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INS — RAF1
Text-mined interactions from Literome
Kim et al., J Biol Chem 2001
:
Activation of AMPK by AICAR in NIH-3T3 cells resulted in drastic inhibitions of Ras,
Raf-1 , and Erk activation
induced by
insulin-like growth factor 1 (IGF-1)
Kayampilly et al., Endocrinology 2006
:
DHT treatment also reduced the
insulin mediated insulin receptor substrate-1 and
Raf-1 phosphorylation, the upstream molecules of ERK in insulin signaling pathway
Lee et al., J Biol Chem 1992
:
We recently presented evidence that
insulin and certain other growth factors
activated one or more
Raf-1 kinase kinase activities ( Lee, R.M., Rapp, U. R., and Blackshear, P.J. ( 1991 ) J. Biol. Chem. 266, 10351-10357 )
Izumi et al., J Biol Chem 1991
:
Both
insulin and platelet derived growth factor
stimulated phosphorylation of the
c-raf protein about 2- to 3-fold
Ku et al., Am J Physiol Cell Physiol 2009
:
Pretreatment of preadipocytes with 67LR antiserum prevented the effects of EGCG on
insulin stimulated phosphorylation of IRS2,
RAF1 , and ERK1/2 and insulin stimulated preadipocyte proliferation ( cell number and bromodeoxyuridine incorporation )
Monaco et al., Cell cycle (Georgetown, Tex.) 2009
:
Concomitantly,
insulin stimulation
induced Raf-1 and ERK activation, followed by thymidine uptake ... Inhibition of CaMKII abrogated the
insulin induced
Raf-1 and ERK activation, resulting also in the inhibition of thymidine incorporation
Lee et al., J Biol Chem 1991
:
In three different insulin-sensitive cell types,
insulin activated
Raf-1 kinase kinase activity in crude cytosolic cellular fractions
Alejandro et al., FASEB J 2011
:
As
Raf-1 activity is
critical for basal apoptosis and
insulin secretion in vitro, we hypothesized that Raf-1 may play an important role in glucose homeostasis in vivo ... This work provides the first direct evidence that
Raf-1 signaling is
essential for the regulation of basal
insulin transcription and the supply of releasable insulin in vivo
Kovacina et al., J Biol Chem 1990
:
In the HeLa cells, 100 pM insulin gave a significant increase in
Raf-1 kinase activity, and 100 nM
insulin caused a maximal 2-5-fold increase in activity ... Moreover, a serine/threonine-specific phosphatase, phosphatase 1, but not two tyrosine-specific phosphatases, was found to deactivate the
insulin activated
Raf-1 kinase activity
Blackshear et al., J Biol Chem 1990
:
In several cell lines expressing relatively large numbers of insulin receptors,
insulin rapidly
stimulated the phosphorylation of immunoreactive
Raf-1 protein ... The
insulin stimulated increase in
Raf-1 protein phosphorylation occurred concurrently with a 3-fold increase in Raf-1 protein kinase activity
Fingar et al., J Biol Chem 1994
:
In contrast, activated
Raf-1 affects neither the expression of the
`` insulin-responsive '' glucose transporter ( GLUT4 ) nor its cellular distribution ; GLUT4 is virtually undetectable on the plasma membrane in the absence of insulin and translocates normally following the addition of hormone
Ueki et al., J Biol Chem 1994
:
Feedback
regulation of mitogen activated protein kinase kinase kinase activity of
c-Raf-1 by
insulin and phorbol ester stimulation
Kyriakis et al., J Biol Chem 1993
:
c-Raf-1 activation is also
induced by
insulin , phorbol ester, thrombin, and endothelin ... Although
PDGF/insulin stimulated
c-Raf-1 Ser/Thr phosphorylation may be necessary to sustain the active state, a role for mitogen activated protein kinase/extracellular signal regulated kinase-2 phosphorylation in the initiation of c-Raf-1 activation is unlikely
Carel et al., Endocrinology 1996
:
Insulin stimulated
Raf-1 binding to p21Ras in HIRc ( wild-type ), delta CT ( insulin receptor lacking a 43-amino acid C-terminal domain ), and Y/F2 ( tyrosine 1316 and 1322 replaced by phenylalanine ) cells