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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to MAPK3

KRAS — MAPK3

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Choi et al., Oncogene 2004 : Taken together, these findings explain the opposite effects of Ha-Ras and Ki-Ras on modulation of radiosensitivity, and suggest that differential activation of PI3K/Akt and Rac/p38 MAPK signaling by Ha-Ras and Ki-Ras may account for the opposing response to the ionizing radiation
Whitwam et al., Oncogene 2007 (Cell Transformation, Neoplastic...) : Although both NRAS and KRAS activate mitogen activated protein kinase signaling, only NRAS enhances MYC activity in these cells
Luo et al., Oncogene 2007 (Intestinal Neoplasms...) : Expression of K-ras ( V12 ) in tumours caused activation of the mitogen activated protein kinase and Akt/protein kinase B signaling pathways, demonstrated by phosphorylation of p44MAPK, Akt and GSK3beta, as well as transcriptional upregulation of Pem, Tcl-1 and Trap1a genes ( known targets of K-ras ( V12 ) expression in stem cells )
Lee et al., Int J Oncol 2009 (Adenoma...) : ATP synthase, Ras oncogene family, cytochrome c oxidase, flavoprotein, TEF 1, adipoprotein A-1 BP, glutathione oxidase, fatty acid BP 4, diaphorase 1, MAPK4 and transgelin were up-regulated by K-ras oncogene
Moretó et al., Cell Signal 2009 (MAP Kinase Signaling System) : These findings suggest that modulation of K-Ras activity via CaM regulates MAPK signaling only in certain cell types
Van Schaeybroeck et al., Cancer Res 2011 (Colorectal Neoplasms) : Collectively, our findings indicate that oncogenic Kras regulates ADAM17 activity and thereby growth factor ligand shedding in a MEK1/2/Erk1/2 dependent manner and that KrasMT CRC tumors are vulnerable to MEK1/2 inhibitors, at least in part, due to their dependency on ADAM17 activity
Lopez et al., Cell Death Differ 2012 (MAP Kinase Signaling System...) : Importantly, in a set of human cancer cells with Src-, Kras- or BRAF dependent activation of Erk1/2 , resistances to staurosporine or thapsigargin were also shown to depend on Bik degradation rate via a similar mechanism
Mulay et al., PloS one 2013 (MAP Kinase Signaling System) : We demonstrate that in Chinese Hamster Ovary ( CHO ) cells and human hepatic HuH7 cells, extracellular signal regulated kinase 1/2 ( Erk1/2 ) inhibition reduces PPARa-inducible ABCA1 protein levels, while ectopic expression of constitutively active H-Ras, K-Ras and MAPK/Erk kinase 1 (Mek1) increases ABCA1 protein expression, respectively
Lerner et al., J Biol Chem 1995 (Cell Transformation, Neoplastic) : FTI-277 also inhibited oncogenic K-Ras4B processing and constitutive activation of MAPK , but the concentrations required were 100-fold higher than those needed for H-Ras inhibition