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).
| 元の言語 | English |
|---|---|
| ページ（範囲） | 199-204 |
| ページ数 | 6 |
| ジャーナル | Oncogene |
| 巻 | 13 |
| 発行部数 | 1 |
| 出版物ステータス | Published - 1996 |
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ASJC Scopus subject areas
- Molecular Biology
- Cancer Research
- Genetics
これを引用
Impaired development of CD4+ CD8+ thymocytes by csk-'knock-in' into fyn locus. / Kanazawa, Satoshi; Ilić, Dusko; Hashiyama, Motohiro; Okada, Masato; Noumura, Tetsuo; Aizawa, Shinichi; Suda, Toshio.
：: Oncogene, 巻 13, 番号 1, 1996, p. 199-204.研究成果: Article
}
TY - JOUR
T1 - Impaired development of CD4+ CD8+ thymocytes by csk-'knock-in' into fyn locus
AU - Kanazawa, Satoshi
AU - Ilić, Dusko
AU - Hashiyama, Motohiro
AU - Okada, Masato
AU - Noumura, Tetsuo
AU - Aizawa, Shinichi
AU - Suda, Toshio
PY - 1996
Y1 - 1996
N2 - 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).
AB - 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).
KW - Knock-in
KW - p50(csk)
KW - p56(lck)
KW - p59(fyn)
KW - T cell development
KW - Thymocytes
UR - http://www.scopus.com/inward/record.url?scp=0029931282&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029931282&partnerID=8YFLogxK
M3 - Article
C2 - 8700547
AN - SCOPUS:0029931282
VL - 13
SP - 199
EP - 204
JO - Oncogene
JF - Oncogene
SN - 0950-9232
IS - 1
ER -