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

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MRE11A — SRC

Text-mined interactions from Literome

Xing et al., Mol Cell Biol 2000 (MAP Kinase Signaling System) : In addition, we found that Rap1 also mediates oncogenic Src signaling
Schmitt et al., Mol Cell 2002 : Src was required for cAMP activation of Rap1 and the inhibition of ERKs and cell growth
Schmitt et al., J Biol Chem 2002 (MAP Kinase Signaling System) : Interestingly, beta-adrenergic stimulation of both Rap1 and ERKs, but not Ras and AKT, can be blocked by a Src mutant ( SrcS17A ) that is incapable of being phosphorylated and activated by PKA ... Furthermore, a Src mutant ( SrcS17D ), which mimics PKA phosphorylation at serine 17, stimulates Rap1 activation, Rap1/B-Raf association, and ERK activation but does not stimulate Ras or AKT
Ling et al., J Biol Chem 2003 (MAP Kinase Signaling System) : Src-CrkII-C3G dependent activation of Rap1 switches growth hormone stimulated p44/42 MAP kinase and JNK/SAPK activities
Fukuyama et al., J Biol Chem 2005 : These results indicate that Rap1 is activated by nectins through the c-Src-Crk-C3G signaling and involved in the nectin induced, c-Src- and FRG mediated activation of Cdc42 and formation of AJs
Obara et al., J Cell Sci 2004 : The activation of Rap1 by both cAMP and NGF was blocked by PP2, an inhibitor of Src family kinases, and by a Src mutant incapable of being phosphorylated by PKA ( SrcS17A ), consistent with the requirement of PKA phosphorylation of Src at S17 in these actions ... PKA phosphorylation of Src may therefore be required for Rap1 activation in PC12 cells
Fukuyama et al., Oncogene 2006 : The c-Src catalysed tyrosine phosphorylation was not sufficient for the activation of Vav2 and the c-Src induced activation of Rap1 was additionally necessary for it, although activated Rap1 alone was not sufficient for the activation of non-tyrosine phosphorylated Vav2
Oh et al., Oncogene 2006 : Therefore, TIMP-2 mediated inhibition of Src kinase activity leads to the signaling switch from Rac1 to Rap1 , thereby leading to enhanced RECK expression
Sakamoto et al., J Biol Chem 2006 : An immunoglobulin-like cell-cell adhesion molecule nectin first trans-interacts with each other to form cell-cell adhesion and induces activation of Rap1 , Cdc42, and Rac small G proteins through c-Src
Guidetti et al., Journal of thrombosis and haemostasis : JTH 2009 : Importantly, alpha ( IIb ) beta3 induced phosphorylation and activation of PLCgamma2, as well as accumulation of active Rap1b , were totally suppressed by Src inhibition