, E. T., György, A., Bicher, J., Genger, J.-W., Köcher,
T., … Siekhaus, D. E. (2022). Macrophage mitochondrial bioenergetics and tissue
invasion are boosted by an Atossa-Porthos axis in Drosophila. The Embo Journal.
Embo Press. https://doi.org/10.15252/embj.2021109049
chicago: Emtenani, Shamsi, Elliot T Martin, Attila György, Julia Bicher, Jakob-Wendelin
Genger, Thomas Köcher, Maria Akhmanova, et al. “Macrophage Mitochondrial Bioenergetics
and Tissue Invasion Are Boosted by an Atossa-Porthos Axis in Drosophila.” The
Embo Journal. Embo Press, 2022. https://doi.org/10.15252/embj.2021109049.
ieee: S. Emtenani et al., “Macrophage mitochondrial bioenergetics and tissue
invasion are boosted by an Atossa-Porthos axis in Drosophila,” The Embo Journal,
vol. 41. Embo Press, 2022.
ista: Emtenani S, Martin ET, György A, Bicher J, Genger J-W, Köcher T, Akhmanova
M, Pereira Guarda M, Roblek M, Bergthaler A, Hurd TR, Rangan P, Siekhaus DE. 2022.
Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an Atossa-Porthos
axis in Drosophila. The Embo Journal. 41, e109049.
mla: Emtenani, Shamsi, et al. “Macrophage Mitochondrial Bioenergetics and Tissue
Invasion Are Boosted by an Atossa-Porthos Axis in Drosophila.” The Embo Journal,
vol. 41, e109049, Embo Press, 2022, doi:10.15252/embj.2021109049.
short: S. Emtenani, E.T. Martin, A. György, J. Bicher, J.-W. Genger, T. Köcher,
M. Akhmanova, M. Pereira Guarda, M. Roblek, A. Bergthaler, T.R. Hurd, P. Rangan,
D.E. Siekhaus, The Embo Journal 41 (2022).
date_created: 2022-03-24T13:23:09Z
date_published: 2022-03-23T00:00:00Z
date_updated: 2023-08-03T06:13:14Z
day: '23'
ddc:
- '570'
department:
- _id: DaSi
- _id: LoSw
doi: 10.15252/embj.2021109049
ec_funded: 1
external_id:
isi:
- '000771957000001'
file:
- access_level: open_access
checksum: dba48580fe0fefaa4c63078d1d2a35df
content_type: application/pdf
creator: siekhaus
date_created: 2022-03-24T13:22:41Z
date_updated: 2022-03-24T13:22:41Z
file_id: '10919'
file_name: Macrophage mitochondrial bioenergetics and tissue invasion are boosted
by an Atossa-Porthos axis in Drosopila.pdf
file_size: 4344585
relation: main_file
file_date_updated: 2022-03-24T13:22:41Z
has_accepted_license: '1'
intvolume: ' 41'
isi: 1
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
project:
- _id: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
- _id: 264CBBAC-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02379
name: Modeling epithelial tissue mechanics during cell invasion
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: Drosophila TNFa´s Funktion in Immunzellen
publication: The Embo Journal
publication_identifier:
eissn:
- 1460-2075
publication_status: published
publisher: Embo Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Macrophage mitochondrial bioenergetics and tissue invasion are boosted by an
Atossa-Porthos axis in Drosophila
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
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 41
year: '2022'
...
---
_id: '10614'
abstract:
- lang: eng
text: 'The infiltration of immune cells into tissues underlies the establishment
of tissue-resident macrophages and responses to infections and tumors. Yet the
mechanisms immune cells utilize to negotiate tissue barriers in living organisms
are not well understood, and a role for cortical actin has not been examined.
Here, we find that the tissue invasion of Drosophila macrophages, also known as
plasmatocytes or hemocytes, utilizes enhanced cortical F-actin levels stimulated
by the Drosophila member of the fos proto oncogene transcription factor family
(Dfos, Kayak). RNA sequencing analysis and live imaging show that Dfos enhances
F-actin levels around the entire macrophage surface by increasing mRNA levels
of the membrane spanning molecular scaffold tetraspanin TM4SF, and the actin cross-linking
filamin Cheerio, which are themselves required for invasion. Both the filamin
and the tetraspanin enhance the cortical activity of Rho1 and the formin Diaphanous
and thus the assembly of cortical actin, which is a critical function since expressing
a dominant active form of Diaphanous can rescue the Dfos macrophage invasion defect.
In vivo imaging shows that Dfos enhances the efficiency of the initial phases
of macrophage tissue entry. Genetic evidence argues that this Dfos-induced program
in macrophages counteracts the constraint produced by the tension of surrounding
tissues and buffers the properties of the macrophage nucleus from affecting tissue
entry. We thus identify strengthening the cortical actin cytoskeleton through
Dfos as a key process allowing efficient forward movement of an immune cell into
surrounding tissues. '
acknowledged_ssus:
- _id: LifeSc
acknowledgement: 'We thank the following for their contributions: Plasmids were supplied
by the Drosophila Genomics Resource Center (NIH 2P40OD010949-10A1); fly stocks were
provided by K. Brueckner, B. Stramer, M. Uhlirova, O. Schuldiner, the Bloomington
Drosophila Stock Center (NIH P40OD018537) and the Vienna Drosophila Resource Center,
FlyBase for essential genomic information, and the BDGP in situ database for data.
For antibodies, we thank the Developmental Studies Hybridoma Bank, which was created
by the Eunice Kennedy Shriver National Institute of Child Health and Human Development
of the NIH and is maintained at the University of Iowa, as well as J. Zeitlinger
for her generous gift of Dfos antibody. We thank the Vienna BioCenter Core Facilities
for RNA sequencing and analysis and the Life Scientific Service Units at IST Austria
for technical support and assistance with microscopy and FACS analysis. We thank
C. P. Heisenberg, P. Martin, M. Sixt, and Siekhaus group members for discussions
and T. Hurd, A. Ratheesh, and P. Rangan for comments on the manuscript.'
article_processing_charge: No
article_type: original
author:
- first_name: Vera
full_name: Belyaeva, Vera
id: 47F080FE-F248-11E8-B48F-1D18A9856A87
last_name: Belyaeva
- first_name: Stephanie
full_name: Wachner, Stephanie
id: 2A95E7B0-F248-11E8-B48F-1D18A9856A87
last_name: Wachner
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Shamsi
full_name: Emtenani, Shamsi
id: 49D32318-F248-11E8-B48F-1D18A9856A87
last_name: Emtenani
orcid: 0000-0001-6981-6938
- first_name: Igor
full_name: Gridchyn, Igor
id: 4B60654C-F248-11E8-B48F-1D18A9856A87
last_name: Gridchyn
orcid: 0000-0002-1807-1929
- first_name: Maria
full_name: Akhmanova, Maria
id: 3425EC26-F248-11E8-B48F-1D18A9856A87
last_name: Akhmanova
orcid: 0000-0003-1522-3162
- first_name: M
full_name: Linder, M
last_name: Linder
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: M
full_name: Sibilia, M
last_name: Sibilia
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
citation:
ama: Belyaeva V, Wachner S, György A, et al. Fos regulates macrophage infiltration
against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila.
PLoS Biology. 2022;20(1):e3001494. doi:10.1371/journal.pbio.3001494
apa: Belyaeva, V., Wachner, S., György, A., Emtenani, S., Gridchyn, I., Akhmanova,
M., … Siekhaus, D. E. (2022). Fos regulates macrophage infiltration against surrounding
tissue resistance by a cortical actin-based mechanism in Drosophila. PLoS Biology.
Public Library of Science. https://doi.org/10.1371/journal.pbio.3001494
chicago: Belyaeva, Vera, Stephanie Wachner, Attila György, Shamsi Emtenani, Igor
Gridchyn, Maria Akhmanova, M Linder, Marko Roblek, M Sibilia, and Daria E Siekhaus.
“Fos Regulates Macrophage Infiltration against Surrounding Tissue Resistance by
a Cortical Actin-Based Mechanism in Drosophila.” PLoS Biology. Public Library
of Science, 2022. https://doi.org/10.1371/journal.pbio.3001494.
ieee: V. Belyaeva et al., “Fos regulates macrophage infiltration against
surrounding tissue resistance by a cortical actin-based mechanism in Drosophila,”
PLoS Biology, vol. 20, no. 1. Public Library of Science, p. e3001494, 2022.
ista: Belyaeva V, Wachner S, György A, Emtenani S, Gridchyn I, Akhmanova M, Linder
M, Roblek M, Sibilia M, Siekhaus DE. 2022. Fos regulates macrophage infiltration
against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila.
PLoS Biology. 20(1), e3001494.
mla: Belyaeva, Vera, et al. “Fos Regulates Macrophage Infiltration against Surrounding
Tissue Resistance by a Cortical Actin-Based Mechanism in Drosophila.” PLoS
Biology, vol. 20, no. 1, Public Library of Science, 2022, p. e3001494, doi:10.1371/journal.pbio.3001494.
short: V. Belyaeva, S. Wachner, A. György, S. Emtenani, I. Gridchyn, M. Akhmanova,
M. Linder, M. Roblek, M. Sibilia, D.E. Siekhaus, PLoS Biology 20 (2022) e3001494.
date_created: 2022-01-12T10:18:17Z
date_published: 2022-01-06T00:00:00Z
date_updated: 2024-03-25T23:30:15Z
day: '06'
ddc:
- '570'
department:
- _id: DaSi
- _id: JoCs
doi: 10.1371/journal.pbio.3001494
ec_funded: 1
external_id:
isi:
- '000971223700001'
pmid:
- '34990456'
file:
- access_level: open_access
checksum: f454212a5522a7818ba4b2892315c478
content_type: application/pdf
creator: cchlebak
date_created: 2022-01-12T13:50:04Z
date_updated: 2022-01-12T13:50:04Z
file_id: '10615'
file_name: 2022_PLOSBio_Belyaeva.pdf
file_size: 5426932
relation: main_file
success: 1
file_date_updated: 2022-01-12T13:50:04Z
has_accepted_license: '1'
intvolume: ' 20'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: e3001494
pmid: 1
project:
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: Drosophila TNFa´s Funktion in Immunzellen
- _id: 26199CA4-B435-11E9-9278-68D0E5697425
grant_number: '24800'
name: Tissue barrier penetration is crucial for immunity and metastasis
- _id: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
publication: PLoS Biology
publication_identifier:
eissn:
- 1545-7885
issn:
- 1544-9173
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
related_material:
link:
- relation: earlier_version
url: https://www.biorxiv.org/content/10.1101/2020.09.18.301481
- description: News on the ISTA Website
relation: press_release
url: https://ista.ac.at/en/news/resisting-the-pressure/
record:
- id: '8557'
relation: earlier_version
status: public
- id: '11193'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Fos regulates macrophage infiltration against surrounding tissue resistance
by a cortical actin-based mechanism in Drosophila
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
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 20
year: '2022'
...
---
_id: '10536'
abstract:
- lang: eng
text: TGFβ overexpression is commonly detected in cancer patients and correlates
with poor prognosis and metastasis. Cancer progression is often associated with
an enhanced recruitment of myeloid-derived cells to the tumor microenvironment.
Here we show that functional TGFβ-signaling in myeloid cells is required for metastasis
to the lungs and the liver. Myeloid-specific deletion of Tgfbr2 resulted in reduced
spontaneous lung metastasis, which was associated with a reduction of proinflammatory
cytokines in the metastatic microenvironment. Notably, CD8+ T cell depletion in
myeloid-specific Tgfbr2-deficient mice rescued lung metastasis. Myeloid-specific
Tgfbr2-deficiency resulted in reduced liver metastasis with an almost complete
absence of myeloid cells within metastatic foci. On contrary, an accumulation
of Tgfβ-responsive myeloid cells was associated with an increased recruitment
of monocytes and granulocytes and higher proinflammatory cytokine levels in control
mice. Monocytic cells isolated from metastatic livers of Tgfbr2-deficient mice
showed increased polarization towards the M1 phenotype, Tnfα and Il-1β expression,
reduced levels of M2 markers and reduced production of chemokines responsible
for myeloid-cell recruitment. No significant differences in Tgfβ levels were observed
at metastatic sites of any model. These data demonstrate that Tgfβ signaling in
monocytic myeloid cells suppresses CD8+ T cell activity during lung metastasis,
while these cells actively contribute to tumor growth during liver metastasis.
Thus, myeloid cells modulate metastasis through different mechanisms in a tissue-specific
manner.
acknowledgement: The authors acknowledge the assistance of the Laboratory Animal Services
Center (LASC) – UZH, Center for Microscopy and Image Analysis, and the Flow Cytometry
Center of the University of Zurich.
article_number: '765151'
article_processing_charge: No
article_type: original
author:
- first_name: Cristina
full_name: Stefanescu, Cristina
last_name: Stefanescu
- first_name: Merel
full_name: Van Gogh, Merel
last_name: Van Gogh
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: Mathias
full_name: Heikenwalder, Mathias
last_name: Heikenwalder
- first_name: Lubor
full_name: Borsig, Lubor
last_name: Borsig
citation:
ama: Stefanescu C, Van Gogh M, Roblek M, Heikenwalder M, Borsig L. TGFβ signaling
in myeloid cells promotes lung and liver metastasis through different mechanisms.
Frontiers in Oncology. 2021;11. doi:10.3389/fonc.2021.765151
apa: Stefanescu, C., Van Gogh, M., Roblek, M., Heikenwalder, M., & Borsig, L.
(2021). TGFβ signaling in myeloid cells promotes lung and liver metastasis through
different mechanisms. Frontiers in Oncology. Frontiers. https://doi.org/10.3389/fonc.2021.765151
chicago: Stefanescu, Cristina, Merel Van Gogh, Marko Roblek, Mathias Heikenwalder,
and Lubor Borsig. “TGFβ Signaling in Myeloid Cells Promotes Lung and Liver Metastasis
through Different Mechanisms.” Frontiers in Oncology. Frontiers, 2021.
https://doi.org/10.3389/fonc.2021.765151.
ieee: C. Stefanescu, M. Van Gogh, M. Roblek, M. Heikenwalder, and L. Borsig, “TGFβ
signaling in myeloid cells promotes lung and liver metastasis through different
mechanisms,” Frontiers in Oncology, vol. 11. Frontiers, 2021.
ista: Stefanescu C, Van Gogh M, Roblek M, Heikenwalder M, Borsig L. 2021. TGFβ signaling
in myeloid cells promotes lung and liver metastasis through different mechanisms.
Frontiers in Oncology. 11, 765151.
mla: Stefanescu, Cristina, et al. “TGFβ Signaling in Myeloid Cells Promotes Lung
and Liver Metastasis through Different Mechanisms.” Frontiers in Oncology,
vol. 11, 765151, Frontiers, 2021, doi:10.3389/fonc.2021.765151.
short: C. Stefanescu, M. Van Gogh, M. Roblek, M. Heikenwalder, L. Borsig, Frontiers
in Oncology 11 (2021).
date_created: 2021-12-12T23:01:27Z
date_published: 2021-11-18T00:00:00Z
date_updated: 2023-08-17T06:20:32Z
day: '18'
ddc:
- '610'
department:
- _id: DaSi
doi: 10.3389/fonc.2021.765151
external_id:
isi:
- '000726603400001'
pmid:
- '34868988'
file:
- access_level: open_access
checksum: 56cbac80e6891ce750511a30161b7792
content_type: application/pdf
creator: alisjak
date_created: 2021-12-13T13:32:37Z
date_updated: 2021-12-13T13:32:37Z
file_id: '10539'
file_name: 2021_Frontiers_Stefanescu.pdf
file_size: 9245199
relation: main_file
success: 1
file_date_updated: 2021-12-13T13:32:37Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: Frontiers in Oncology
publication_identifier:
eissn:
- 2234-943X
publication_status: published
publisher: Frontiers
quality_controlled: '1'
scopus_import: '1'
status: public
title: TGFβ signaling in myeloid cells promotes lung and liver metastasis through
different mechanisms
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
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2021'
...
---
_id: '6187'
abstract:
- lang: eng
text: Aberrant display of the truncated core1 O-glycan T-antigen is a common feature
of human cancer cells that correlates with metastasis. Here we show that T-antigen
in Drosophila melanogaster macrophages is involved in their developmentally programmed
tissue invasion. Higher macrophage T-antigen levels require an atypical major
facilitator superfamily (MFS) member that we named Minerva which enables macrophage
dissemination and invasion. We characterize for the first time the T and Tn glycoform
O-glycoproteome of the Drosophila melanogaster embryo, and determine that Minerva
increases the presence of T-antigen on proteins in pathways previously linked
to cancer, most strongly on the sulfhydryl oxidase Qsox1 which we show is required
for macrophage tissue entry. Minerva’s vertebrate ortholog, MFSD1, rescues the
minerva mutant’s migration and T-antigen glycosylation defects. We thus identify
a key conserved regulator that orchestrates O-glycosylation on a protein subset
to activate a program governing migration steps important for both development
and cancer metastasis.
acknowledged_ssus:
- _id: LifeSc
article_number: e41801
article_processing_charge: No
author:
- first_name: Katarina
full_name: Valosková, Katarina
id: 46F146FC-F248-11E8-B48F-1D18A9856A87
last_name: Valosková
- first_name: Julia
full_name: Biebl, Julia
id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87
last_name: Biebl
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: Shamsi
full_name: Emtenani, Shamsi
id: 49D32318-F248-11E8-B48F-1D18A9856A87
last_name: Emtenani
orcid: 0000-0001-6981-6938
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Michaela
full_name: Misova, Michaela
id: 495A3C32-F248-11E8-B48F-1D18A9856A87
last_name: Misova
orcid: 0000-0003-2427-6856
- first_name: Aparna
full_name: Ratheesh, Aparna
id: 2F064CFE-F248-11E8-B48F-1D18A9856A87
last_name: Ratheesh
orcid: 0000-0001-7190-0776
- first_name: Patricia
full_name: Rodrigues, Patricia
id: 2CE4065A-F248-11E8-B48F-1D18A9856A87
last_name: Rodrigues
- first_name: Katerina
full_name: Shkarina, Katerina
last_name: Shkarina
- first_name: Ida Signe Bohse
full_name: Larsen, Ida Signe Bohse
last_name: Larsen
- first_name: Sergey Y
full_name: Vakhrushev, Sergey Y
last_name: Vakhrushev
- first_name: Henrik
full_name: Clausen, Henrik
last_name: Clausen
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
citation:
ama: Valosková K, Bicher J, Roblek M, et al. A conserved major facilitator superfamily
member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion.
eLife. 2019;8. doi:10.7554/elife.41801
apa: Valosková, K., Bicher, J., Roblek, M., Emtenani, S., György, A., Misova, M.,
… Siekhaus, D. E. (2019). A conserved major facilitator superfamily member orchestrates
a subset of O-glycosylation to aid macrophage tissue invasion. ELife. eLife
Sciences Publications. https://doi.org/10.7554/elife.41801
chicago: Valosková, Katarina, Julia Bicher, Marko Roblek, Shamsi Emtenani, Attila
György, Michaela Misova, Aparna Ratheesh, et al. “A Conserved Major Facilitator
Superfamily Member Orchestrates a Subset of O-Glycosylation to Aid Macrophage
Tissue Invasion.” ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/elife.41801.
ieee: K. Valosková et al., “A conserved major facilitator superfamily member
orchestrates a subset of O-glycosylation to aid macrophage tissue invasion,” eLife,
vol. 8. eLife Sciences Publications, 2019.
ista: Valosková K, Bicher J, Roblek M, Emtenani S, György A, Misova M, Ratheesh
A, Rodrigues P, Shkarina K, Larsen ISB, Vakhrushev SY, Clausen H, Siekhaus DE.
2019. A conserved major facilitator superfamily member orchestrates a subset of
O-glycosylation to aid macrophage tissue invasion. eLife. 8, e41801.
mla: Valosková, Katarina, et al. “A Conserved Major Facilitator Superfamily Member
Orchestrates a Subset of O-Glycosylation to Aid Macrophage Tissue Invasion.” ELife,
vol. 8, e41801, eLife Sciences Publications, 2019, doi:10.7554/elife.41801.
short: K. Valosková, J. Bicher, M. Roblek, S. Emtenani, A. György, M. Misova, A.
Ratheesh, P. Rodrigues, K. Shkarina, I.S.B. Larsen, S.Y. Vakhrushev, H. Clausen,
D.E. Siekhaus, ELife 8 (2019).
date_created: 2019-03-28T13:37:45Z
date_published: 2019-03-26T00:00:00Z
date_updated: 2024-03-25T23:30:15Z
day: '26'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.7554/elife.41801
ec_funded: 1
external_id:
isi:
- '000462530200001'
file:
- access_level: open_access
checksum: cc0d1a512559d52e7e7cb0e9b9854b40
content_type: application/pdf
creator: dernst
date_created: 2019-03-28T14:00:41Z
date_updated: 2020-07-14T12:47:23Z
file_id: '6188'
file_name: 2019_eLife_Valoskova.pdf
file_size: 4496017
relation: main_file
file_date_updated: 2020-07-14T12:47:23Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
project:
- _id: 253CDE40-B435-11E9-9278-68D0E5697425
grant_number: '24283'
name: Examination of the role of a MFS transporter in the migration of Drosophila
immune cells
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: The role of Drosophila TNF alpha in immune cell invasion
- _id: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
- _id: 25388084-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '329540'
name: 'Breaking barriers: Investigating the junctional and mechanobiological changes
underlying the ability of Drosophila immune cells to invade an epithelium'
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/new-gene-potentially-involved-in-metastasis-identified/
record:
- id: '6530'
relation: dissertation_contains
- id: '8983'
relation: dissertation_contains
status: public
- id: '6546'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation
to aid macrophage tissue invasion
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
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 8
year: '2019'
...
---
_id: '6190'
abstract:
- lang: eng
text: "Increased levels of the chemokine CCL2 in cancer patients are associated
with poor prognosis. Experimental evidence suggests that CCL2 correlates with
inflammatory monocyte recruitment and induction of vascular activation, but the
functionality remains open. Here, we show that endothelial Ccr2 facilitates pulmonary
metastasis using an endothelial-specific Ccr2-deficient mouse model (Ccr2ecKO).
Similar levels of circulating monocytes and equal leukocyte recruitment to metastatic
lesions of Ccr2ecKO and Ccr2fl/fl littermates were observed. The absence of endothelial
Ccr2 strongly reduced pulmonary metastasis, while the primary tumor growth was
unaffected. Despite a comparable cytokine milieu in Ccr2ecKO and Ccr2fl/fl littermates
the absence of vascular permeability induction was observed only in Ccr2ecKO mice.
CCL2 stimulation of pulmonary endothelial cells resulted in increased phosphorylation
of MLC2, endothelial cell retraction, and vascular leakiness that was blocked
by an addition of a CCR2 inhibitor. These data demonstrate that endothelial CCR2
expression is required for tumor cell extravasation and pulmonary metastasis.\r\n\r\nImplications:
The findings provide mechanistic insight into how CCL2–CCR2 signaling in endothelial
cells promotes their activation through myosin light chain phosphorylation, resulting
in endothelial retraction and enhanced tumor cell migration and metastasis."
article_processing_charge: No
article_type: original
author:
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: Darya
full_name: Protsyuk, Darya
last_name: Protsyuk
- first_name: Paul F.
full_name: Becker, Paul F.
last_name: Becker
- first_name: Cristina
full_name: Stefanescu, Cristina
last_name: Stefanescu
- first_name: Christian
full_name: Gorzelanny, Christian
last_name: Gorzelanny
- first_name: Jesus F.
full_name: Glaus Garzon, Jesus F.
last_name: Glaus Garzon
- first_name: Lucia
full_name: Knopfova, Lucia
last_name: Knopfova
- first_name: Mathias
full_name: Heikenwalder, Mathias
last_name: Heikenwalder
- first_name: Bruno
full_name: Luckow, Bruno
last_name: Luckow
- first_name: Stefan W.
full_name: Schneider, Stefan W.
last_name: Schneider
- first_name: Lubor
full_name: Borsig, Lubor
last_name: Borsig
citation:
ama: Roblek M, Protsyuk D, Becker PF, et al. CCL2 is a vascular permeability factor
inducing CCR2-dependent endothelial retraction during lung metastasis. Molecular
Cancer Research. 2019;17(3):783-793. doi:10.1158/1541-7786.MCR-18-0530
apa: Roblek, M., Protsyuk, D., Becker, P. F., Stefanescu, C., Gorzelanny, C., Glaus
Garzon, J. F., … Borsig, L. (2019). CCL2 is a vascular permeability factor inducing
CCR2-dependent endothelial retraction during lung metastasis. Molecular Cancer
Research. AACR. https://doi.org/10.1158/1541-7786.MCR-18-0530
chicago: Roblek, Marko, Darya Protsyuk, Paul F. Becker, Cristina Stefanescu, Christian
Gorzelanny, Jesus F. Glaus Garzon, Lucia Knopfova, et al. “CCL2 Is a Vascular
Permeability Factor Inducing CCR2-Dependent Endothelial Retraction during Lung
Metastasis.” Molecular Cancer Research. AACR, 2019. https://doi.org/10.1158/1541-7786.MCR-18-0530.
ieee: M. Roblek et al., “CCL2 is a vascular permeability factor inducing
CCR2-dependent endothelial retraction during lung metastasis,” Molecular Cancer
Research, vol. 17, no. 3. AACR, pp. 783–793, 2019.
ista: Roblek M, Protsyuk D, Becker PF, Stefanescu C, Gorzelanny C, Glaus Garzon
JF, Knopfova L, Heikenwalder M, Luckow B, Schneider SW, Borsig L. 2019. CCL2 is
a vascular permeability factor inducing CCR2-dependent endothelial retraction
during lung metastasis. Molecular Cancer Research. 17(3), 783–793.
mla: Roblek, Marko, et al. “CCL2 Is a Vascular Permeability Factor Inducing CCR2-Dependent
Endothelial Retraction during Lung Metastasis.” Molecular Cancer Research,
vol. 17, no. 3, AACR, 2019, pp. 783–93, doi:10.1158/1541-7786.MCR-18-0530.
short: M. Roblek, D. Protsyuk, P.F. Becker, C. Stefanescu, C. Gorzelanny, J.F. Glaus
Garzon, L. Knopfova, M. Heikenwalder, B. Luckow, S.W. Schneider, L. Borsig, Molecular
Cancer Research 17 (2019) 783–793.
date_created: 2019-03-31T21:59:12Z
date_published: 2019-03-01T00:00:00Z
date_updated: 2023-08-25T08:57:01Z
day: '01'
department:
- _id: DaSi
doi: 10.1158/1541-7786.MCR-18-0530
external_id:
isi:
- '000460099800012'
pmid:
- '30552233'
intvolume: ' 17'
isi: 1
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1158/1541-7786.MCR-18-0530
month: '03'
oa: 1
oa_version: Published Version
page: 783-793
pmid: 1
publication: Molecular Cancer Research
publication_identifier:
eissn:
- '15573125'
issn:
- '15417786'
publication_status: published
publisher: AACR
quality_controlled: '1'
scopus_import: '1'
status: public
title: CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial
retraction during lung metastasis
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 17
year: '2019'
...
---
_id: '544'
abstract:
- lang: eng
text: Drosophila melanogaster plasmatocytes, the phagocytic cells among hemocytes,
are essential for immune responses, but also play key roles from early development
to death through their interactions with other cell types. They regulate homeostasis
and signaling during development, stem cell proliferation, metabolism, cancer,
wound responses and aging, displaying intriguing molecular and functional conservation
with vertebrate macrophages. Given the relative ease of genetics in Drosophila
compared to vertebrates, tools permitting visualization and genetic manipulation
of plasmatocytes and surrounding tissues independently at all stages would greatly
aid in fully understanding these processes, but are lacking. Here we describe
a comprehensive set of transgenic lines that allow this. These include extremely
brightly fluorescing mCherry-based lines that allow GAL4-independent visualization
of plasmatocyte nuclei, cytoplasm or actin cytoskeleton from embryonic Stage 8
through adulthood in both live and fixed samples even as heterozygotes, greatly
facilitating screening. These lines allow live visualization and tracking of embryonic
plasmatocytes, as well as larval plasmatocytes residing at the body wall or flowing
with the surrounding hemolymph. With confocal imaging, interactions of plasmatocytes
and inner tissues can be seen in live or fixed embryos, larvae and adults. They
permit efficient GAL4-independent FACS analysis/sorting of plasmatocytes throughout
life. To facilitate genetic analysis of reciprocal signaling, we have also made
a plasmatocyte-expressing QF2 line that in combination with extant GAL4 drivers
allows independent genetic manipulation of both plasmatocytes and surrounding
tissues, and a GAL80 line that blocks GAL4 drivers from affecting plasmatocytes,
both of which function from the early embryo to the adult.
acknowledged_ssus:
- _id: LifeSc
acknowledgement: ' A. Ratheesh also by Marie Curie IIF GA-2012-32950BB:DICJI, Marko
Roblek by the provincial government of Lower Austria, K. Valoskova and S. Wachner
by DOC Fellowships from the Austrian Academy of Sciences, '
article_processing_charge: No
author:
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Marko
full_name: Roblek, Marko
id: 3047D808-F248-11E8-B48F-1D18A9856A87
last_name: Roblek
orcid: 0000-0001-9588-1389
- first_name: Aparna
full_name: Ratheesh, Aparna
id: 2F064CFE-F248-11E8-B48F-1D18A9856A87
last_name: Ratheesh
orcid: 0000-0001-7190-0776
- first_name: Katarina
full_name: Valosková, Katarina
id: 46F146FC-F248-11E8-B48F-1D18A9856A87
last_name: Valosková
- first_name: Vera
full_name: Belyaeva, Vera
id: 47F080FE-F248-11E8-B48F-1D18A9856A87
last_name: Belyaeva
- first_name: Stephanie
full_name: Wachner, Stephanie
id: 2A95E7B0-F248-11E8-B48F-1D18A9856A87
last_name: Wachner
- first_name: Yutaka
full_name: Matsubayashi, Yutaka
last_name: Matsubayashi
- first_name: Besaiz
full_name: Sanchez Sanchez, Besaiz
last_name: Sanchez Sanchez
- first_name: Brian
full_name: Stramer, Brian
last_name: Stramer
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
citation:
ama: 'György A, Roblek M, Ratheesh A, et al. Tools allowing independent visualization
and genetic manipulation of Drosophila melanogaster macrophages and surrounding
tissues. G3: Genes, Genomes, Genetics. 2018;8(3):845-857. doi:10.1534/g3.117.300452'
apa: 'György, A., Roblek, M., Ratheesh, A., Valosková, K., Belyaeva, V., Wachner,
S., … Siekhaus, D. E. (2018). Tools allowing independent visualization and genetic
manipulation of Drosophila melanogaster macrophages and surrounding tissues. G3:
Genes, Genomes, Genetics. Genetics Society of America. https://doi.org/10.1534/g3.117.300452'
chicago: 'György, Attila, Marko Roblek, Aparna Ratheesh, Katarina Valosková, Vera
Belyaeva, Stephanie Wachner, Yutaka Matsubayashi, Besaiz Sanchez Sanchez, Brian
Stramer, and Daria E Siekhaus. “Tools Allowing Independent Visualization and Genetic
Manipulation of Drosophila Melanogaster Macrophages and Surrounding Tissues.”
G3: Genes, Genomes, Genetics. Genetics Society of America, 2018. https://doi.org/10.1534/g3.117.300452.'
ieee: 'A. György et al., “Tools allowing independent visualization and genetic
manipulation of Drosophila melanogaster macrophages and surrounding tissues,”
G3: Genes, Genomes, Genetics, vol. 8, no. 3. Genetics Society of America,
pp. 845–857, 2018.'
ista: 'György A, Roblek M, Ratheesh A, Valosková K, Belyaeva V, Wachner S, Matsubayashi
Y, Sanchez Sanchez B, Stramer B, Siekhaus DE. 2018. Tools allowing independent
visualization and genetic manipulation of Drosophila melanogaster macrophages
and surrounding tissues. G3: Genes, Genomes, Genetics. 8(3), 845–857.'
mla: 'György, Attila, et al. “Tools Allowing Independent Visualization and Genetic
Manipulation of Drosophila Melanogaster Macrophages and Surrounding Tissues.”
G3: Genes, Genomes, Genetics, vol. 8, no. 3, Genetics Society of America,
2018, pp. 845–57, doi:10.1534/g3.117.300452.'
short: 'A. György, M. Roblek, A. Ratheesh, K. Valosková, V. Belyaeva, S. Wachner,
Y. Matsubayashi, B. Sanchez Sanchez, B. Stramer, D.E. Siekhaus, G3: Genes, Genomes,
Genetics 8 (2018) 845–857.'
date_created: 2018-12-11T11:47:05Z
date_published: 2018-03-01T00:00:00Z
date_updated: 2024-03-25T23:30:15Z
day: '01'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.1534/g3.117.300452
ec_funded: 1
external_id:
isi:
- '000426693300011'
file:
- access_level: open_access
checksum: 7d9d28b915159078a4ca7add568010e8
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:48Z
date_updated: 2020-07-14T12:46:56Z
file_id: '4905'
file_name: IST-2018-990-v1+1_2018_Gyoergy_Tools_allowing.pdf
file_size: 2251222
relation: main_file
file_date_updated: 2020-07-14T12:46:56Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
issue: '3'
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call_identifier: FWF
grant_number: P29638
name: Drosophila TNFa´s Funktion in Immunzellen
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: The role of Drosophila TNF alpha in immune cell invasion
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grant_number: 'LSC16-021 '
name: Investigating the role of the novel major superfamily facilitator transporter
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call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
publication: 'G3: Genes, Genomes, Genetics'
publication_status: published
publisher: Genetics Society of America
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relation: dissertation_contains
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relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Tools allowing independent visualization and genetic manipulation of Drosophila
melanogaster macrophages and surrounding tissues
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
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 8
year: '2018'
...