TY - JOUR
T1 - Hypoxia and hypoxia/reoxygenation activate Src family tyrosine kinases and p21(ras) in cultured rat cardiac myocytes
AU - Seko, Yoshinori
AU - Tobe, Kazuyuki
AU - Takahashi, Naoyuki
AU - Kaburagi, Yasushi
AU - Kadowaki, Takashi
AU - Yazaki, Yoshio
N1 - Funding Information:
This work was supported by a grant for cardiomyopathy and a grant for intractable vasculitis from the Ministry of Health and Welfare, Japan; a grant for scientific research from the Ministry of Education, Science and Culture, Japan; a grant from Kowa Life Science Foundation; a grant from Ichiro Kanehara Foundation; and a grant from Kanae Foundation of Research for New Medicine. We thank Kaori Takahashi for excellent technical assistance.
PY - 1996/9/13
Y1 - 1996/9/13
N2 - We previously reported that both hypoxia and hypoxia followed by reoxygenation (hypoxia/reoxygenation) rapidly and sequentially activate mitogen-activated protein kinase kinase kinase (MAPKKK) activity of Raf-1. This was followed by the sequential activation of MAP kinase kinase (MAPKK), MAP kinases (p42(mapk) and p44(mapk)), and S6 kinase (p90(rsk)) In this study, we demonstrated that both hypoxia and hypoxia/ reoxygenation caused rapid activation of Src family tyrosine kinases, p60(c-src) and p59(c-fyn), which are upstream mediators of MAP kinase activation. This was followed by the activation of p21(ras). Because Src family tyrosine kinases are known to be cell-surface-associated kinases and upstream regulators of p21(ras), these results strongly suggested that activation of Src family tyrosine kinases plays a key role in triggering intracellular signaling cascades in cardiac myocytes in response to hypoxia and hypoxia/reoxygenation.
AB - We previously reported that both hypoxia and hypoxia followed by reoxygenation (hypoxia/reoxygenation) rapidly and sequentially activate mitogen-activated protein kinase kinase kinase (MAPKKK) activity of Raf-1. This was followed by the sequential activation of MAP kinase kinase (MAPKK), MAP kinases (p42(mapk) and p44(mapk)), and S6 kinase (p90(rsk)) In this study, we demonstrated that both hypoxia and hypoxia/ reoxygenation caused rapid activation of Src family tyrosine kinases, p60(c-src) and p59(c-fyn), which are upstream mediators of MAP kinase activation. This was followed by the activation of p21(ras). Because Src family tyrosine kinases are known to be cell-surface-associated kinases and upstream regulators of p21(ras), these results strongly suggested that activation of Src family tyrosine kinases plays a key role in triggering intracellular signaling cascades in cardiac myocytes in response to hypoxia and hypoxia/reoxygenation.
UR - http://www.scopus.com/inward/record.url?scp=0030582381&partnerID=8YFLogxK
U2 - 10.1006/bbrc.1996.1389
DO - 10.1006/bbrc.1996.1389
M3 - 学術論文
C2 - 8806668
AN - SCOPUS:0030582381
SN - 0006-291X
VL - 226
SP - 530
EP - 535
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -