Enables JUN kinase kinase activity. Involved in several processes, including cellular response to sorbitol; positive regulation of JNK cascade; and positive regulation of macromolecule metabolic process. Located in axon; dendrite cytoplasm; and perikaryon. Used to study transient cerebral ischemia. Human ortholog(s) of this gene implicated in colorectal cancer; ovarian serous carcinoma; pancreatic cancer; respiratory system cancer (multiple); and urinary bladder cancer. Orthologous to human MAP2K4 (mitogen-activated protein kinase kinase 4); PARTICIPATES IN c-Jun N-terminal kinases MAPK signaling pathway; Rho/Rac/Cdc42 mediated signaling pathway; ceramide signaling pathway; INTERACTS WITH 2,3,7,8-tetrachlorodibenzodioxine; 6-propyl-2-thiouracil; acetamide.
alvocidib promotes the reaction [Bortezomib results in increased phosphorylation of and results in increased activity of MAP2K4 protein] and Bortezomib results in increased phosphorylation of and results in increased activity of MAP2K4 protein
[Copper co-treated with pyrrolidine dithiocarbamic acid] results in increased phosphorylation of MAP2K4 protein and Acetylcysteine inhibits the reaction [[Copper co-treated with pyrrolidine dithiocarbamic acid] results in increased phosphorylation of MAP2K4 protein]
[Copper co-treated with pyrrolidine dithiocarbamic acid] results in increased phosphorylation of MAP2K4 protein and Acetylcysteine inhibits the reaction [[Copper co-treated with pyrrolidine dithiocarbamic acid] results in increased phosphorylation of MAP2K4 protein]
[[[cypermethrin results in decreased expression of MIR155 mRNA] which results in increased expression of BCL6 mRNA] which results in decreased expression of MAP2K4 protein] which results in decreased phosphorylation of and results in decreased activity of MAPK8 protein more ...
MAP2K4 protein affects the reaction [diallyl trisulfide results in increased abundance of Reactive Oxygen Species] and MAP2K4 protein affects the reaction [diallyl trisulfide results in increased degradation of FTL protein]
licochalcone A promotes the reaction [Sorafenib results in decreased phosphorylation of MAP2K4 protein] and Sorafenib promotes the reaction [licochalcone A results in decreased phosphorylation of MAP2K4 protein]
MYD88 protein promotes the reaction [Lipopolysaccharides results in increased phosphorylation of MAP2K4 protein] and TLR2 protein promotes the reaction [Lipopolysaccharides results in increased phosphorylation of MAP2K4 protein]
Acetylcysteine inhibits the reaction [[Copper co-treated with pyrrolidine dithiocarbamic acid] results in increased phosphorylation of MAP2K4 protein] and Acetylcysteine inhibits the reaction [Cadmium Chloride results in increased phosphorylation of MAP2K4 protein]
Diethylnitrosamine results in increased phosphorylation of and results in increased activity of MAP2K4 protein and MAPK14 protein inhibits the reaction [Diethylnitrosamine results in increased phosphorylation of and results in increased activity of MAP2K4 protein]
MAP2K4 protein affects the reaction [Paclitaxel results in increased activity of CASP3 protein] and MAP2K4 protein affects the reaction [Paclitaxel results in increased cleavage of PARP1 protein]
Acetaminophen results in increased phosphorylation of and results in increased activity of MAP2K4 protein and MAP2K4 mutant form inhibits the reaction [Acetaminophen results in increased activity of MAPK8 protein]
[Copper co-treated with pyrrolidine dithiocarbamic acid] results in increased phosphorylation of MAP2K4 protein and Acetylcysteine inhibits the reaction [[Copper co-treated with pyrrolidine dithiocarbamic acid] results in increased phosphorylation of MAP2K4 protein]
[Cisplatin co-treated with Quercetin] results in increased expression of MAP2K4 mRNA and Quercetin inhibits the reaction [[CYP2E1 protein results in increased susceptibility to Docosahexaenoic Acids] which results in increased phosphorylation of MAP2K4 protein]
MAP2K4 mutant form affects the reaction [sodium arsenite results in increased expression of TP53 protein] and MAP2K4 mutant form inhibits the reaction [sodium arsenite results in increased expression of CDKN1A protein]
licochalcone A promotes the reaction [Sorafenib results in decreased phosphorylation of MAP2K4 protein] and Sorafenib promotes the reaction [licochalcone A results in decreased phosphorylation of MAP2K4 protein]
[Streptozocin co-treated with Dietary Fats] results in increased phosphorylation of MAP2K4 protein and Sodium Selenite promotes the reaction [[Streptozocin co-treated with Dietary Fats] results in increased phosphorylation of MAP2K4 protein]
Map2k4 functions as a tumor suppressor in lung adenocarcinoma and inhibits tumor cell invasion by decreasing peroxisome proliferator-activated receptor γ2 expression.
Toll-like receptor 2-mediated sequential activation of MyD88 and MAPKs contributes to lipopolysaccharide-induced sp-a gene expression in human alveolar epithelial cells.
Immunolocalization of the mitogen-activated protein kinases p42MAPK and JNK1, and their regulatory kinases MEK1 and MEK4, in adult rat central nervous system.
Overexpression of mitogen-activated protein kinase kinase 4 and nuclear factor-kappaB in laryngeal squamous cell carcinoma: a potential indicator for poor prognosis.
Mitogen-activated protein kinase kinase 4 metastasis suppressor gene expression is inversely related to histological pattern in advancing human prostatic cancers.
Inhibition of MLK3-MKK4/7-JNK1/2 pathway by Akt1 in exogenous estrogen-induced neuroprotection against transient global cerebral ischemia by a non-genomic mechanism in male rats.
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.
Blockade of the translocation and activation of mitogen-activated protein kinase kinase 4 (MKK4) signaling attenuates neuronal damage during later ischemia-reperfusion.
Mitogen-activated protein kinase kinase 4 deficiency in cardiomyocytes causes connexin 43 reduction and couples hypertrophic signals to ventricular arrhythmogenesis.
