Gene interactions and pathways from curated databases and text-mining

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CDK5 — EPHB2

Text-mined interactions from Literome

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 )
Chen et al., Cancer Res 2004 : Additionally, Cdk5/p35 phosphorylates MEK1 and inhibits its ability to phosphorylate its downstream target Erk2
Lee et al., J Neurochem 2004 (Neuroblastoma) : Furthermore, Cdk5 and p35 expression was decreased by ERK1/2 inhibition with PD98059 and increased by overexpression of a constitutive active mitogen activated protein kinase kinase 1 ( MEK1 ) mutant, suggesting the critical role of ERK1/2 in the induction of Cdk5 and p35
Wang et al., Cell Death Differ 2006 : Inhibition of Cdk5 inhibits PI3K/Akt and ERK phosphorylation and Bcl-2 expression, and thus sensitizes the differentiated cells to DNA-damage
Peng et al., Am J Physiol Endocrinol Metab 2009 (Synaptic Transmission) : This study investigated whether Cdk5 dependent ERK activation underlies the estrogen elicited facilitation on the repetitive stimulation induced spinal reflex potentiaton ( SRP ) that is presumed to be involved in postinflammatory/neuropathic hyperalgesia and allodynia
Saito et al., J Exp Med 2010 (Cell Transformation, Neoplastic...) : In nonpolarized epithelial cells, Erk activation results in oncogenic stress, up-regulation of the p21 ( Waf1/Cip1 ) cyclin dependent kinase inhibitor, and induction of senescence
Wang et al., J Cell Biochem 2011 (Brain Neoplasms...) : In addition, induction of LRRC4 or knockdown of STMN1 expression induced cell cycle arrest in U251 cells, which was associated with modulating the p21, cyclin D1, and cyclin B expression, and the ERK phosphorylation, and inhibiting the CDK5 and cdc2 kinase activities, but increasing the microtubulin polymerization in U251 cells
Hong et al., Exp Cell Res 2011 (Prostatic Neoplasms) : Ectopic expression of a constitutively active AR inhibited Raf/MEK/ERK mediated regulation of the differentiation markers, neuron-specific enolase and neutral endopeptidase, and the cyclin dependent kinase inhibitors, p16(INK4A) and p21 ( CIP1 ), but not Rb phosphorylation and E2F1 expression, indicating that AR has a specific role in the pathway mediated differentiation and growth inhibitory signaling