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

研究成果: Article

4 引用 (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).

出版物ステータスPublished - 1996 8 10

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

フィンガープリント Impaired development of CD4<sup>+</sup> CD8<sup>+</sup> thymocytes by csk-'knock-in' into fyn locus' の研究トピックを掘り下げます。これらはともに一意のフィンガープリントを構成します。

  • これを引用

    Kanazawa, S., Ilić, D., Hashiyama, M., Okada, M., Noumura, T., Aizawa, S., & Suda, T. (1996). Impaired development of CD4+ CD8+ thymocytes by csk-'knock-in' into fyn locus. Oncogene, 13(1), 199-204.