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Publication : Congenital nephrotic syndrome in mice lacking CD2-associated protein.

First Author  Shih NY Year  1999
Journal  Science Volume  286
Issue  5438 Pages  312-5
PubMed ID  10514378 Mgi Jnum  J:57971
Mgi Id  MGI:1346257 Doi  10.1126/science.286.5438.312
Citation  Shih NY, et al. (1999) Congenital nephrotic syndrome in mice lacking CD2-associated protein [see comments]. Science 286(5438):312-5
abstractText  CD2-associated protein (CD2AP) is an 80-kilodalton protein that is critical for stabilizing contacts between T cells and antigen-presenting cells. In CD2AP-deficient mice, immune function was compromised, but the mice died at 6 to 7 weeks of age from renal failure. In the kidney, CD2AP was expressed primarily in glomerular epithelial cells. Knockout mice exhibited defects in epithelial cell foot processes, accompanied by mesangial cell hyperplasia and extracellular matrix deposition. Supporting a role for CD2AP in the specialized cell junction known as the slit diaphragm, CD2AP associated with nephrin, the primary component of the slit diaphragm.
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