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MAPK1 — NTRK1
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
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Gene Ontology Complexes protein complex:
protein complex complex (HSF1-TRMT112-HIST1H4A-UBQLN1-CDX2-USP28-HDAC5-CAV3-CANX-LHX1-TUBA3C-TUBA3E-PI4K2A-NR0B2-RYR2-NTRK1-MPP5-N6AMT1-STAP1-ZFP42-FADD-ATP6V0D1-PRKCDBP-AQP2-FNTB-PRPSAP2-WIPI2-CRB3-CRB2-PEX11A-LDB1-RBP4-TMEM102-GATA2-ADCY2-DZIP1-SYK-TUBB4B-PTPN11-KAT5-CEP290-SYP-ASF1B-PLEKHA2-KIF24-MYO5B-RGP1-CFTR-SPTBN5-VPS72-ACTA2-PRKCI-CNST-SNX4-GNAO1-NFKBIA-UBE2D2-EPB41-RAB5A-GLUL-BSND-GSK3B-SKI-XRCC6-PPM1E-TTR-TUBA1A-SUCLG1-TRIAP1-AKT1S1-MYD88-NPPB-GDF11-INCENP-PLCB3-BECN1-PRKAB1-SOD1-TUBB1-NPHS2-NPHS1-EPS8L1-GDI1-TUBB2A-TUBB2B-SUCLG2-PEX3-TUBAL3-ERLIN1-MAGED1-GCH1-TUBB-CPS1-MEF2C-ZNF703-SLC22A6-CPLX1-EIF4EBP1-TUBE1-FLNA-CD19-STX1A-HDAC2-TOMM40L-HDAC6-SMAD6-SMAD7-TLE6-SMAD2-PARD6B-STXBP1-ACR-TRPC1-PARD6A-TRPC4-PANX1-DCTN1-SOX9-PXMP2-BCR-SET-MALT1-BHMT-RILP-TRADD-HIST1H3A-MAPK1-PVALB-NFKB1-NUFIP1-ACVR2B-TAL1-FOXP3-SSX2IP-GNB2-SLC27A5-GOPC-PAX2-CXADR-AIF1L-APBA1-MYL12A-LMO2-ID2-CCDC113-DDOST-SPP2-GATAD2B-PLN-ERCC8-BIRC8-ASF1A-CAB39-BIRC3-BIRC2-CTNNB1-CORO1A-PRELID1-HAND2-CHAF1B-SCAP-GNAT3-CDC20-SMARCA4-IQGAP1-YWHAZ-CEBPA-PRPS2-AXIN1-XRCC5-YWHAQ-UVRAG-SLC51B-RGS4-RGS6-HTT-YWHAB-APCS-CDCA8-RIPK1-MTA2-SIN3A-ANXA1-NOS1-SNTA1-TRAF6-KPNB1-VCL-VCP-PTRF-PRKCZ-SKIL-RAB3A-KRIT1-SSBP3-PRPSAP1-PPP1CC-TAB1-MYO6-ACTL7A-TUBG2-MBD2-COL6A1-COL6A2-BCL3)
Helps et al., Biochem J 2000, Lauderdale et al., Proc Natl Acad Sci U S A 2000, Didichenko et al., FEBS Lett 2000, Koh et al., Curr Biol 2002, Fan et al., Mol Cell Biol 2002, Groisman et al., Cell 2003, Offenhäuser et al., Mol Biol Cell 2004, Tagami et al., Cell 2004, Doyon et al., Mol Cell Biol 2004, Moore et al., Genomics 2004, Sun et al., Mol Cell 2004, Zang et al., J Cell Biochem 2004, Tian et al., Cancer Res 2005, An et al., Biochemistry 2005, Mahajan et al., Proc Natl Acad Sci U S A 2005, Vader et al., EMBO Rep 2006, Yeh et al., J Biol Chem 2006, Li et al., Immunol Rev 2006, Agbas et al., Biochem J 2007, Swiatecka-Urban et al., J Biol Chem 2007, McKeegan et al., Mol Cell Biol 2007, Shono et al., J Am Soc Nephrol 2007, Popov et al., Cell cycle (Georgetown, Tex.) 2007, Sato et al., J Biol Chem 2008, Fitzgerald et al., J Biol Chem 2008, Lyssand et al., J Biol Chem 2008, Figaro et al., FEBS Lett 2008, Ueda et al., Proc Natl Acad Sci U S A 2008, Shimojo et al., J Biol Chem 2008, Costantini et al., Blood 2009, Mitsuishi et al., J Biol Chem 2010, Masuda et al., J Biol Chem 2010, Koch et al., J Cell Sci 2010, Boëda et al., J Biol Chem 2011, Sircoulomb et al., EMBO Mol Med 2011, Hoxhaj et al., J Cell Sci 2012, Uckun et al., Proc Natl Acad Sci U S A 2012, Pusapati et al., J Biol Chem 2012, Ghai et al., Proc Natl Acad Sci U S A 2013, Kelly et al., PLoS Biol 2013, Chiang et al., PloS one 2013, Dauphinee et al., J Immunol 2013, Potting et al., Cell Metab 2013, Ludwig et al., PLoS Biol 2013, Lee et al., Proc Natl Acad Sci U S A 2013, Kobayashi et al., J Cell Biol 2014, Zheng et al., Am J Physiol 1994, Kumar et al., Biochem Biophys Res Commun 1998, Watabe-Uchida et al., J Cell Biol 1998, Haft et al., Mol Cell Biol 1998
Text-mined interactions from Literome
Zhu et al., Mol Carcinog 2002
(Disease Progression...) :
NGF has the potential to stimulate the growth of some pancreatic cancer cell lines, and this effect is mediated by the phosphorylation of
tyrosine kinase receptor A and
mitogen activated protein kinase activation ; it is dependent on the expression levels of tyrosine kinase receptor A and p75 receptors
Parran et al., Toxicological sciences : an official journal of the Society of Toxicology 2005
(Neuroblastoma) :
In controls, the activation of TrkA
MAPK and PKC-delta peaked after 5 min of exposure to NGF and then decreased but was still detectable at 60 min. Concurrent exposure to increasing concentrations of thimerosal and NGF for 5 min
resulted in a concentration dependent decrease in
TrkA and MAPK phosphorylation, which was evident at 50 nM for TrkA and 100 nM for MAPK
Appert-Collin et al., Int J Immunopathol Pharmacol 2005
:
These findings suggest that this compound does not involve
MAPK activation by
TrkA receptor stimulation but acts by MAP kinase pathway by a pertussis toxin-sensitive mechanism involving 5-HT1A receptors, p21 Ras and MEK-1 and by PKC and Akt pathways
Cushing et al., J Neurosci Res 2005
(Neuroblastoma) :
Immunoblot analysis demonstrated that Cx43 and the
mitogen activated protein kinase ( MAPK ), ERK-1/2, were phosphorylated in
response to
TrkA activation via NGF and that phosphorylation could be prevented by treatment with the MEK-1/2 inhibitor U0126
Moughal et al., J Neurochem 2006
:
In contrast, the stimulation of PC12 cells with LPA leads to a predominant G ( i ) alpha2 mediated
Trk A-independent activation of p42/p44
MAPK , where Gbetagamma subunits play a diminished role
Jin et al., Cancer Res 2007
(Cell Transformation, Neoplastic) :
Here, we define some aspects of the molecular mechanisms regulating
ETV6-NTRK dependent
Ras-Erk1/2 and PI3K-Akt activation
Akpan et al., Brain Res 2008
(Chagas Disease) :
It also requires
TrkA dependent PI3K and
MAPK/Erk signaling pathways because PDNF stimulation of cholinergic transcripts is abolished by specific pharmacological inhibitors
Schmitz et al., Cell Mol Neurobiol 2011
:
Our data showed that cavtratin suppresses the NGF induced phosphorylation of
TrkA as well as the
activation of
MAPK in porcine oligodendrocytes significantly
Alsina et al., PloS one 2012
(MAP Kinase Signaling System) :
At molecular level, our findings indicate that ectopic expression of a mutated form of Spry4 ( Y53A ), in which a conserved tyrosine residue was replaced, fail to block both
TrkA mediated
Erk/MAPK activation and neurite outgrowth induced by NGF, suggesting that an intact tyrosine 53 site is required for the inhibitory effect of Spry4 on NGF signaling
Chaves et al., Zygote 2013
:
The
TrkA receptor
activates predominantly phosphatidylinositol-3-kinase (PI3K) and mitogenic activated protein kinase (
MAPK ) to promote cell survival and proliferation
Cattaneo et al., International journal of molecular sciences 2013
:
Upon activation, intracellular domains of FPR2 mediate signaling to G-proteins, which trigger several agonist dependent signal transduction pathways, including activation of phospholipase C (PLC), protein kinase C ( PKC ) isoforms, the phosphoinositide 3-kinase (PI3K)/protein kinase B ( Akt ) pathway, the
mitogen activated protein kinase ( MAPK ) pathway, p38MAPK, as well as the phosphorylation of cytosolic tyrosine kinases,
tyrosine kinase receptor transactivation , phosphorylation and nuclear translocation of regulatory transcriptional factors, release of calcium and production of oxidants
Tam et al., Blood 1997
:
NGF stimulation of HMC-1 cells induced tyrosine phosphorylation of
TrkA protein,
increased expression of the early response genes c-fos and NGF1-A, and activation of
ERK-mitogen activated protein ( MAP ) kinase , results which indicate that TrkA receptors in HMC-1 cells are fully functional