Complex MAP3K5:TNFRSF1B:TRAF2 map
Complex composition:

  1. TRAF2 map
  2. TNFRSF1B map
  3. MAP3K5 map


MAP3K5|​pho:​TNFRSF1B:​TRAF2@Cytoplasm

Identifiers
NAME:MAP3K5:TNFRSF1B:TRAF2

References
su_mpk1_mpk1_re148( Survival  map ):
TNF-dependent production of ROS triggers the dissociation of Trx from ASK1 and the consequently liberalised ASK1 binds to TRAF2. Finally TRAF2 appears to activate ASK1 (by phosphorylation) by enhancing and stabilising the oligomerisation of ASK1.
PMID:12655147
su_mpk1_mpk1_re153( Survival  map ):
MLK3 and MLK2 two MAP3Ks of JNK pathway can interact with RAC1 in a GTP-dependent manner.
MEKK2 and MEKK3 can activate JNK P38 and ERK pathways.
TAO kinases are novel MAP3Ks that specifically regulate P38s.
ASK1 is a MAP3K and can activate both JNK and P38 pathways.
MEKK1 selectively activates the endogenous JNK pathway. MEKK1 can activate MEK4 and MEK7 in vivo.
MEKK4 is a MAP3K and can activate both JNK and P38 pathways.
TAK1 is a MAP3K. It is able to activate both JNK and P38 pathways.
Endogenous TAK1 is activated by TGF-beta IL-1 and TNF. TAK1 can phosphorylate and activate MEK4 MEK3 and MEK6.
MLK3 has the potential to positively regulate the ERK / MAPK  map pathway by directly phosphorylating and activating MEK.
Expression of GADD45 genes in mammalian cells strongly activates co-expressed MTK1 as well as P38 and JNK the MAPKs downstream of MTK1. TAO kinases are MAP3Ks that function upstream of P38 and JNK.
PMID:11274345 PMID:12738796 PMID:18855897 PMID:21614932


Modifications:
Participates in complexes:
In compartment: Cytoplasm
  1. MAP3K5|​pho:​TNFRSF1B:​TRAF2@Cytoplasm map
Participates in reactions:
As Reactant or Product:
  1. TNFRSF1B:​TRAF2@Plasma Membrane map + MAP3K5@Cytoplasm map map MAP3K5|​pho:​TNFRSF1B:​TRAF2@Cytoplasm map
As Catalyser:
  1. MAP2K4@Cytoplasm map map MAP2K4|​pho|​pho@Cytoplasm map
  2. MAP2K3@Cytoplasm map map MAP2K3|​pho|​pho@Cytoplasm map
  3. MAP2K7@Cytoplasm map map MAP2K7|​pho|​pho@Cytoplasm map
  4. MAP2K6@Cytoplasm map map MAP2K6|​pho|​pho@Cytoplasm map