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IGF1 — PI3

Text-mined interactions from Literome

Cospedal et al., Cardiovasc Res 1999 : IGF-I also stimulated migration of VSMCs, and, relative to the effect of PDGF-BB, induced smaller increases in PI3-kinase and MAP kinase activities
Yano et al., Endocrinology 1999 : Treatment with either PMA or GF109203X did not significantly affect the effects of IGF-I on PI3 kinase activation or PKB/Akt phosphorylation
Duan et al., Circ Res 2000 : The IGF-I induced increase in IRS-I associated PI3 kinase activity was concentration dependent
Ballou et al., J Biol Chem 2000 : Furthermore, phenylephrine blocked the insulin-like growth factor-I (IGF-I) induced activation of PI 3-kinase and the phosphorylation and activation of Akt-1
Chandrasekher et al., Invest Ophthalmol Vis Sci 2000 : Insulin and IGF-1 stimulated the PI-3K activity in epithelial cells in culture by more than 100 %, and activation of the enzyme resulted in tyrosine phosphorylation of the p85 subunit
Lawlor et al., Mol Cell Biol 2000 (MAP Kinase Signaling System) : Transient transfection of a constitutively active PI3-kinase or an inducible Akt promoted myoblast viability in the absence of growth factors, while inhibition of PI3-kinase activity by the drug LY294002 selectively blocked IGF- but not PDGF mediated muscle cell survival
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
Cheng et al., J Biol Chem 2000 (MAP Kinase Signaling System) : In parallel, IGF-I activates IGF-I receptor, insulin receptor substrate-1 (IRS-1), phosphatidylinositol 3 (PI-3)-kinase , and FAK
Baudry et al., FEBS Lett 2001 : Stimulation of IR ( -/- ) myotubes with IGF-1 ( 10 ( -10 ) to 10 ( -7 ) M ) increased glucose uptake and incorporation into glycogen, induced IRS-1 phosphorylation and activated PI 3-kinase and MAP kinase, two enzymes of major signaling pathways
Alexander et al., Am J Physiol Gastrointest Liver Physiol 2001 : Involvement of PI 3-kinase in IGF-I stimulation of jejunal Na+-K+-ATPase activity and nutrient absorption ... The results suggest that the effect of IGF-I on jejunal ion and nutrient transport involves activation of PI 3-kinase and stimulation of Na+-K+-ATPase activity in enterocytes
Kimpinski et al., J Neurosci Res 2001 (MAP Kinase Signaling System) : Activation of PI 3-kinase and SNT by both NGF and IGF-1 correlated with their effects on neurite growth
Pozios et al., Am J Physiol Regul Integr Comp Physiol 2001 (MAP Kinase Signaling System) : These results indicate that both IGF-I and -II are potent mitogens for zebrafish embryonic cells and that activation of both the MAPK and PI3 kinase signaling pathways is required for the mitogenic action of IGFs in zebrafish embryonic cells
Isenović et al., Biochem Biophys Res Commun 2001 : Role of PI3-kinase in isoproterenol and IGF-1 induced ecNOS activity
Gooch et al., J Biol Chem 2001 (Hypertrophy) : IGF-I also activated both Erk1/Erk2 MAPK and phosphatidylinositol 3-kinase (PI3K) in MCs
Bartucci et al., Cancer Res 2001 (Breast Neoplasms...) : Also, the acute ( 15-min ) IGF-I activation of PI-3 and Akt kinases was similar in ER-negative and ER-positive cells
Friehs et al., Ann Thorac Surg 2001 (Cardiomegaly) : Insulin-like growth factor-1 restored glucose uptake and PI-3-kinase activity to control levels in the hypertrophied hearts and both effects were blocked by wortmannin ( a PI-3-kinase inhibitor )
Strle et al., J Neuroimmunol 2002 : In contrast to IL-10, IGF-I increases enzymatic activity of PI 3-kinase and causes phosphorylation on serine ( 473 ) of Akt but does not prevent microglial apoptosis ... In contrast to IL-10, IGF-I increases enzymatic activity of PI 3-kinase and causes phosphorylation on serine ( 473 ) of Akt but does not prevent microglial apoptosis
Kuemmerle et al., Am J Physiol Gastrointest Liver Physiol 2003 : Endogenous IGF-I regulates growth of human intestinal smooth muscle cells by jointly activating phosphatidylinositol 3-kinase (PI3K) and ERK1/2
Krystal et al., Mol Cancer Ther 2002 (Carcinoma, Small Cell...) : Both stem cell factor (SCF) and insulin-like growth factor (IGF)-I , components of prominent small cell lung cancer ( SCLC ) autocrine loops, as well as FCS, can potently activate phosphatidylinositol 3-kinase (PI3K)-Akt signaling, albeit with different kinetics
Galvan et al., J Biol Chem 2003 : IGF-IR binding to its ligand, insulin-like growth factor ( IGF-I ) activates phosphoinositide 3-kinase (PI3K) , promotes cell proliferation by activating the mitogen activated protein kinase ( MAPK ) cascade, and blocks apoptosis by inducing the phosphorylation and inhibition of proapoptotic proteins such as BAD
Oh et al., J Biol Chem 2003 : IGF-1 induced chondrogenesis of limb bud mesenchymal cells during micromass culture through the activation of phosphatidylinositol 3-kinase (PI3K) and Akt
Liu et al., Pediatr Res 2003 : These effects are mediated through both MEK and PI 3-kinase pathways but not through the IGF-I induction of TNF-alpha production by the DC
Etgen et al., Endocrinology 2003 : Because E ( 2 ) and IGF-I can activate phosphatidylinositol-3-kinase (PI3K) and MAPK, we infused agents that block PI3K and/or MAPK activity as described above
Lassarre et al., Endocrinology 2003 (Breast Neoplasms) : However, IGF-I induced PI 3-kinase activity was decreased by 24 h of pretreatment with EGF or PDGF but not with FGF ... They further suggest that the FGF induced increase in IRS-1 counterbalances the inhibition of IRS-1 tyrosine phosphorylation to allow normal stimulation of IGF-I induced PI 3-kinase activity
Chandrasekher et al., Invest Ophthalmol Vis Sci 2003 : The PI-3K inhibitors wortmannin and LY294002 blocked the insulin-, insulin-like growth factor (IGF)-1- , and fibroblast growth factor (FGF)-2 promoted cell proliferation in rabbit lens epithelial cells ... Insulin and IGF-1 stimulated activation of PI-3K in proliferating and differentiating cultures ... Whereas there was a gradual decrease in insulin/IGF-1 mediated activation of PI-3K and its downstream target Akt, with progression of differentiation in chicken lens epithelial cells, Erk2 phosphorylation induced by these growth factors was not decreased ; rather, it remained increased in early stages of differentiation
Hu et al., Mol Endocrinol 2004 (MAP Kinase Signaling System) : IGF-I activated both the phosphoinositide 3'-OH kinase (PI3K) and the MAPK pathways
González-Timón et al., Cardiovasc Res 2004 (Arteriosclerosis) : These observations correlated with opposite changes exerted by native and oxidized LDL on the insulin receptor substrate-1 (IRS) associated PI3 kinase/Akt response to IGF-I
Chandrasekher et al., Curr Eye Res 2004 (Cataract...) : Insulin and IGF-1 also stimulated rat lens PI-3K activity ... Further, the ability of IGF-1 to stimulate PI-3K activity was significantly reduced in lens epithelial cells treated with selenium
Seimi et al., Circ J 2004 (Cardiomegaly) : The phosphatidylinositol (PI) 3-kinase/Akt/GSK-3 beta signaling induced by IGF-1 was investigated using inhibitors of PI 3-kinase and Ad AktAA, a dominant negative form of Akt
Kataoka et al., J Radiat Res 2004 : We have investigated the role of insulin-like growth factor I receptor ( IGF-IR ) in heat shock induced activation of the mitogen activated protein kinase ( MAPK ) and phosphatidylinositol-3 ' kinase (PI3-K) pathways
Digicaylioglu et al., Proc Natl Acad Sci U S A 2004 : The synergistic effect of EPO+IGF-I was mediated , at least in part, by activation of phosphatidylinositol 3-kinase (PI3-K)
Meyer et al., Cell Mol Life Sci 2005 (Neuroblastoma) : In this study, we show that IGF-I stimulated phosphatidylinositol 3-kinase (PI-3K) activity promotes rac activation and subsequent activation of the down- stream effectors LIM kinase and cofilin
Itakura et al., J Neurochem 2005 : In striking contrast, IGF-1 activated the PI3-kinase pathway but not the MAPK pathway, and IGF-1 dependent enhancement was suppressed by a PI3-kinase inhibitor but not by a MAPK kinase inhibitor ... In striking contrast, IGF-1 activated the PI3-kinase pathway but not the MAPK pathway, and IGF-1 dependent enhancement was suppressed by a PI3-kinase inhibitor but not by a MAPK kinase inhibitor ... These results indicate that PI3-kinase participates in the enhancement of neurotransmitter release by two distinct mechanisms : EGF and NGF activate PI3-kinase in the plasma membrane, whereas IGF-1 activates PI3-kinase possibly in the intracellular membrane, leading to enhancement of neurotransmitter release in a MAPK dependent and -independent manner respectively
Luo et al., J Cell Biol 2005 : Phosphoinositide (PI) 3-kinase is required for most insulin and insulin-like growth factor (IGF) 1-dependent cellular responses
Zhang et al., Breast Cancer Res Treat 2005 (Breast Neoplasms) : Both Erk1,2 and phosphatidyl-3 kinase (PI3K) were required for IGF-I stimulated cell motility, but only PI3K appeared to be directly downstream of IGF-I
Kwon et al., Endocrinology 2006 : Recruitment of the tyrosine phosphatase Src homology 2 domain tyrosine phosphatase-2 to the p85 subunit of phosphatidylinositol-3 (PI-3) kinase is required for insulin-like growth factor-I dependent PI-3 kinase activation in smooth muscle cells ... Cells stably expressing this p85 mutant also showed a decrease in IGF-I stimulated PI-3 kinase activity and cell migration
Mukherjee et al., Comp Biochem Physiol A Mol Integr Physiol 2006 : These data suggest that PI-3 kinase activity is required for IGF-I , b-insulin and HCG induction of GVBD in C. carpio
Riobó et al., Proc Natl Acad Sci U S A 2006 (Neoplasms) : Stimulation of PI3-kinase/Akt by insulin-like growth factor I potentiates Gli activation induced by low levels of Shh ; however, insulin-like growth factor I alone is insufficient to induce Gli dependent transcription
Lackey et al., Oncogene 2007 : These effects on IGF/insulin signaling include a reduction of up to five- to tenfold in IGF stimulated PI 3-kinase activation, a failure to activate the ERK kinases and, in some cells, reduced expression of insulin receptor substrate 1, and both IGF1 and insulin receptors
Mutiara et al., Mol Cell Endocrinol 2008 : Akt/PKB activation by GnRH and IGF-1 was completely eliminated in the presence of the PI3-kinase inhibitor, LY 294002, but not in the presence of an Akt/PKB inhibitor
Fukushima et al., Endocrinology 2008 : In contrast, IGF-I dependent PI 3-kinase activation was required for the increase in cyclin D1 mRNA levels and degradation of p27 ( Kip1 ) ... In contrast, IGF-I dependent PI 3-kinase activation was required for the increase in cyclin D1 mRNA levels and degradation of p27 ( Kip1 ) ... Together, the present study elucidates the role of cAMP and IGF-I in differentially activating PI 3-kinase as a mediator of multiple molecular events
Mani et al., Reproduction 2010 : IGF1 stimulated the phosphoinositide 3'-OH kinase (PI3K) but not the MAPK pathway in granulosa cells, as evidenced by increased phosphorylation of AKT but not extracellular regulated kinase 1/2
Arvisais et al., Mol Endocrinol 2010 : Serine phosphorylation of IRS1 was associated with reduced formation of IGF-I stimulated IRS1/PI3Kp85 complexes
Furundzija et al., Biochem Biophys Res Commun 2010 (Atherosclerosis) : Pharmacological blocking experiments with specific inhibitors of Akt, PKC and p38 MAP-kinase revealed that IGF-1 dependent activation of focal adhesion kinase ( FAK ) and paxillin, and consecutively IGF-1 facilitated migration, required IGF-1/IGF-1R mediated PI3-kinase/PKC/p38 dependent integrin inside-out signaling
Zhao et al., Ethn Dis 2010 (Cardiomegaly) : This raises an important implication relative to the role of IGF-1 dependent activation of PI-3K , which may translate into a differential prognostic for cardiac hypertrophy among ethnic groups
Xi et al., Endocrinology 2010 (Hyperglycemia) : Disruption of p66shc-Src interaction using either a blocking peptide or by expressing a p66shc mutant that did not bind to Src rescued IGF-I stimulated PI-3 kinase/AKT activation as well as IGF-I dependent cell survival
Pinzon-Guzman et al., J Neurosci 2011 : In adult retinas, IGF1 activates PI-3 kinase (PI3K) , but in neonatal retinas its action is identical to the action of an PI3K inhibitor
Logan et al., J Bone Miner Res 2013 (Breast Neoplasms...) : Functional studies in osteoclasts showed that PQIP inhibited both IGF-1 and conditioned medium induced osteoclast formation by preventing phosphatidylinositol 3-kinase (PI3K)/protein kinase B ( Akt ) activation without interfering with RANKL or M-CSF signaling
King et al., Journal of ovarian research 2013 : This may be due partly to altered collagen IV deposition and organization in the ovary in response to insulin and IGF signaling mediated by PI 3-kinase
O' Neill et al., Exp Gerontol 2013 (Alzheimer Disease) : Therapeutic approaches targeted at normalizing signaling through either the neuronal PI3-kinase/Akt/mTOR pathway or its activation by insulin and IGF-1 have been shown to be protective against the development of AD pathology and cognitive decline in animal models of AD and some of these therapies are entering clinical trials in patients with the disease
Lassarre et al., Biochim Biophys Acta 2013 (Breast Neoplasms) : PDGF inhibited IGF-I stimulated IRS-1 tyrosine phosphorylation and subsequent IGF-I induced PI 3-kinase activity, and stimulated IRS-1 serine 307 phosphorylation
Sizer et al., Mol Cell Endocrinol 1994 : Insulin- and IGF-I induced changes in PI 3-kinase were each half-maximal at 3-5 nM of hormone and were not additive
Pomerance et al., J Neurosci Res 1995 : In astroglial cells cultured in serum-free medium, IGF1 , PDGF, and EGF, which stimulate cell proliferation, increased PI(3)-kinase activity immunoprecipitated with anti-phosphotyrosine antibodies as shown by thin layer chromatography and high performance liquid chromatography ... IGF1 and PDGF, to a lesser degree, also increased the PI(3)-kinase activity associated with pp60c-src protein
Kato et al., J Cell Physiol 1993 : Overexpression of IGF-I receptors in NIH-3T3 cells resulted in increased sensitivity and maximal responsiveness of thymidine incorporation, 2-deoxyglucose uptake, and phosphatidylinositol-3 (PI3) kinase activation to IGF-I stimulation
Chang et al., J Biol Chem 1995 : In contrast, insulin-like growth factor 1 modestly stimulated PI 3-kinase in both control and transgenic muscle
Sizer et al., Mol Cell Endocrinol 1994 : Insulin- and IGF-I induced changes in PI 3-kinase were each half-maximal at 3-5 nM of hormone and were not additive
Minshall et al., J Immunol 1996 : In this work, we show that IL-3 dependent FDCP-1/Mac-1 murine hemopoietic progenitors express receptors for another growth factor, insulin-like growth factor-I (IGF-I), and that both IL-3 and IGF-I stimulate PI 3-kinase activity
Jullien et al., Diabetes 1996 (Body Weight...) : To determine through which receptor IGF-I was activating PI 3-kinase , the ability of IGF-I to activate both its own receptor and insulin receptor was simultaneously measured ... In muscles of obese insulin-resistant mice, although the defect of PI 3-kinase activation in response to IGF-I was relatively less pronounced ( 45 % ) than in response to insulin ( 70 % ) when compared with lean mice, PI 3-kinase stimulation was still markedly altered in response to IGF-I
Takahashi et al., Endocrinology 1997 : Rather, phosphatidylinositol (PI) 3-kinase activity, which was activated by IGF-I about 5- to 10-fold more strongly than EGF, appeared to correlate with mitogenesis
Dudek et al., Science 1997 : IGF-1 activation of phosphoinositide 3-kinase (PI3-K) triggered the activation of two protein kinases, the serine-threonine kinase Akt and the p70 ribosomal protein S6 kinase ( p70 ( S6K ) )
Brüning et al., Mol Cell Biol 1997 : Increasing the level of IRS-2 in these cells by using a retrovirus reconstitutes IGF-1 activation of PI 3-kinase and immediate-early gene expression to the same degree as expression of IRS-1 ; however, IRS-2 overexpression has only a minor effect on IGF-1 stimulation of cell cycle progression
Giorgino et al., J Biol Chem 1997 : The stimulation of phosphatidylinositol (PI) 3-kinase by insulin-like growth factor I (IGF-I) in L6 cultured skeletal muscle cells is inhibited by the glucocorticoid dexamethasone
Miller et al., J Biol Chem 1997 : PI-3-K inhibition completely blocked the survival promoting activity of IGF-I , but had no effect on cAMP mediated survival ... These data indicate that the survival promoting effects of depolarization and IGF-I , but not cAMP, require PI-3-K activity
Scrimgeour et al., Endocrinology 1997 (Cell Transformation, Neoplastic) : We have also examined IGF-I induced phosphatidylinositol (PI) 3-kinase activation in the same cell lines ... By each method we show that the IGF-I induced MAP kinase phosphorylation/activation and PI 3-kinase activation, are not different between cells overexpressing wild-type IGF-I receptors and cells carrying IGF-I receptors having tyrosine motifs replaced at positions 1250 and 1251
Esposito et al., Endocrinology 1997 (Cell Transformation, Neoplastic) : IGF-I induced activation of phosphatidylinositol (PI) 3'-kinase was equivalent in cells expressing either mutant or wild-type IGF-IRs
Mañes et al., J Biol Chem 1997 : We show that IGFBP-1 inhibits IGF-I induced survival and proliferation of BAF/3 cells, as well as IGF-I mediated activation of phosphatidylinositol 3-kinase (PI 3-K)
Liu et al., J Immunol 1998 : IGF-I , but not vitamin D3, caused a sevenfold increase in the enzymatic activity of both PI 3-kinase and atypical PKC-zeta
Valverde et al., Mol Endocrinol 1998 : Insulin/IGF-I rapidly stimulated IRS-1 and IRS-2 tyrosine phosphorylation, their association with p85alpha, and IRS-1- and IRS-2 associated phosphatidylinositol (PI) 3-kinase activation to the same extent, the effect of insulin being stronger than the effect of IGF-I at the same physiological dose ( 10 nM )
Zhang et al., J Neurochem 1998 : The inhibition of IGF-1 protection by ethanol corresponded to a marked reduction in the phosphorylation of insulin receptor substrate 1, the binding of phosphatidylinositol 3-kinase ( PI 3-kinase ), and a block of IGF-1 stimulated PI 3-kinase activity
Blakesley et al., J Biol Chem 1998 : In addition, these mutant IGF-I receptors do not affect IGF-I stimulated p42/p44 mitogen activated protein kinase activation or phosphatidylinositol (PI) 3'-kinase activity
Kornmann et al., Cancer Res 1998 (Colonic Neoplasms...) : Insulin, IGF-I , and IGF-II enhanced the growth of both cell lines, stimulated tyrosine phosphorylation of IRS-2, and increased IRS-2 associated phosphatidylinositol (PI) 3-kinase activity
Hayashi et al., J Biol Chem 1998 : In cultured cells, IGF-I specifically activated phosphatidylinositol 3-kinase ( PI3-kinase ) and its downstream target, protein kinase B, but not mitogen activated protein kinases ... In cultured cells, IGF-I specifically activated phosphatidylinositol 3-kinase ( PI3-kinase ) and its downstream target, protein kinase B, but not mitogen activated protein kinases
Cui et al., Brain Res Dev Brain Res 1998 : Phosphoinositide 3-kinase (PI3-K) activation by IGF-I can lead to phosphorylation and inactivation of GSK-3
Takahashi et al., J Cell Physiol 1999 : IGF-I induced PI 3-kinase activation is generally mediated via insulin receptor substrate (IRS)-1, but EGF induced PI 3-kinase activation is mediated by various signalling molecules such as ErbB3 and c-Cbl in different cells