@article{3385,
  author       = {Sixt, Michael K},
  journal      = {Immunology Letters},
  number       = {1},
  pages        = {32 -- 34},
  publisher    = {Elsevier},
  title        = {{Interstitial locomotion of leukocytes}},
  doi          = {10.1016/j.imlet.2011.02.013},
  volume       = {138},
  year         = {2011},
}

@article{3392,
  abstract     = {Migrating lymphocytes acquire a polarized phenotype with a leading and a trailing edge, or uropod. Although in vitro experiments in cell lines or activated primary cell cultures have established that Rho-p160 coiled-coil kinase (ROCK)-myosin II-mediated uropod contractility is required for integrin de-adhesion on two-dimensional surfaces and nuclear propulsion through narrow pores in three-dimensional matrices, less is known about the role of these two events during the recirculation of primary, nonactivated lymphocytes. Using pharmacological antagonists of ROCK and myosin II, we report that inhibition of uropod contractility blocked integrin-independent mouse T cell migration through narrow, but not large, pores in vitro. T cell crawling on chemokine-coated endothelial cells under shear was severely impaired by ROCK inhibition, whereas transendothelial migration was only reduced through endothelial cells with high, but not low, barrier properties. Using three-dimensional thick-tissue imaging and dynamic two-photon microscopy of T cell motility in lymphoid tissue, we demonstrated a significant role for uropod contractility in intraluminal crawling and transendothelial migration through lymph node, but not bone marrow, endothelial cells. Finally, we demonstrated that ICAM-1, but not anatomical constraints or integrin-independent interactions, reduced parenchymal motility of inhibitor-treated T cells within the dense lymphoid microenvironment, thus assigning context-dependent roles for uropod contraction during lymphocyte recirculation.},
  author       = {Soriano, Silvia and Hons, Miroslav and Schumann, Kathrin and Kumar, Varsha and Dennier, Timo and Lyck, Ruth and Sixt, Michael K and Stein, Jens},
  issn         = {1550-6606},
  journal      = {Journal of Immunology},
  number       = {5},
  pages        = {2356 -- 2364},
  publisher    = {American Association of Immunologists},
  title        = {{In vivo analysis of uropod function during physiological T cell trafficking}},
  doi          = {10.4049/jimmunol.1100935},
  volume       = {187},
  year         = {2011},
}

@article{3505,
  abstract     = {Cell migration on two-dimensional (2D) substrates follows entirely different rules than cell migration in three-dimensional (3D) environments. This is especially relevant for leukocytes that are able to migrate in the absence of adhesion receptors within the confined geometry of artificial 3D extracellular matrix scaffolds and within the interstitial space in vivo. Here, we describe in detail a simple and economical protocol to visualize dendritic cell migration in 3D collagen scaffolds along chemotactic gradients. This method can be adapted to other cell types and may serve as a physiologically relevant paradigm for the directed locomotion of most amoeboid cells.},
  author       = {Sixt, Michael K and Lämmermann, Tim},
  journal      = {Cell Migration},
  pages        = {149 -- 165},
  publisher    = {Springer},
  title        = {{In vitro analysis of chemotactic leukocyte migration in 3D environments}},
  doi          = {10.1007/978-1-61779-207-6_11},
  volume       = {769},
  year         = {2011},
}

@article{491,
  abstract     = {In their search for antigens, lymphocytes continuously shuttle among blood vessels, lymph vessels, and lymphatic tissues. Chemokines mediate entry of lymphocytes into lymphatic tissues, and sphingosine 1-phosphate (S1P) promotes localization of lymphocytes to the vasculature. Both signals are sensed through G protein-coupled receptors (GPCRs). Most GPCRs undergo ligand-dependent homologous receptor desensitization, a process that decreases their signaling output after previous exposure to high ligand concentration. Such desensitization can explain why lymphocytes do not take an intermediate position between two signals but rather oscillate between them. The desensitization of S1P receptor 1 (S1PR1) is mediated by GPCR kinase 2 (GRK2). Deletion of GRK2 in lymphocytes compromises desensitization by high vascular S1P concentrations, thereby reducing responsiveness to the chemokine signal and trapping the cells in the vascular compartment. The desensitization kinetics of S1PR1 allows lymphocytes to dynamically shuttle between vasculature and lymphatic tissue, although the positional information in both compartments is static.},
  author       = {Eichner, Alexander and Sixt, Michael K},
  journal      = {Science Signaling},
  number       = {198},
  publisher    = {American Association for the Advancement of Science},
  title        = {{Setting the clock for recirculating lymphocytes}},
  doi          = {10.1126/scisignal.2002617},
  volume       = {4},
  year         = {2011},
}

@article{518,
  abstract     = {Cancer stem cells or cancer initiating cells are believed to contribute to cancer recurrence after therapy. MicroRNAs (miRNAs) are short RNA molecules with fundamental roles in gene regulation. The role of miRNAs in cancer stem cells is only poorly understood. Here, we report miRNA expression profiles of glioblastoma stem cell-containing CD133 + cell populations. We find that miR-9, miR-9 * (referred to as miR-9/9 *), miR-17 and miR-106b are highly abundant in CD133 + cells. Furthermore, inhibition of miR-9/9 * or miR-17 leads to reduced neurosphere formation and stimulates cell differentiation. Calmodulin-binding transcription activator 1 (CAMTA1) is a putative transcription factor, which induces the expression of the anti-proliferative cardiac hormone natriuretic peptide A (NPPA). We identify CAMTA1 as an miR-9/9 * and miR-17 target. CAMTA1 expression leads to reduced neurosphere formation and tumour growth in nude mice, suggesting that CAMTA1 can function as tumour suppressor. Consistently, CAMTA1 and NPPA expression correlate with patient survival. Our findings could provide a basis for novel strategies of glioblastoma therapy.},
  author       = {Schraivogel, Daniel and Weinmann, Lasse and Beier, Dagmar and Tabatabai, Ghazaleh and Eichner, Alexander and Zhu, Jia and Anton, Martina and Sixt, Michael K and Weller, Michael and Beier, Christoph and Meister, Gunter},
  journal      = {EMBO Journal},
  number       = {20},
  pages        = {4309 -- 4322},
  publisher    = {Wiley-Blackwell},
  title        = {{CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells}},
  doi          = {10.1038/emboj.2011.301},
  volume       = {30},
  year         = {2011},
}