English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

γ-Parvin Is Dispensable for Hematopoiesis, Leukocyte Trafficking, and T-Cell-Dependent Antibody Response

MPS-Authors
/persons/resource/persons204285

Lämmermann,  Tim
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

External Resource
Fulltext (public)

Chu et al 2006.pdf
(Publisher version), 722KB

Supplementary Material (public)
There is no public supplementary material available
Citation

Chu, H., Thievessen, I., Sixt, M., Lämmermann, T., Waisman, A., Braun, A., et al. (2006). γ-Parvin Is Dispensable for Hematopoiesis, Leukocyte Trafficking, and T-Cell-Dependent Antibody Response. Molecular and Cellular Biology (Washington, DC), 26, 1817-1825. doi:10.1128/MCB.26.5.1817-1825.2006.


Cite as: http://hdl.handle.net/21.11116/0000-0007-74B8-7
Abstract
Integrins regulate cell behavior through the assembly of multiprotein complexes at the site of cell adhesion. Parvins are components of such a multiprotein complex. They consist of three members (α-, β-, and γ-parvin), form a functional complex with integrin-linked kinase (ILK) and PINCH, and link integrins to the actin cytoskeleton. Whereas α- and β-parvins are widely expressed, γ-parvin has been reported to be expressed in hematopoietic organs. In the present study, we report the expression pattern of the parvins in hematopoietic cells and the phenotypic analysis of γ-parvin-deficient mice. Whereas α-parvin is not expressed in hematopoietic cells, β-parvin is only found in myeloid cells and γ-parvin is present in both cells of the myeloid and lymphoid lineages, where it binds ILK. Surprisingly, loss of γ-parvin expression had no effect on blood cell differentiation, proliferation, and survival and no consequence for the T-cell-dependent antibody response and lymphocyte and dendritic cell migration. These data indicate that despite the high expression of γ-parvin in hematopoietic cells it must play a more subtle role for blood cell homeostasis.