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Rap1A-deficient T and B cells show impaired integrin-mediated cell adhesion

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons50662

Zemojtel,  Tomasz
Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons50389

Kolanczyk,  Mateusz
Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Zitation

Duchniewicz, M., Zemojtel, T., Kolanczyk, M., Grossmann, S., Scheele, J. S., & Zwartkruis, F. J. T. (2006). Rap1A-deficient T and B cells show impaired integrin-mediated cell adhesion. Molecular and Cellular Biology, 26(2), 643-653. doi:10.1128/MCB.26.2.643-653.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0010-84EB-1
Zusammenfassung
Studies in tissue culture cells have demonstrated a role for the Ras-like GTPase Rap1 in the regulation of integrin-mediated cell-matrix and cadherin-mediated cell-cell contacts. To analyze the function of Rap1 in vivo, we have disrupted the Rap1A gene by homologous recombination. Mice homozygous for the deletion allele are viable and fertile. However, primary hematopoietic cells isolated from spleen or thymus have a diminished adhesive capacity on ICAM and fibronectin substrates. In addition, polarization of T cells from Rap1–/– cells after CD3 stimulation was impaired compared to that of wild-type cells. Despite this, these defects did not result in hematopoietic or cell homing abnormalities. Although it is possible that the relatively mild phenotype is a consequence of functional complementation by the Rap1B gene, our genetic studies confirm a role for Rap1A in the regulation of integrins.