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査読

5 被引用数 (Scopus)

抄録

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).

本文言語English
ページ(範囲)199-204
ページ数6
ジャーナルOncogene
13
1
出版ステータスPublished - 1996 8 10

ASJC Scopus subject areas

  • 分子生物学
  • 遺伝学
  • 癌研究

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