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11 results on '"Brakebusch, Cord"'

7. Megakaryocyte-specific RhoA deficiency causes macrothrombocytopenia and defective platelet activation in hemostasis and thrombosis

Author

Pleines, Irina, primary, Hagedorn, Ina, additional, Gupta, Shuchi, additional, May, Frauke, additional, Chakarova, Lidija, additional, van Hengel, Jolanda, additional, Offermanns, Stefan, additional, Krohne, Georg, additional, Kleinschnitz, Christoph, additional, Brakebusch, Cord, additional, and Nieswandt, Bernhard, additional

Published
2012
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8. RhoH is important for positive thymocyte selection and T-cell receptor signaling

Author

Dorn, Tatjana, primary, Kuhn, Ursula, additional, Bungartz, Gerd, additional, Stiller, Sebastian, additional, Bauer, Martina, additional, Ellwart, Joachim, additional, Peters, Thorsten, additional, Scharffetter-Kochanek, Karin, additional, Semmrich, Monika, additional, Laschinger, Melanie, additional, Holzmann, Bernhard, additional, Klinkert, Wolfgang E. F., additional, Straten, Per Thor, additional, Køllgaard, Tania, additional, Sixt, Michael, additional, and Brakebusch, Cord, additional

Published
2006
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10. RhoH is important for positive thymocyte selection and T-cell receptor signaling

Author

Dorn, Tatjana, Kuhn, Ursula, Bungartz, Gerd, Stiller, Sebastian, Bauer, Martina, Ellwart, Joachim, Peters, Thorsten, Scharffetter-Kochanek, Karin, Semmrich, Monika, Laschinger, Melanie, Holzmann, Bernhard, Klinkert, Wolfgang E. F., Straten, Per Thor, Køllgaard, Tania, Sixt, Michael, and Brakebusch, Cord

Abstract

RhoH is a small GTPase expressed only in the hematopoietic system. With the use of mice with targeted disruption of the RhoH gene, we demonstrated that RhoH is crucial for thymocyte maturation during DN3 to DN4 transition and during positive selection. Furthermore, the differentiation and expansion of DN3 and DN4 thymocytes in vitro were severely impaired. These defects corresponded to defective TCR signaling. Although RhoH is not required for TCR-induced activation of ZAP70 and ZAP70-mediated activation of p38, it is crucial for the tyrosine phosphorylation of LAT, PLCγ1, and Vav1 and for the activation of Erk and calcium influx. These data suggest that RhoH is important for pre–TCR and TCR signaling because it allows the efficient interaction of ZAP70 with the LAT signalosome, thus regulating thymocyte development.

Published
2007
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11. Adult murine hematopoiesis can proceed without beta1 and beta7 integrins.

Author

Bungartz G, Stiller S, Bauer M, Müller W, Schippers A, Wagner N, Fässler R, and Brakebusch C

Subjects
Anemia, Hemolytic blood, Anemia, Hemolytic pathology, Animals, B-Lymphocytes cytology, B-Lymphocytes physiology, Cell Movement, Colony-Forming Units Assay, Erythropoiesis, Gene Expression, Hematopoietic Stem Cells cytology, Hematopoietic Stem Cells physiology, Integrin beta Chains genetics, Integrin beta1 genetics, Lymphopoiesis, Mice, Mice, Knockout, Myelopoiesis, T-Lymphocytes cytology, T-Lymphocytes physiology, Hematopoiesis physiology, Integrin beta Chains physiology, Integrin beta1 physiology
Abstract

The function of alpha4beta1 and alpha4beta7 integrins in hematopoiesis is controversial. While some experimental evidence suggests a crucial role for these integrins in retention and expansion of progenitor cells and lymphopoiesis, others report a less important role in hematopoiesis. Using mice with a deletion of the beta1 and the beta7 integrin genes restricted to the hematopoietic system we show here that alpha4beta1 and alpha4beta7 integrins are not essential for differentiation of lymphocytes or myelocytes. However, beta1beta7 mutant mice displayed a transient increase of colony-forming unit (CFU-C) progenitors in the bone marrow and, after phenylhydrazine-induced anemia, a decreased number of splenic erythroid colony-forming units in culture (CFUe's). Array gene expression analysis of CD4(+)CD8(+) double-positive (DP) and CD4(-)CD8(-) double-negative (DN) thymocytes and CD19(+) and CD4(+) splenocytes did not provide any evidence for a compensatory mechanism explaining the mild phenotype. These data show that alpha4beta1 and alpha4beta7 are not required for blood cell differentiation, although in their absence alterations in numbers and distribution of progenitor cells were observed.

Published
2006
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