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Synergistic action of R‐Ras and IGF‐1 on Bcl‐xL expression and caspase‐3 inhibition in BaF3 cells: R‐Ras and IGF‐1 control distinct anti‐apoptotic kinase pathways
Author(s) -
Suzuki Jotaro,
Kaziro Yoshito,
Koide Hiroshi
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01213-7
Subject(s) - mapk/erk pathway , bcl xl , protein kinase b , microbiology and biotechnology , signal transduction , growth factor , apoptosis , kinase , caspase , anti apoptotic ras signalling cascade , chemistry , insulin like growth factor , caspase 3 , biology , receptor , biochemistry , programmed cell death
R‐Ras and insulin‐like growth factor‐1 (IGF‐1) synergistically inhibit apoptosis of BaF3 cells upon interleukin‐3 deprivation. To characterize the mechanism of this synergistic inhibition, we examined the effect of R‐Ras and IGF‐1 on several apoptosis‐related proteins. Extracellular signal‐regulated kinase (ERK) was activated by IGF‐1, but not by R‐Ras. In contrast, Akt was activated strongly by R‐Ras, but weakly by IGF‐1. It was also found that R‐Ras and IGF‐1 cooperatively induced Bcl‐xL expression and inhibited caspase‐3 activation.