◀ Back to EPHB2

CCND1 — EPHB2

Text-mined interactions from Literome

Roovers et al., Mol Biol Cell 1999 : Cell attachment to fibronectin or anti-alpha5beta1 integrin is sufficient to sustain the ERK signal and to induce cyclin D1 in growth factor treated cells
Corre et al., Oncogene 1999 (Cell Transformation, Viral...) : Expression of alpha i2-G204A resulted in decreased Src-kinase activity, delayed activation of p42 ERK-MAPK , decreased cyclin D1 expression and reduced proliferation in response to serum
Seddighzadeh et al., Clin Exp Metastasis 1999 (Breast Neoplasms...) : Inhibition of ERK1/2 activity also led to decreased cell proliferation and to decreased cyclin D1 expression
Fribourg et al., Cell Growth Differ 2000 (Adenocarcinoma...) : Although V12Ras was able to stimulate ERK phosphorylation and induce cyclin D1 expression in the absence of androgen, it was not sufficient to promote androgen independent cell cycle progression
Lotfi et al., Braz J Med Biol Res 2000 (Adrenal Cortex Neoplasms) : FGF2 elicits a strong mitogenic response in G0/G1 arrested Y1 adrenocortical cells, that includes a ) rapid and transient activation of extracellular signal regulated kinases-mitogen activated protein kinases ( ERK-MAPK) (2 to 10 min ), b ) transcription activation of c-fos, c-jun and c-myc genes ( 10 to 30 min ), c ) induction of c-Fos and c-Myc proteins by 1 h and cyclin D1 protein by 5 h, and d ) onset of DNA synthesis stimulation within 8 h. ACTH, itself a weak mitogen, interacts with FGF2 in a complex manner, blocking the FGF2 mitogenic response during the early and middle G1 phase, keeping ERK-MAPK activation and c-Fos and cyclin D1 induction at maximal levels, but post-transcriptionally inhibiting c-Myc expression
Osada et al., Jpn J Cancer Res 2000 (Pancreatic Neoplasms) : EGF induced cell proliferation through ERK phosphorylation, since U0126, which is an inhibitor of ERK phosphorylation, abrogated the increase of cyclin D1 by EGF
Wagner et al., Genes Dev 2001 (Disease Models, Animal...) : Activation of Ras and Erk causes induction of cyclin D1-Cdk4 without increase of cyclin E or PCNA in ductal lesions
Bauerfeld et al., Am J Physiol Lung Cell Mol Physiol 2001 : Cdc42 induced cyclin D1 promoter activation was independent of ERK as evidenced by insensitivity to PD-98059, an inhibitor of mitogen activated protein kinase/ERK kinase ( MEK )
Crépieux et al., Oncogene 2001 (MAP Kinase Signaling System) : Consistently, we show that the ERK mediated FSH mitogenic effect triggers upregulation of cyclin D1
Guillemot et al., J Biol Chem 2001 (MAP Kinase Signaling System) : Taken together, these findings demonstrate that Ang II-induced cyclin D1 up-regulation is mediated by the activation and specific interaction of Egr-1 with the -136 to -96 bp region of the cyclin D1 promoter and by activation of the -29 to +139 bp region, both in a p21(ras)/Raf-1/MEK/ERK dependent manner, and also involves PI3K and SHP-2
Masuda et al., Clin Cancer Res 2001 : Treatment with EGCG inhibited phosphorylation of the EGFR, signal transducer and activator of transcription3 ( Stat3 ), and extracellular regulated kinase (ERK) proteins and also inhibited basal and transforming growth factor-alpha stimulated c-fos and cyclin D1 promoter activity
Takami et al., Am J Respir Cell Mol Biol 2002 : IFN-gamma does not interfere with the effects of HGF on either ERK activation or cyclin D1 induction ; however, it prevents the downregulation of p27 ( kip1 ) CDK inhibitor that takes place in response to a combination of HGF and serum
Jirmanova et al., Oncogene 2002 : Differentiation induced by retinoic acid results in the gain of ERK dependent control of cyclin D1 expression and of S phase progression
Hecquet et al., Invest Ophthalmol Vis Sci 2002 (MAP Kinase Signaling System) : The requirement for Ras and the regulatory role of ERK2 in cyclin D1 production and in cell proliferation suggest that the Ras/Raf/MEK/ERK pathway plays a key role in the control of RPE cell proliferation
Lents et al., J Biol Chem 2002 : Taken together, these data show a new role for ERK in G1 cell cycle progression : In addition to its role in stimulating cyclin D1 expression and nuclear translocation of CDK2, ERK regulates Thr-160 phosphorylation of CDK2-cyclin E
Roovers et al., Mol Cell Biol 2003 (MAP Kinase Signaling System) : We recently reported that Rho kinase is required for sustained ERK signaling and the consequent mid-G ( 1 ) phase induction of cyclin D1 in fibroblasts
Zhang et al., Acta Pharmacol Sin 2003 : Fourthly, ET-1 increased the phosphorylated level of ERK and the expression of cylin D1, an inhibitor of ERK blocked phosphorylated level of ERK and cyclin D1 expression
Park et al., Am J Physiol Gastrointest Liver Physiol 2003 (Colorectal Neoplasms) : Transient ERK activation and subsequent cyclin D1 induction were observed on adding 10 microM ZnCl2 in MSSM in the presence of cell proliferation ... Moreover, this ERK activation and cyclin D1 and p21 ( Cip/WAF1 ) induction were abolished by PD-98059 pretreatment ... The differential regulations of cell growth, ERK activities, and cyclin D1 and p21 ( Cip/WAF1 ) inductions were also observed in serum enriched medium containing higher zinc concentrations
Alldridge et al., Exp Cell Res 2003 (MAP Kinase Signaling System) : Moreover, ANXA1 reduces proliferation by ERK mediated disruption of the actin cytoskeleton and ablation of cyclin D1 protein expression and not by ERK mediated induction of the cyclin dependent kinase, CDK2, inhibitor p21 ( cip/waf )
Kuemmerle et al., Am J Physiol Gastrointest Liver Physiol 2004 : IGF-I elicited a time dependent increase in cyclin D1 protein levels mediated jointly by ERK1/2 dependent and PI3-kinase dependent mechanisms
Chen et al., FASEB J 2004 (MAP Kinase Signaling System) : Taken together, our findings define a critical role for SAMe in ERK signaling and cyclin D1 regulation during regeneration and suggest chronic hepatic SAMe depletion results in loss of responsiveness to mitogenic signals
Li et al., Am J Physiol Cell Physiol 2004 (MAP Kinase Signaling System) : Trypsinization of high-density MDCK cells immediately increased phospho-ERK1/2 and was followed by a transient increase in cyclin D1 levels
Ko et al., Exp Cell Res 2004 (Adenocarcinoma...) : Decreasing phospho-ERK with the pharmacological inhibitors, PD98059 and U0126, markedly suppresses hyperoxia stimulated phospho-p53 ( Ser15 ), p53, and p21 ( CIP1 ), and also restores the hyperoxia reduced kinase activities of cyclin D1/E1-Cdks
Yuan et al., Cancer Res 2004 (Lung Neoplasms...) : In response to 10 % serum, a proliferative stimulus, phosphorylated ERK1/2 initially accumulated in the nucleus, and reduction of nuclear phospho-ERK1/2 after 2 to 4 hours was followed by expression of cyclin D1 and S-phase entry
Huynh et al., Int J Oncol 2004 (Carcinoma, Hepatocellular...) : Our data indicate that activated ERK plays an important role in cyclin D1 and Cdk-2 expression and phosphorylation of pRB at Ser780 and Ser795 in liver cancer cells
Shi et al., J Biol Chem 2005 : Furthermore, we show that cyclin D1 and c-myc IRES function is enhanced following exposure to rapamycin and requires both p38 MAPK and RAF/MEK/ERK signaling, as specific inhibitors of these pathways reduce IRES mediated translation and protein levels under conditions of quiescent AKT activity
Swant et al., J Biol Chem 2005 (Cell Transformation, Neoplastic...) : Our studies reveal that recombinant MIF induces cyclin D1 expression in a Rho-, Rho kinase-, MLC kinase-, and ERK dependent manner in asynchronous NIH 3T3 fibroblasts
Talora et al., Blood 2006 (Cell Transformation, Neoplastic...) : We therefore conclude not only that cyclin D1 is a target of the Tal1/Sp1 complex, but also that Notch3 dependent activation of pre-TCR/ERK signaling regulates SCL/Tal1 function
Kim et al., J Endocrinol 2006 : Although EX induced phosphorylation of Raf-1 and extracellular-signal regulated kinase ( ERK ), both PD98059 and exogenous ERK1 had no effect on the cyclin D1 induction by EX
Dekanty et al., FEBS Lett 2006 : We also show that ERK1-2 , but not p38MAPK activation is required to induce cyclin D1 expression, strongly suggesting that the concerted action of cyclin D1 gene expression and other events are required to induce complete phosphorylation of retinoblastoma protein and S-phase entry in response to PGF2alpha
Sawant et al., Toxicology 2007 (Carbon Tetrachloride Poisoning...) : In contrast to the non-DB rats, CCl ( 4 ) administration led to lower plasma IL-6, decreased ERK1/2 activation , lower cyclin D1 , and cdk 4/6 expression resulting in decreased p-pRB and inhibition of liver cell division in the DB rats
Villanueva et al., Mol Biol Cell 2007 : ERK activity regulates the induction of cyclin D1 , and a sustained ERK signal is thought to be required for this effect, at least in fibroblasts
Klein et al., Cell cycle (Georgetown, Tex.) 2007 : Inhibition of NFkappaB signaling with the IkappaB super-repressor blocked the Rac dependent expression of cyclin D1 mRNA, and this effect was selective since ERK dependent cyclin D1 mRNA induction was minimally affected by super-repressor expression ... We conclude that, in MEFs, Rac mediated induction of cyclin D1 mRNA requires activation of a parallel NFkappaB pathway whereas ERK induces cyclin D1 transcription independent of NFkappaB
Yang et al., Biochem J 2008 (Breast Neoplasms) : Heregulin beta1 promotes breast cancer cell proliferation through Rac/ERK dependent induction of cyclin D1 and p21Cip1
Kothapalli et al., J Biol Chem 2008 : HMW-HA binding to CD44 selectively inhibits the GTP loading of Rac and Rac dependent signaling to the cyclin D1 gene, whereas LMW-HA binding to CD44 selectively stimulates ERK activation and ERK dependent cyclin D1 gene expression
Parrales et al., J Cell Physiol 2010 (Vitreoretinopathy, Proliferative) : Our results show that ERK activation is necessary but not sufficient for the induction of cyclin D1 expression and proliferation, since the inhibition of PI3K or cPKC prevents this outcome
Humtsoe et al., Oncogene 2010 (MAP Kinase Signaling System...) : The expression of cyclin D1 required both EGFR mediated ERK and AKT activation
Go et al., Mar Biotechnol (NY) 2011 : Cf-PS treatment induced the translocation of ß-catenin, an effector of the Wnt signaling pathway, from the cytosol to the nucleus and increased the expression of cyclinD1 and c-myc. Cf-PS also induced ERK1/2 phosphorylation, which is activated by mitogenic and proliferative stimuli such as growth factors, but the phosphorylation of JNK and p38 was not enhanced
Hwang et al., Adv Food Nutr Res 2011 : Further, Cf-PS treatment induced the translocation of ß-catenin, an effector of the Wnt signaling pathway, from the cytosol to the nucleus and increased the expression of cyclinD1 and c-myc. Cf-PS also induced ERK1/2 phosphorylation, which is activated by mitogenic and proliferative stimuli such as growth factors, but the phosphorylation of JNK and p38 was not enhanced
Pan et al., Biochem Biophys Res Commun 2012 : Endoglin inhibits ERK induced c-Myc and cyclin D1 expression to impede endothelial cell proliferation
Li et al., PloS one 2012 : Pharmacological inhibition of JAK/STAT3, PI3K/Akt or MEK/ERK signaling by AG490, Wortmannin or U0126, respectively, reduced leptin induced cyclin D1 expression and NP cell proliferation
Weber et al., J Biol Chem 1997 : Overexpression of dominant negative ERK resulted in inhibition of PDGF induced cyclin D1 expression but had no effect on PDGF induced p27 ( KIP1 ) degradation
Ito et al., Hepatology 1998 (Carcinoma, Hepatocellular...) : Furthermore, in 25 of 26 cases of HCC which genomic DNA was available, 22 cases without genomic DNA amplification exhibited positive correlation, not only between protein expression of c-Fos and cyclin D1 , but also between MAPK/ERK activation and cyclin D1 expression ... In conclusion, these findings suggest that MAPK/ERK activation in human HCC may play an important role in multistep hepatocarcinogenesis, especially in the progression of HCC ; at least in part, through cyclin D1 up-regulation primarily induced by MAPK/ERK via c-Fos