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MAPK3 — TNFSF10
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
MAPK3
→
TNFSF10
(increases)
Mezosi et al., J Clin Endocrinol Metab 2004*
Evidence: Modified assertion
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NCI Pathway Database TRAIL signaling pathway:
Erk1-2 (MAPK3/MAPK1)
→
TRAIL (trimer) complex (TNFSF10)
(modification, collaborate)
Tran et al., J Biol Chem 2001, Secchiero et al., Circulation 2003*
Evidence: mutant phenotype, assay
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NCI Pathway Database TRAIL signaling pathway:
Erk1-2-active (MAPK3/MAPK1)
→
TRAIL/TRAILR1/DAP3/GTP/FADD complex (TNFRSF10A-FADD-TNFSF10-DAP3)
(modification, inhibits)
Bodmer et al., Nat Cell Biol 2000, Sprick et al., Immunity 2000, Kischkel et al., Immunity 2000, Tran et al., J Biol Chem 2001, Miyazaki et al., Nat Immunol 2001, Jin et al., Mol Cell Biol 2006, Walczak et al., EMBO J 1997
Evidence: mutant phenotype, assay, physical interaction
Text-mined interactions from Literome
Secchiero et al., Blood 2004
(MAP Kinase Signaling System) :
Among the intracellular pathways investigated,
TRAIL significantly
stimulated the extracellular signal regulated kinase 1/2 ( ERK1/2 ) but not the
p38/mitogen activated protein kinase ( MAPK ) or the c-Jun NH2-terminal kinase (JNK) pathway
Belyanskaya et al., Lung Cancer 2008
(Carcinoma, Small Cell...) :
TRAIL induced SCLC cell proliferation was mediated by
extracellular signal regulated kinase 1 and 2, and
dependent on the expression of surface
TRAIL-receptor 2 (TRAIL-R2) and lack of caspase-8, which is frequent in SCLC
Sun et al., Oncol Rep 2011
:
Taken together, we show herein that the upstream molecule of the
TRAIL induced
MAPK activation is MEKK, as opposed to ASK1, via the mediation of its signal through JNK/p38 in a caspase-8 dependent manner