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HRAS — MAPK14

Pathways - manually collected, often from reviews:

• KEGG Neurotrophin signaling pathway: HRAS/KRAS/NRAS → MAPK11/MAPK12/MAPK13/MAPK14 (protein-protein, activation)
  
• 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)
  

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• MIPS Negatome - no physical interaction between proteins Interaction: HRAS — MAPK14 (Absence of interaction, pull down) Waskiewicz et al., EMBO J 1997

Text-mined interactions from Literome

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
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
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
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