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抗Human MAP3K11 抗体:
抗Mouse (Murine) MAP3K11 抗体:
抗Rat (Rattus) MAP3K11 抗体:
Human Polyclonal MAP3K11 Primary Antibody for WB - ABIN4334888
Chien, Lin, Wang, Lee, Chen, Fong, Shih: Acacetin inhibits the invasion and migration of human non-small cell lung cancer A549 cells by suppressing the p38α MAPK signaling pathway. in Molecular and cellular biochemistry 2011
Data indicate that BTG2 (显示 BTG2 抗体), MAP3K11, RPS6KA1 (显示 RPS6KA1 抗体) and PRDM1 (显示 PRDM1 抗体) as putative targets of microRNA miR (显示 MLXIP 抗体)-125b.
Increased expression of MAP3K11 is associated with esophageal cancer.
During hepatocyte lipotoxicity, activated MLK3 induces the release of CXCL10 (显示 CXCL10 抗体)-bearing vesicles from hepatocytes, which are chemotactic for macrophages.
MLK3 serves as a common upstream kinase of AMPK (显示 PRKAA1 抗体) and JNK (显示 MAPK8 抗体) and functions as a direct upstream kinase for AMPK (显示 PRKAA1 抗体) independent of LKB1 (显示 STK11 抗体)
MLK3 represents a newly recognized integral component of HER2 (显示 ERBB2 抗体) biology in HER2 (显示 ERBB2 抗体)+ breast tumors.
MLK3 is a critical factor controlling the activity of kinase networks that control the cellular responses to different concentrations of reactive oxygen species.
Signaling pathways associated with the Pro252His mutation in MLK3 are located in the kinase domain which is an important domain for the regulation of downstream signaling pathways.
CHIP modulates MLK3 protein levels in response to Geldanamycin and stress stimuli, and CHIP-dependent regulation of MLK3 is required for suppression of SKOV3 ovarian cancer cell invasion.
Data indicate URMC-099 as an orally bioavailable, potent mixed lineage kinase 3 MLK3 inhibitor.
CTGF acting through Rac1 activates the MLK3/JNK signaling pathway, which in turn initiates AP-1 activation and recruitment of c-Jun and c-Fos to the collagen I promoter and ultimately induces collagen I expression in human lung fibroblasts
MAP3K11 might function as an important tumor suppressor neutralized by oncomiR-125b in B-cell leukemia.
During hepatocyte lipotoxicity, activated MLK3 (显示 KCNK7 抗体) induces the release of CXCL10 (显示 CXCL10 抗体)-bearing vesicles from hepatocytes, which are chemotactic for macrophages.
TRB3 (显示 TRIB3 抗体)(-/-) islets show a decrease in both the amplitude and duration of cytokine-stimulated MLK3 (显示 KCNK7 抗体) induction and JNK (显示 MAPK8 抗体) activation.
MLK3 (显示 KCNK7 抗体) limits RhoA (显示 RHOA 抗体) activation and injury-induced neointima formation by binding to and inhibiting the activation of p63Rho guanine nucleotide exchange factor (显示 ARHGEF12 抗体), a RhoA (显示 RHOA 抗体) activator.
Genetic or pharmacologic inhibition of MLK3 (显示 KCNK7 抗体) blocks fMLP (显示 FPR1 抗体)-mediated motility of neutrophils both in vitro and in vivo, suggesting that MLK3 (显示 KCNK7 抗体) may be a therapeutic target in human diseases characterized by exuberant neutrophil migration.
Data from knockout mice suggest that MLK3 (显示 KCNK7 抗体) plays role in saturated fatty acid-induced activation of MAP kinase (显示 MAPK1 抗体) signaling; MLK3 (显示 KCNK7 抗体) appears to be involved in pathogenesis of obesity, adipose tissue in fl ammation, insulin (显示 INS 抗体) resistance, and fatty liver disease.
Lysine 63-linked ubiquitination modulates mixed lineage kinase-3 interaction with JIP1 (显示 MAPK8IP1 抗体) scaffold protein (显示 HOMER1 抗体) in cytokine-induced pancreatic beta cell death
These results reveal a novel role for MLK3 (显示 KCNK7 抗体) signaling in the regulation of intestinal epithelial migration in vivo and suggest that MLK3 (显示 KCNK7 抗体) may be an important target for the regulation of intestinal mucosal healing.
mice with a targeted deletion of Mlk3 (显示 KCNK7 抗体) displayed multiple skeletal defects, including dental abnormalities, deficient calvarial mineralization, and reduced bone mass
The protein encoded by this gene is a member of the serine/threonine kinase family. This kinase contains a SH3 domain and a leucine zipper-basic motif. This kinase preferentially activates MAPK8/JNK kinase, and functions as a positive regulator of JNK signaling pathway. This kinase can directly phosphorylate, and activates IkappaB kinase alpha and beta, and is found to be involved in the transcription activity of NF-kappaB mediated by Rho family GTPases and CDC42.
SH3 domain-containing proline-rich kinase
, mixed lineage kinase 3
, protein-tyrosine kinase PTK1
, src-homology 3 domain-containing proline-rich kinase
, mitogen activated protein kinase kinase kinase 11