Enables MAP kinase kinase kinase activity. Involved in several processes, including endothelial cell apoptotic process; positive regulation of cardiac muscle cell apoptotic process; and positive regulation of p38MAPK cascade. Located in external side of plasma membrane. Used to study cerebral infarction and myocardial infarction. Biomarker of membranous glomerulonephritis; transient cerebral ischemia; and visual epilepsy. Human ortholog(s) of this gene implicated in Huntington's disease. Orthologous to human MAP3K5 (mitogen-activated protein kinase kinase kinase 5); PARTICIPATES IN c-Jun N-terminal kinases MAPK signaling pathway; p38 MAPK signaling pathway; phosphatidylinositol 3-kinase-Akt signaling pathway; INTERACTS WITH 17beta-estradiol; 2,3,7,8-Tetrachlorodibenzofuran; 4-vinylcyclohexene dioxide.
[Estradiol co-treated with Tetrachlorodibenzodioxin] results in decreased expression of MAP3K5 mRNA and [Estradiol co-treated with TGFB1 protein] results in decreased expression of MAP3K5 mRNA
[[[[Glucose results in decreased expression of MIR17 mRNA] which results in increased expression of TXNIP mRNA] which results in increased expression of TXNIP protein] promotes the reaction [TXNIP protein binds to TXN1 protein]] which results in increased activity of MAP3K5 protein more ...
Glucose deficiency promotes the reaction [DAXX protein binds to MAP3K5 protein] and Glucose results in increased phosphorylation of and results in increased activity of MAP3K5 protein
Berberine inhibits the reaction [[lipopolysaccharide and Escherichia coli O111 B4 co-treated with TNF protein] results in decreased expression of and results in increased phosphorylation of MAP3K5 protein]
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Acetaminophen] results in decreased expression of MAP3K5 mRNA and [Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Tartrazine] results in increased expression of MAP3K5 mRNA
[Chelating Agents binds to Copper] which results in decreased expression of MAP3K5 mRNA and [NSC 689534 binds to Copper] which results in decreased expression of MAP3K5 mRNA
[Chelating Agents binds to Copper] which results in decreased expression of MAP3K5 mRNA and [NSC 689534 binds to Copper] which results in decreased expression of MAP3K5 mRNA
[[[[Glucose results in decreased expression of MIR17 mRNA] which results in increased expression of TXNIP mRNA] which results in increased expression of TXNIP protein] promotes the reaction [TXNIP protein binds to TXN1 protein]] which results in increased activity of MAP3K5 protein more ...
Glucose deficiency promotes the reaction [DAXX protein binds to MAP3K5 protein] and Glucose results in increased phosphorylation of and results in increased activity of MAP3K5 protein
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Acetaminophen] results in decreased expression of MAP3K5 mRNA and [Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Tartrazine] results in increased expression of MAP3K5 mRNA
[NOG protein co-treated with entinostat co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of MAP3K5 mRNA
[lipopolysaccharide and Escherichia coli O111 B4 co-treated with Okadaic Acid co-treated with Fingolimod Hydrochloride] results in increased expression of MAP3K5 mRNA
[[[[Glucose results in decreased expression of MIR17 mRNA] which results in increased expression of TXNIP mRNA] which results in increased expression of TXNIP protein] promotes the reaction [TXNIP protein binds to TXN1 protein]] which results in increased activity of MAP3K5 protein more ...
Glucose deficiency promotes the reaction [DAXX protein binds to MAP3K5 protein] and Glucose results in increased phosphorylation of and results in increased activity of MAP3K5 protein
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Acetaminophen] results in decreased expression of MAP3K5 mRNA and [Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Tartrazine] results in increased expression of MAP3K5 mRNA
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Acetaminophen] results in decreased expression of MAP3K5 mRNA and [Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Tartrazine] results in increased expression of MAP3K5 mRNA
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Acetaminophen] results in decreased expression of MAP3K5 mRNA and [Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Tartrazine] results in increased expression of MAP3K5 mRNA
ASK1 protein inhibits the reaction [Hydrogen Peroxide promotes the reaction [MAP3K5 protein binds to MAP2K7 protein]] and Hydrogen Peroxide promotes the reaction [MAP3K5 protein binds to MAP2K7 protein]
[NOG protein co-treated with mercuric bromide co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of MAP3K5 mRNA
N-acetylsphingosine affects the phosphorylation of and results in increased activity of MAP3K5 protein and TXNIP affects the reaction [N-acetylsphingosine affects the phosphorylation of and results in increased activity of MAP3K5 protein]
neoechinulin A inhibits the reaction [[APP protein binds to APP protein binds to APP protein] which results in increased phosphorylation of MAP3K5 protein]
[lipopolysaccharide and Escherichia coli O111 B4 co-treated with Okadaic Acid co-treated with Fingolimod Hydrochloride] results in increased expression of MAP3K5 mRNA
MAP3K5 protein affects the reaction [Paclitaxel results in increased activity of CASP3 protein] and MAP3K5 protein affects the reaction [Paclitaxel results in increased cleavage of PARP1 protein]
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Acetaminophen] results in decreased expression of MAP3K5 mRNA
[perfluorooctane sulfonic acid co-treated with Cellulose] results in decreased expression of MAP3K5 mRNA and [perfluorooctane sulfonic acid co-treated with Inulin] results in decreased expression of MAP3K5 mRNA
CAMK2D protein promotes the reaction [Phenylephrine results in increased activity of MAP3K5 protein] and KN 93 inhibits the reaction [Phenylephrine results in increased activity of MAP3K5 protein]
[NOG protein co-treated with Phenylmercuric Acetate co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of MAP3K5 mRNA
Acetylcysteine inhibits the reaction [platycodin D affects the phosphorylation of and results in increased activity of MAP3K5 protein] and platycodin D affects the phosphorylation of and results in increased activity of MAP3K5 protein
Acetylcysteine inhibits the reaction [Quercetin results in decreased phosphorylation of and results in increased activity of MAP3K5 protein] and Quercetin results in decreased phosphorylation of and results in increased activity of MAP3K5 protein
Acetylcysteine inhibits the reaction [Rotenone inhibits the reaction [TXN protein binds to and results in decreased activity of MAP3K5 protein]] and Rotenone inhibits the reaction [TXN protein binds to and results in decreased activity of MAP3K5 protein]
[Succimer binds to Magnetite Nanoparticles] which results in decreased expression of MAP3K5 mRNA and [Succimer co-treated with Magnetite Nanoparticles] results in decreased expression of MAP3K5 mRNA
4-methylumbelliferone 8-carbaldehyde inhibits the reaction [surfactin peptide results in increased phosphorylation of MAP3K5 protein] and KIRA6 inhibits the reaction [surfactin peptide results in increased phosphorylation of MAP3K5 protein]
4-methylumbelliferone 8-carbaldehyde inhibits the reaction [surfactin peptide results in increased phosphorylation of MAP3K5 protein] and KIRA6 inhibits the reaction [surfactin peptide results in increased phosphorylation of MAP3K5 protein]
[Glycochenodeoxycholic Acid co-treated with Deoxycholic Acid co-treated with Chenodeoxycholic Acid co-treated with Glycodeoxycholic Acid co-treated with Glycocholic Acid co-treated with Tartrazine] results in increased expression of MAP3K5 mRNA
[NOG protein co-treated with Valproic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of MAP3K5 mRNA
Tumor necrosis factor-alpha and apoptosis signal-regulating kinase 1 control reactive oxygen species release, mitochondrial autophagy, and c-Jun N-terminal kinase/p38 phosphorylation during necrotizing enterocolitis.
Inhibition of apoptosis signal-regulating kinase 1 reduces endoplasmic reticulum stress and nuclear huntingtin fragments in a mouse model of Huntington disease.
Activation of the stress-activated MAP kinase, p38, but not JNK in cortical motor neurons during early presymptomatic stages of amyotrophic lateral sclerosis in transgenic mice.
Endogenous nitric oxide induces activation of apoptosis signal-regulating kinase 1 via S-nitrosylation in rat hippocampus during cerebral ischemia-reperfusion.
Induction of apoptosis signal regulating kinase 1 (ASK1) after spinal cord injury in rats: possible involvement of ASK1-JNK and -p38 pathways in neuronal apoptosis.
Formation of a tumour necrosis factor receptor 1 molecular scaffolding complex and activation of apoptosis signal-regulating kinase 1 during seizure-induced neuronal death.
Biphasic activation of apoptosis signal-regulating kinase 1-stress-activated protein kinase 1-c-Jun N-terminal protein kinase pathway is selectively mediated by Ca2+-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors involving oxidative stress following brain ischemia in rat hippocampus.
