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

Satoshi Kanazawa, Dusko Ilić, Motohiro Hashiyama, Masato Okada, Tetsuo Noumura, Shinichi Aizawa, Toshio Suda

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


p59(fyn) 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 p59(fyn) 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 p120(cbl).

Original languageEnglish
Pages (from-to)199-204
Number of pages6
Issue number1
Publication statusPublished - 1996
Externally publishedYes


  • Knock-in
  • T cell development
  • Thymocytes
  • p50(csk)
  • p56(lck)
  • p59(fyn)

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


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