◀ Back to IGF1
ANXA6 — IGF1
Text-mined interactions from Literome
Hosoi et al., Cancer Res 1999
(Rhabdomyosarcoma) :
To examine the rate at which the mTOR pathway recovered, the ability of
IGF-I to
stimulate p70S6K activity was followed in cells treated for 1 h with rapamycin and then allowed to recover in medium containing > or =100-fold excess of FK506 ( to prevent rapamycin from rebinding to its cytosolic receptor FKBP-12 )
Shah et al., Biochem J 2000
:
Quiescent L6 skeletal myoblasts pretreated for 4 h with the synthetic glucocorticoid dexamethasone exhibited a marked attenuation of
IGF-I induced activation of the ribosomal protein S6 kinase (
p70 ( S6k ) )
Chung et al., Cell Signal 2000
:
In serum starved CK expressor cells, insulin and
IGF-I stimulated DNA synthesis,
p70 S6 kinase (p70 S6K) activity, phosphatidylinositol 3-kinase (PI3K) activity, and activating phosphorylation of p42/p44 mitogen activated protein kinases ( MAPK ) to greater extents than in the corresponding vector control cells
Law et al., J Biol Chem 2000
:
Interestingly, low salicylate concentrations ( < /=250 microm ) inhibit p70 ( s6k ) activation by phorbol myristate acetate, while higher salicylate concentrations ( > /=5 mm ) are required to block
p70 ( s6k )
activation by epidermal growth factor +
insulin-like growth factor-1
Lingohr et al., Diabetes 2002
(MAP Kinase Signaling System) :
Phosphorylation of
p70 ( S6K ) was also
increased by
IGF-1/glucose , but not by TGF-alpha/EGF, despite upstream PKB activation
Shah et al., Biochem J 2002
:
In the present study, we have shown that 4-amino-5- ( 4-methylphenyl ) -7- ( t-butyl ) pyrazolo [ 3,4-d ] pyrimidine ( PP1 ), a selective inhibitor of the Src family of non-receptor tyrosine kinases, interferes with the
activation of 70 and 85 kDa S6K gene products (
p70S6K1 and p85S6K1 ) by insulin,
insulin-like growth factor 1 , sodium orthovanadate and activated alleles of phosphoinositide 3-kinase and H-Ras
Grey et al., Endocrinology 2003
:
In addition, abrogation of PI-3 kinase dependent Akt signaling, which does not inhibit
IGF-I induced
p70s6 kinase phosphorylation, also inhibited the antiapoptotic effects of IGF-I in osteoblasts
Grzelkowska-Kowalczyk et al., Pol J Vet Sci 2005
:
The impairment of
IGF-I stimulated protein synthesis and activation of protein kinase B,
p70 ( S6k ), MAP kinase, and p90 ( rsk ) in mouse C2C12 myogenic cells exposed to high glucose and high insulin
Bridle et al., J Lab Clin Med 2006
:
Both
IGF-1 and PDGF
increased ERK, PI3-K and
p70-S6-K activity ... When evaluating potential crosstalk between these signaling pathways, we observed that PI3-K is required for
p70-S6-K activation by
IGF-1 and PDGF, and is partially responsible for PDGF induced ERK activation
Chen et al., Biochemistry 2006
:
We also found that IGF-1 initiated activation of Akt is significantly enhanced after siRNA mediated Gbeta1 knockdown, while
IGF-1 induced
p70S6K activation is markedly suppressed following transfection of Gbeta1 siRNA
Grzelkowska-Kowalczyk et al., Cell Mol Biol Lett 2010
:
Pretreatment of myogenic cells with IL-1beta did not modify the
IGF-I stimulated phosphorylation of PKB,
p70 ( S6k ), p42(MAPK) and p90 ( rsk )
Matheny et al., Biochem Biophys Res Commun 2009
:
Conversely, levels of
IGF-I stimulated
p70S6K phosphorylation in cells simultaneously deficient in both Akt1 and Akt3 were increased beyond those seen with loss of any single Akt isoform, suggesting an alternate, Akt independent mechanism that activates mTOR/p70S6K
Cascella et al., Endocrinology 2010
:
Aldosterone resulted in significant increases in the Akt ( 1.87 ± 0.24, P < 0.001 ), MAPK ( 1.78 ± 0.13, P < 0.001 ),
p70S6kinase ( 1.92 ± 0.15, P < 0.001 ), IGF-I receptor ( 1.69 ± 0.05, P < 0.01 ), and insulin receptor substrate-1 ( 1.7 ± 0.04, P < 0.01 ) ( fold increase, mean ± SEM, n = 3 ) phosphorylation
responses to
IGF-I compared with IGF-I treatment alone
Tsai et al., J Nutr Biochem 2011
(Neovascularization, Pathologic) :
Western blotting and immunoprecipitation demonstrated that denbinobin causes more efficient inhibition of
IGF-1 induced
activation of IGF-1R and its downstream signaling targets, including, extracellular signal regulated kinase, Akt, mTOR,
p70S6K , 4EBP and cyclin D1
Xie et al., J Steroid Biochem Mol Biol 2011
(Carcinoma...) :
In parallel,
IGF-II increases phosphorylation of AKT and
p70S6K , while metformin increases AMPK phosphorylation and decreases p70S6K phosphorylation
Liu et al., Mol Med Report 2013
:
Rosiglitazone inhibits
insulin-like growth factor-1 induced polycystic kidney disease cell growth and
p70S6 kinase activation ... Moreover, rosiglitazone ( at the same concentration ) was shown to inhibit the
IGF-1 induced activation of
p70S6K ... The present study showed that PPAR? small interfering RNA ( siRNA ) did not block the effect of rosiglitazone in inhibiting the
IGF-1 induced phosphorylation of
p70S6K ... This effect of rosiglitazone was demonstrated to be partially due to the inhibition of
IGF-1 induced activation of
p70S6K
Graves et al., Proc Natl Acad Sci U S A 1995
:
Both PDGF and
IGF-I activated
p70S6K , but only PDGF increased mitogen activated protein kinase activity ... The
effects of PDGF and
IGF-I on increasing PHAS-I phosphorylation, on dissociating the PHAS-I-eIF-4E complex, and on increasing
p70S6K were abolished by rapamycin
Dardevet et al., Endocrinology 1996
:
Although
p70S6K activation by insulin and
IGF-I may be mediated by PI3 kinase in epitrochlearis muscle, the specific inhibition of this kinase by rapamycin caused only partial ( 25 % ) inhibition of the stimulation of protein synthesis by these two hormones
Band et al., J Biol Chem 1997
:
Phosphatidylinositol 3'-kinase and
p70s6k are
required for insulin but not bisperoxovanadium 1,10-phenanthroline ( bpV ( phen ) ) inhibition of
insulin-like growth factor binding protein gene expression
Canicio et al., Endocrinology 1998
:
p70 S6 kinase activation is not
required for
insulin-like growth factor induced differentiation of rat, mouse, or human skeletal muscle cells