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MAPK1 — NRAS
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
MAPK1
→
NRAS
(increases, NRAS 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)
Text-mined interactions from Literome
Giehl et al., Oncogene 2000
(Pancreatic Neoplasms) :
Stimulation of cells with epidermal growth factor (EGF) or fetal calf serum ( FCS ) resulted in
activation of
N-Ras , but not K-Ras, as well as activation of c-Raf, MEK-1, and p42
MAPK
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
Hamilton et al., Oncogene 1998
:
Ha-ras and
N-ras regulate
MAPK activity by distinct mechanisms in vivo