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IGF1 — PCNA

Text-mined interactions from Literome

Takahashi et al., Biochim Biophys Acta 2001 : In addition, these inhibitors depressed the synergistic increase in cyclin D1 and cyclin D- or cyclin E-associated cyclin dependent kinase (CDK) activity that is induced by TSH and IGF-I
Gao et al., J Clin Endocrinol Metab 2001 (Leiomyoma...) : Up-regulation by IGF-I of proliferating cell nuclear antigen and Bcl-2 protein expression in human uterine leiomyoma cells ... In addition, we examined the effect of IGF-I on proliferating cell nuclear antigen ( PCNA ) expression in cultured leiomyoma cells ... The effects of IGF-I on Bcl-2 protein and PCNA expression in cultured leiomyoma cells were assessed by Western immunoblot analysis and immunocytochemical staining, whereas the effects of IGF-I on the cell viability and apoptosis of the cultured cells were determined by 3- ( 4,5-dimethylatriazol-2-yl ) -2,5diphenyltetrasodium bromide ( MTT ) assay and terminal deoxynucleotidyl transferase mediated 2'-deoxyuridine 5'-triphosphate nick end labeling assay, respectively
Shen et al., J Biol Chem 2004 (Adenocarcinoma...) : Deletion of an E2F recognition site from this reporter eliminates the regulatory effects of both IGF-I and TNFalpha on cyclin A transcription, indicating the essential role of E2F-1 in mediating their cross-talk
Frederick et al., Mol Cell Neurosci 2004 : IGF-I and FGF-2 coordinately enhance cyclin D1 and cyclin E-cdk2 association and activity to promote G1 progression in oligodendrocyte progenitor cells ... IGF-I enhanced FGF-2 induction of cyclin D1, activation of G ( 1 ) cyclin-cyclin dependent kinase (cdk) complexes, and hyperphosphorylation of retinoblastoma protein ( pRb )
Jiang et al., J Cell Biochem 2006 (Hypertrophy) : IGF-1 increases laminin, cyclin D1, and p21Cip1 expression in glomerular mesangial cells : an investigation of the intracellular signaling pathway and cell-cycle progression
Beckert et al., J Surg Res 2007 (Skin Ulcer) : However, in these animals only IGF-I released from the hydrogel dressing stimulated SMA- ( P = 0.03 ) as well as PCNA-expression ( P = 0.001 ) and increased granulation tissue formation ( P = 0.018 )
Mairet-Coello et al., J Neurosci 2009 : Moreover, blockade of the PI3K/Akt pathway in vivo decreased DNA synthesis and cyclin E, increased p27 ( KIP1 ) and p57(KIP2) expression, and prevented IGF-1 induced cyclin E mRNA upregulation
Ma et al., Biochem Biophys Res Commun 2009 : However, IGF-1 enhanced NOS activity, NO content, and the expression level of cyclin E protein, and reduced the expression level of AT(1) mRNA
Al-Musawi et al., Differentiation 2011 : However, from ED16, myogenin and IGF-I mRNAs were similar to that of layers and PCNA was reduced leading to similar fibre area, nuclei numbers and muscle mass at ED18
Yamamoto et al., Endocrinology 1996 : TSH pretreatment induced the expression of G1 cyclin in FRTL-5 cells, and IGF-I caused the accumulation of enough G1 cyclins to drive the cell cycle from G1 to S phase in a short time, which accounts for the effect of TSH on IGF-I induced DNA synthesis
Reiss et al., Exp Cell Res 1997 (Myocardial Infarction) : Cyclin E- and A-associated histone H1 kinase activity and cyclin D1-associated retinoblastoma protein associated kinase activity also increased, but cyclin B kinase activity was not enhanced by IGF-1
Dufourny et al., J Biol Chem 1997 (Breast Neoplasms) : In contrast, all of the observed stimulatory effects of IGF-I on cell cycle progression, cyclin D1 synthesis, and pRb hyperphosphorylation were blocked by the specific phosphatidylinositol 3-kinase inhibitor LY294002, suggesting that phosphatidylinositol 3-kinase activity but not MAPK activity is required for transduction of the mitogenic IGF-I signal in MCF-7 cells