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Oncogene. 1996 Jul 4;13(1):199-204.

Impaired development of CD4+ CD8+ thymoyctes by csk-'knock-in' into fyn locus.

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1
Department of Morphogenesis, Institute of Molecular Embryology and Genetics, Kumamoto University School of Medicine, Japan.

Erratum in

  • Oncogene 1996 Nov 21;13(10):2295.

Abstract

p59fyn is one of the Src-family kinases thought to play an important role in signaling through T cell receptor. However, Fyn deficiency has caused no overt defects in vivo on T cell development, nor has it caused any changes in the phosphorylation status of molecules such as ZAP-70 which have been proposed as p59fyn substrates. This could be explained as being due to compensation of Fyn deficiency by other Src-family kinases. Here, we have 'knocked-in' the csk gene, a negative regulator of Src-family kinases, into fyn locus to challenge the problem of redundant functions among Src-family kinases. The csk-'knock-in' mice displayed atrophy of the thymic cortex and impaired development of CD4+ CD8+ thymocytes. This was concomitant with decrease in tyrosine phosphorylation of ZAP-70 and p120cbl.

PMID:
8700547
[Indexed for MEDLINE]

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