Gene interactions and pathways from curated databases and text-mining

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IGF1 — PIK3CA

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Li et al., Am J Physiol 1999 : IGF-I activated a wortmannin-sensitive PI3K and its purported effector, the atypical protein kinase C (PKC)-zeta
Campana et al., J Neurosci Res 1999 : Phosphatidylinositol 3-kinase and Akt protein kinase mediate IGF-I- and prosaptide induced survival in Schwann cells
Chandrasekher et al., Invest Ophthalmol Vis Sci 2000 : Phosphatidylinositol 3-kinase in bovine lens and its stimulation by insulin and IGF-1
Zheng et al., J Biol Chem 2000 (MAP Kinase Signaling System) : PMA also decreased IGF-1 induced tyrosine phosphorylation of insulin receptor substrate-1 and its association with PI3K
Tu et al., Cancer Res 2000 (MAP Kinase Signaling System...) : IGF-I effectively activated PI 3-K in 8226 and OCI-My5 MM cells, but IL-6 was ineffective ... IGF-I also successfully activated PI 3-K in four of four MM patient specimens, and IL-6 activated PI 3-K in three of four specimens
Gagnon et al., Endocrinology 2001 : Exogenous PI ( 3,4,5 ) P3 ( 10 microM ), the principal product of IGF-1 stimulated PI3K in 3T3-L1 preadipocytes, had a modest survival effect on its own, reducing cell death from 47.9 +/- 3.4 % to 35.6 +/- 3.5 %
Trümper et al., Ann N Y Acad Sci 2000 : Insulin and IGF-1 stimulated PI 3-K activity was mainly associated with insulin receptor substrate (IRS) isoforms IRS-1 and IRS-2 and less so with the IRS-isoform Grb-2 associated binder-1 (Gab-1)
Weber et al., Comp Biochem Physiol B Biochem Mol Biol 2001 : These data suggest that PI 3-K activity is required for GtH- MIS- and IGF-I induction of GVBD in striped bass
Richards et al., Endocrinology 2001 : Collectively, these data suggest that the E2-induced decrease in uterine insulin receptor substrate-2 requires IGF-I signaling, is not dependent solely on insulin receptor substrate-1 and PI3K , and is blocked by progesterone as well as by pharmacological inhibition of proteasomal protease activity
Mehrhof et al., Circulation 2001 : In summary, our data demonstrate that in cardiomyocytes, the antiapoptotic effect of IGF-I requires both PI3K- and MEK1 dependent pathways leading to the activation of the transcription factor CREB, which then induces the expression of the antiapoptotic factor bcl-2
García et al., Mol Endocrinol 2002 : PI3K is involved in the IGF-I inhibition of TSH induced sodium/iodide symporter gene expression ... Interestingly, inhibition of PI3K blocked IGF-I repression of TSHinduced NIS mRNA and protein levels
Hermanto et al., Mol Cell Biol 2002 : While IGF-I induced activation of IRS-1, Shc, PI3K , and MAPK pathways was unaffected, IGF-I-inducible beta1 integrin associated kinase activity and association of Crk with p130 ( CAS ) were significantly inhibited by RACK1 overexpression
Khan et al., Endocrinology 2002 : Furthermore, FSH amplifies IGF-I mediated PI3K/AKT signaling in Sertoli cells
Hallmann et al., J Biol Chem 2003 (MAP Kinase Signaling System) : Although, IGF-1 stimulated PI3K activity associated with insulin receptor substrates was unaltered in all cell lines, p85alpha-null ES cells showed diminished protein kinase B activation despite increased PI3K activity associated with the p85beta subunit
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
Neudauer et al., Exp Cell Res 2003 (MAP Kinase Signaling System...) : In contrast, similar concentrations of either wortmannin or LY294002 were required to inhibit both IGF-I induced PI3K activation and migration
Oh et al., J Biol Chem 2003 : Stimulation of PI3K by IGF-1 resulted in blockage of NO-induced activation of p38 kinase and ERK1/2 and inhibition of PKCalpha and PKCzeta, which in turn suppressed dedifferentiation and apoptosis
Etgen et al., Endocrinology 2003 : These data suggest that activation of both PI3K and MAPK by E ( 2 ) and IGF-I mediates hormonal facilitation of lordosis behavior
Sundgren et al., Am J Physiol Regul Integr Comp Physiol 2003 (Cardiomegaly...) : We conclude that 1 ) IGF-1 through IGF1R stimulates cardiomyocyte division in vivo ; hyperplastic growth is the most likely explanation of IGF-1 stimulated heart growth in vivo ; 2 ) IGF-1 through IGF1R does not stimulate binucleation in vitro or in vivo ; 3 ) IGF-1 through IGF1R does not stimulate hypertrophy either in vivo or in vitro ; and 4 ) IGF-1 through IGF1R requires both ERK and PI3K signaling for proliferation of near-term fetal sheep cardiomyocytes in vitro
Tai et al., Cancer Res 2003 (Multiple Myeloma) : IGF-I induces a 1.7-2.2 ( MM.1S ) and 2-2.5-fold ( OPM6 ) increase in migration, whereas blocking anti-IGF-I and anti-beta1 integrin monoclonal antibodies, PI3-K inhibitors, as well as cytochalasin D abrogate IGF-I induced MM cell transmigration
Yamagishi et al., Brain Res Mol Brain Res 2003 (Potassium Deficiency) : Here we found that IGF-1 had a greater survival promoting effect than BDNF, and activated PI3-K to a higher level and maintained the level for a longer time
Lu et al., Biochem Biophys Res Commun 2004 (Breast Neoplasms...) : They are consistent with the view that the IGF-IR mediated attenuation of trastuzumab induced growth inhibition we recently described is dependent on IGF-I induced PI3K signaling rather than IGF-I induced MAPK signaling
Pfeil et al., Prostate 2004 (Prostatic Neoplasms) : IGF-1 , EGF, and heregulin but not PDGF or activators of protein kinase A induced phosphorylation of Akt in DU145 cells and activation was completely blocked by the PI3K inhibitor LY294002
Meroni et al., J Endocrinol 2004 (MAP Kinase Signaling System) : At the same time, it was proposed that in 8-day-old Sertoli cells the effects of FSH on phosphorylated PKB ( P-PKB ) levels can be explained by a combination of increased secretion of endogenous IGF-I, decreased IGF binding protein-3 (IGFBP-3) production, and a synergistic action of FSH on IGF-I dependent PI3K activation
Aikin et al., Endocrinology 2004 : In addition, IGF-I suppressed cytokine mediated JNK activation in a PI3K dependent manner ... In addition, IGF-I suppressed cytokine mediated JNK activation in a PI3K dependent manner
Descamps et al., J Immunol 2004 (Multiple Myeloma) : Altogether, these results suggest that CD45 negatively regulates IGF-1 dependent activation of PI3K
Weber et al., Biol Reprod 2005 : Our data suggest that gap junctions and PI 3-K activity are necessary for GtH and IGF-I to induce and maintain OMC in white bass
Laurino et al., J Cell Sci 2005 : PI3K activation by IGF-1 is essential for the regulation of membrane expansion at the nerve growth cone ... Our results show that IGF-1 , but not BDNF, significantly and rapidly stimulates IRS/PI3K/Akt and membrane expansion ... Finally, our results show that, upon stimulation with IGF-1 , most active PI3K becomes associated with distal microtubules in the proximal or central domain of the growth cone
Zhang et al., J Mol Endocrinol 2005 (Breast Neoplasms...) : Moreover, these same IGF-I induced responses were also inhibited by the antiestrogen ICI 182780 and this was in contrast to a previous report suggesting that ICI 182780 did not affect IGF-I dependent activation of PI3-K or induction of cyclin D1 expression
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
Risinger et al., J Biol Chem 2006 : Both PDGF-BB and IGF-I activated PI3K/Akt to similar degrees ; however, only PDGF-BB concomitantly stimulated an inhibitory signaling pathway that antagonized the effects of Akt but did not alter the extent or duration of Akt activation
Baregamian et al., J Surg Res 2006 (Enterocolitis, Necrotizing) : Wortmannin, an inhibitor of PI3-K, was used to show PI3-K dependent mechanism of action for IGF-1 ... A better understanding of the exact role of IGF-1 mediated activation of PI3-K may allow us to facilitate the development of novel therapy against NEC
Dhar et al., Cancer Res 2007 (Breast Neoplasms) : Because a pure anti-ER ICI 182,780 is not only able to suppress the up-regulation of WISP-2/CCN5 mRNA expression by IGF-1, it also suppresses the PI3K/Akt activity induced by IGF-1 in MCF-7 cells ; we anticipate that the membrane ER receptor may participate in this event
Lilja et al., J Neurosci Res 2007 (Neuroblastoma) : By blocking phosphatidylinositol-3-kinase [ PI(3)K ] or mitogen activated protein kinase ( MAPK ) signaling, we concluded that the increase in total TRPV1 protein content induced by IGF-I was controlled by PI(3)K signaling, whereas insulin seemed to regulate TRPV1 protein expression via both PI(3)K and MAPK pathways
Ray et al., Int J Oncol 2007 (Breast Neoplasms...) : MCF-7 cells expressed higher levels of Ob-Rb, Jak2, PI3K , Stat3 and p-Stat3 in a dose dependent manner to 50 ng/ml at 24 h ; and IGF-IRalpha increased at 24 h. Cyclin D1 and Cox-2 levels increased with leptin treatment
Carelli et al., Mol Med 2007 (Angiomyolipoma...) : Interestingly, single or simultaneous inhibition of PI3K by LY294002 and ERK by PD98059 does not prevent IGF-1 mediated survivin expression
Fernández et al., Biochim Biophys Acta 2008 : We analyzed IGF-I signalling on astrocytes through the canonical phosphatidylinositol 3-kinase (PI3K)/Akt pathway and focused on possible changes in PTEN, a phosphatase that modulates IGF-I signalling by inhibiting Akt activation and, in turn is positively regulated by PI3K ... Subsequent recovery of reduced PTEN required also activation by IGF-I of PI3K to recruit in this case protein kinase A (PKA) which stimulated Egr-1 levels and, consequently PTEN synthesis
Brady et al., Growth Horm IGF Res 2008 : IGF-I and -II caused significant increases in PI3-K , but not MAPK, activity
Radhakrishnan et al., J Biol Chem 2008 (MAP Kinase Signaling System) : In contrast to MAPK activation the role of Shc in modulating PI3K in response to IGF-I has not been determined ... In this study we show that impaired Shc association with Grb2 results in decreased Grb2-p85 association, SHPS-1-p85 recruitment, and PI3K activation in response to IGF-I
Rodríguez-Pérez et al., Int J Biochem Cell Biol 2009 : Inhibitors of PI3K and PKC essentially blocked insulin-, IGF-I- and EGF induced desensitizations
Frost et al., J Cell Biochem 2009 : The PI3K inhibitor LY294002 blocked IGF-I but not Dex induced REDD1
Park et al., Haematologica 2010 (Leukemia, Myeloid, Acute) : Constitutive PI3K activation is the result of autocrine IGF-1/IGF-1R signaling in 70 % of acute myeloid leukemia samples but specific inhibition of this pathway does not induce apoptosis
Chapuis et al., Haematologica 2010 (Blast Crisis...) : Autocrine IGF-1/IGF-1R signaling is responsible for constitutive PI3K/Akt activation in acute myeloid leukemia : therapeutic value of neutralizing anti-IGF-1R antibody ... As we previously reported IGF-1 autocriny in acute myeloid leukemia cells, we investigated whether IGF-1 signaling was involved in the constitutive activation of PI3K
Thimmaiah et al., Cancer Res 2010 (Rhabdomyosarcoma) : Results indicate that IGF-I signaling to Bad requires activation of PI3K and PKC ( mu, theta, epsilon ) but not mTOR, Ras-extracellular signal regulated kinase 1/2, protein kinase A, or p90 ( RSK )
Koutros et al., Cancer Res 2010 (Genetic Predisposition to Disease...) : In conclusion, we observed a significant association between PIK3C2B and prostate cancer risk, especially for familial, early-onset disease, which may be attributable to IGF dependent PI3K signaling
Wang et al., J Bone Miner Res 2010 : T ( 3 ) activates IGF-1/IGF1R signaling and IGF-1 dependent PI3K/Akt/GSK-3beta signaling in growth plate chondrocytes undergoing proliferation and differentiation to prehypertrophy
Jia et al., Exp Mol Pathol 2010 : IGF-1 induced proliferation in both SV and IMA SMCs was inhibited by a PI3K inhibitor, wortmannin ... These data demonstrate differential activity of IGF-1 induced PI3K-Akt activation , which was quantitatively and temporally greater in SV SMCs than in the IMA
Leen et al., Endocrinology 2011 : The role of PI3K/Akt in GLP-2 induced IGF-I mRNA levels in the murine jejunum was also confirmed in vivo
Liu et al., Cell Mol Neurobiol 2012 : Activation of ERK1/2 and PI3K/Akt by IGF-1 on GAP-43 expression in DRG neurons with excitotoxicity induced by glutamate in vitro
Fox et al., Cancer Res 2011 (Adenocarcinoma...) : Inhibition of InsR and IGF-IR with the dual tyrosine kinase inhibitor OSI-906 prevented the emergence of hormone independent cells and tumors in vivo, inhibited parental and LTED cell growth and PI3K/AKT signaling, and suppressed growth of established MCF-7 xenografts in ovariectomized mice, whereas treatment with the neutralizing IGF-IR monoclonal antibody MAB391 was ineffective
Takahashi et al., Aging Cell 2012 : Finally, small interfering RNA ( siRNA ) -mediated knockdown of p85a expression in acinar cells from young mice resulted in markedly attenuated activation of PI3K/Akt downstream signaling in response to IGF-1
Kumari et al., Indian J Dermatol Venereol Leprol 2013 (Acne Vulgaris...) : Milk consumption and hyperglycemic diets can induce insulin and IGF-1 mediated PI3K / Akt-activation inducing sebaceous lipogenesis, sebocyte, and keratinocyte proliferation, which can aggravate acne
Mañes et al., J Biol Chem 1997 : IGFBP-1 complex with hST-3 restores IGF-I induced proliferation and PI 3-K kinase activity in these cells