◀ Back to MAPK1
KRAS — MAPK1
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
MAPK1
→
KRAS
(increases, KRAS Activity)
Evidence: ERK phosphorylation that was constitutive in mutant ras MM cells was completely abolished by the MEK inhibitor PD98059 (Figure 2C, left panels), as was the ERK phosphorylation reinduced in wild-type cells by readdition of IL-6 (Figure 2C, right panel).......In addition, re-exposure to IL-6 could reinduce AKT phosphorylation in wild-type cells in a wortmannin-sensitive fashion. Moreover, the constitutively maintained AKT phosphorylation in the mutation-containing cells was also sensitive to wortm...
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KEGG Axon guidance:
HRAS/KRAS/NRAS
→
MAPK1/MAPK3
(protein-protein, indirect effect)
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KEGG Neurotrophin signaling pathway:
MAPK1/MAPK3
→
HRAS/KRAS/NRAS
(protein-protein, inhibition)
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WikiPathways DNA Damage Response (only ATM dependent):
HRAS/KRAS/NRAS
→
MAPK1
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
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
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
Kuroda et al., J Biol Chem 1995
:
We have highly purified REKS by successive column chromatographies using a cell-free assay system in which REKS activates recombinant
extracellular signal regulated kinase 2 through recombinant MEK in a guanosine 5'-O- ( thiotriphosphate ) ( GTP gamma S )
-Ki-Ras dependent manner