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MAP3K1 — RAC1
Pathways - manually collected, often from reviews:
-
BioCarta rac1 cell motility signaling pathway:
RAC1
→
MEKK1 (MAP3K1)
(modification, activates)
-
KEGG Neurotrophin signaling pathway:
RAC1
→
MAP3K1
(protein-protein, activation)
-
KEGG MAPK signaling pathway:
CDC42/RAC1/RAC2/RAC3
→
MAP3K1
(protein-protein, activation)
-
NCI Pathway Database BCR signaling pathway:
RAC1 (RAC1)
→
MEKK1 (MAP3K1)
(modification, activates)
Han et al., Immunity 2003
Evidence: assay, physical interaction, other species
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
RAC1/GTP complex (RAC1)
→
MEKK1 (MAP3K1)
(modification, activates)
Auer et al., Mol Biol Cell 1998*
Evidence: mutant phenotype
-
NCI Pathway Database ErbB1 downstream signaling:
RAC1/GTP complex (RAC1)
→
MEKK1 (MAP3K1)
(modification, activates)
Coso et al., Cell 1995*, Minden et al., Cell 1995*, Minden et al., Science 1994, Fanger et al., EMBO J 1997*, Pomérance et al., J Biol Chem 1998*
Evidence: assay, physical interaction
-
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)
-
WikiPathways MAPK Signaling Pathway:
RAC2/RAC1/CDC42
→
MAP3K1
(activation)
-
WikiPathways p38 MAPK Signaling Pathway:
RAC1
→
MAP3K1
(activation)
-
WikiPathways Cardiac Hypertrophic Response:
RAC1
→
MAP3K1
(activation)
-
WikiPathways DNA Damage Response (only ATM dependent):
Complex of RAC1-RAC2-RAC3
→
MAP3K1
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Lee et al., Mol Endocrinol 2000
(Endometrial Neoplasms...) :
The expression of wild-type MEKK1 and an active Rac1, which functions upstream of MEKK1, also increased the activity of the receptor while coexpression of dominant negative
MEKK1 blocked the
Rac1 induction, indicating that endogenous MEKK1 is capable of activating the receptor
Healy et al., Am J Physiol Cell Physiol 2008
:
Our studies also indicate that
Rac and, to a lesser extent, Cdc42
transactivate MEKK1 , which is, in turn, responsible for activation of mitogen activated protein kinase kinase 7 ( MKK7 )