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HRAS — MAPK3

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: MAPK3 → HRAS (increases, HRAS Activity, MAPK3 Activity)
  Evidence: Expression of N17Ras attenuated activation of ERK (Figure 4A) and JNK (Figure 4B). In contrast, selective activation of Ras was sufficient for ERK but not JNK activation.
• OpenBEL Selventa BEL large corpus: MAPK3 → HRAS (increases)
  Evidence: On the other hand the cell survival effects of Ras were accompanied by a strong upregulation of ERK activity (represented by phosphorylated ERK1/2 Thr202/Tyr204) and by upregulation of the activity of p70S6K (represented by the phosphorylation status of the major p70S6K target S6) (Figures 3b and c)
• OpenBEL Selventa BEL large corpus: MAPK3 → HRAS (increases)
  Evidence: Ras-mediated activation of ERK activity (represented by the phosphorylation status of ERK1/2 Thr202/ Tyr204) and of RSK activity (represented by the phosphorylation status of RSK1 Ser380) could efficiently be blocked by U0126 treatment (Figure 4a).
• KEGG Axon guidance: HRAS/KRAS/NRAS → MAPK1/MAPK3 (protein-protein, indirect effect)
• KEGG Neurotrophin signaling pathway: MAPK1/MAPK3 → HRAS/KRAS/NRAS (protein-protein, inhibition)
• WikiPathways Insulin Signaling: RAC1/GRB2/SOS1/RAC2/RRAD/GRB14/SOS2/RAF1/HRAS/GRB10 → MINK1/MAP4K4/MAP3K2/MAPK12/MAP3K5/MAPK10/MAP3K3/MAP4K1/MAPK3/MAP2K7/MAPK13/MAP3K1/MAP4K3/MAP2K6/MAP3K8/MAP3K12/MAP2K4/MAPK7/MAPK14/MAP3K11/MAP3K7/MAPK11/MAPK9/MAPK6/MAP3K13/MAP2K3/MAPK4/MAP4K2/MAP2K5/MAP3K10/MAPK1/MAP2K1/MAP3K6/MAP3K4/MAP3K9/MAP4K5/MAP2K2/MAPK8/MAP3K14 (activation)
  
• WikiPathways TGF-beta Receptor Signaling: HRAS → MAPK3 (activation)

Text-mined interactions from Literome

Shin et al., Mol Cells 1999 : Elevated Erk1/2 activity in ECV304 cells was suppressed by dominant negative H-Ras , but not by cytochalasin D
Yamamoto et al., Eur J Biochem 1999 : Our data indicate that H-Ras is essential for mitogen activated protein kinase activation, partly required for transcriptional activation by TGF-beta, but not critically involved in the signaling that exerts the antiproliferative effect of TGF-beta
Gendron et al., Mol Endocrinol 1999 : These results support the observation that inhibition of p21ras did not impair the effect of Ang II on its ability to stimulate MAPK activity
Gire et al., Oncogene 1999 : Transient or stable expression of mutant H-ras ( by scrapeloading or retroviral infection ) at levels which stimulated proliferation induced sustained activation and translocation of MAP kinase ( MAPK ) in these cells
Hashimoto et al., J Neurochem 2000 : Delayed and sustained activation of p42/p44 mitogen activated protein kinase induced by proteasome inhibitors through p21(ras) in PC12 cells
Saavedra et al., Oncogene 2000 (MAP Kinase Signaling System...) : The effects of H-RAS ( V12 ) were mediated by activation of MAPK , as treatment with PD98059 at concentrations verified to selectively inhibit MEK1 reduced the frequency of prevalence of cells with micronuclei
Misra et al., Arch Biochem Biophys 2001 (Calcium Signaling...) : We conclude that alpha2M* induced cPLA2 synthesis is controlled by [ Ca2+ ] i levels, tyrosine kinase activity, the p21ras dependent MAPK and PI 3-kinase downstream signaling pathways, and regulation of NFkappaB
Yashima et al., J Cell Physiol 2001 (MAP Kinase Signaling System) : Although dominant negative mutant of Ha-Ras substantially inhibited the basal activities of ERK and p38 MAPK , it exhibited marginal effect on VEGF induced activation of ERK and p38 MAPK in HUVECs and HAECs
Misra et al., Cell Signal 2001 (MAP Kinase Signaling System) : Thus, COX-2 induction is dependent on cPLA(2) activity, Ca ( 2+ ) mobilization, and PKC activity and requires participation of both the p21(ras) dependent MAPK and PI 3-kinase signalling pathways
Misra et al., Cell Signal 2002 (MAP Kinase Signaling System) : Use of selective inhibitors of signal transduction and the quantitation of the levels of phosphorylated MAPK/ERK activating kinase-1 (MEK1), extracellular signal regulated kinase-1 ( ERK1 ), and p38 mitogen activated protein kinase ( MAPK ) suggests that the effects of Cd ( 2+ ) are mediated by the p21(ras) dependent MAPK , but not the phosphoinositide 3 (PI 3)-kinase signalling pathway
Shih et al., J Clin Endocrinol Metab 2002 (Adenocarcinoma, Follicular...) : Inhibition of the MAPK pathway by either H-ras antisense transfection or PD 98059, an MAPK kinase inhibitor , blocked these RV-induced effects
Illario et al., J Clin Endocrinol Metab 2003 : Inhibition of p21Ras activity and inhibition of MAPK enzymatic activity completely arrested cell growth but did not induce cell death
Bulavin et al., Mol Cell Biol 2003 (MAP Kinase Signaling System) : The region of interaction was mapped to amino acids 71 to 96, and the central portion ( amino acids 71 to 124 ) of Gadd45a was required for p38 MAPK activation in the presence of H-ras
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
Kim et al., Cytokine 2005 (Cell Transformation, Neoplastic) : H-ras mediated activation of p38 MAPK and ERK-1/2 was stimulated by TGF-beta
Messina et al., J Neurochem 2008 : The late decline in Ha-Ras levels observed after 60 min was prevented by the proteasome inhibitor, MG132, as well as by the selective mitogen activated protein kinase ( MAPK ) inhibitor, PD98059
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
Agarwal et al., Oncogene 1995 : We observe that activation of ERK-1 via Raf-1 and p21ras dependent signals can result in the hyperphosphorylation of c-jun
Ming et al., Nature 1994 : Activation of p42mapk/p44mapk is triggered by sequential activation of the GDP-GTP exchange factor Sos, the GTP binding protein p21ras , and protein kinases p74raf and p47mek ( refs 7-10 )
Chen et al., Science 1994 (Cell Transformation, Neoplastic) : Expression of activated G alpha s in NIH 3T3 cells increased intracellular concentrations of adenosine 3',5'-monophosphate ( cAMP ) and inhibited H-Ras stimulated DNA synthesis and mitogen activated protein kinase activity
Frost et al., Proc Natl Acad Sci U S A 1994 : The role of ERK-1 and ERK-2 in wild-type ( wt ) Ha-Ras , phorbol 12-myristate 13-acetate ( PMA ), and serum induced AP-1 activity was studied ... Overexpression of ERK-1 augmented wt Ha-Ras stimulation of AP-1, while having no effect upon PMA or serum stimulation ... Overexpression of either kinase-deficient ERK-1 or kinase-deficient ERK-2 partially inhibited AP-1 activation by wt Ha-Ras but had no effect on PMA or serum induced activation
Joneson et al., Science 1996 : In quiescent fibroblasts, ectopic expression of activated H-RAS ( H-RASV12, where V12 indicates valine-12 ) induces membrane ruffling, mitogen activated protein ( MAP ) kinase activation, and stimulation of DNA synthesis
Todaka et al., Biochem J 1996 : Overexpression of wild-type H-ras and the dominant negative mutant H-rass17N in our cell system respectively enhanced and blocked insulin stimulated activation of mitogen activated protein kinase , but did not affect insulin stimulated GLUT4 translocation
Eguchi et al., J Biol Chem 1996 : These data suggest that Ang II-induced MAPK activation through the Ang II type 1 receptor could be mediated by p21(ras)activation through a currently unidentified tyrosine kinase that lies downstream of Gq-coupled Ca2+/calmodulin signals
Csar et al., Biochem J 1997 (Leukemia, Myeloid) : cAMP suppresses p21ras and Raf-1 responses but not the Erk-1 response to granulocyte-colony stimulating factor : possible Raf-1 independent activation of Erk-1 ... The Erk-1 activity was not down-regulated by the increase in intracellular cAMP levels, whereas p21ras and Raf-1 activities were, suggesting that Erk-1 activity might not be dependent on upstream p21ras and/or Raf-1 activity in this system
Schulz et al., Biochem Biophys Res Commun 1997 : Triggering of the T cell receptor ( TCR ) perturbs the guanine nucleotide binding cycle of p21ras and in turn induces phosphorylation and activation of mitogen activated protein kinases ( MAPK )
Hamilton et al., Oncogene 1998 : Ha-ras and N-ras regulate MAPK activity by distinct mechanisms in vivo