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In lipotoxic hepatocytes, MLK3 activates a MAPK (zeige MAPK1 Proteine) signaling cascade, resulting in the activating phosphorylation of STAT1 (zeige STAT1 Proteine), and CXCL10 (zeige CXCL10 Proteine) transcriptional upregulation.
Data indicate that BTG2 (zeige BTG2 Proteine), MAP3K11, RPS6KA1 (zeige RPS6KA1 Proteine) and PRDM1 (zeige PRDM1 Proteine) as putative targets of microRNA miR (zeige MLXIP Proteine)-125b.
Increased expression of MAP3K11 is associated with esophageal cancer.
During hepatocyte lipotoxicity, activated MLK3 induces the release of CXCL10 (zeige CXCL10 Proteine)-bearing vesicles from hepatocytes, which are chemotactic for macrophages.
MLK3 serves as a common upstream kinase of AMPK (zeige PRKAA1 Proteine) and JNK (zeige MAPK8 Proteine) and functions as a direct upstream kinase for AMPK (zeige PRKAA1 Proteine) independent of LKB1 (zeige STK11 Proteine)
MLK3 represents a newly recognized integral component of HER2 (zeige ERBB2 Proteine) biology in HER2 (zeige ERBB2 Proteine)+ 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.
MAP3K11 might function as an important tumor suppressor neutralized by oncomiR-125b in B-cell leukemia.
TRB3 (zeige TRIB3 Proteine)(-/-) islets show a decrease in both the amplitude and duration of cytokine-stimulated MLK3 induction and JNK (zeige MAPK8 Proteine) activation.
MLK3 limits RhoA (zeige RHOA Proteine) activation and injury-induced neointima formation by binding to and inhibiting the activation of p63Rho guanine nucleotide exchange factor (zeige ARHGEF12 Proteine), a RhoA (zeige RHOA Proteine) activator.
Genetic or pharmacologic inhibition of MLK3 blocks fMLP (zeige FPR1 Proteine)-mediated motility of neutrophils both in vitro and in vivo, suggesting that MLK3 may be a therapeutic target in human diseases characterized by exuberant neutrophil migration.
Data from knockout mice suggest that MLK3 plays role in saturated fatty acid-induced activation of MAP kinase (zeige MAPK1 Proteine) signaling; MLK3 appears to be involved in pathogenesis of obesity, adipose tissue in fl ammation, insulin (zeige INS Proteine) resistance, and fatty liver disease.
Lysine 63-linked ubiquitination modulates mixed lineage kinase-3 interaction with JIP1 (zeige MAPK8IP1 Proteine) scaffold protein (zeige HOMER1 Proteine) in cytokine-induced pancreatic beta cell death
These results reveal a novel role for MLK3 signaling in the regulation of intestinal epithelial migration in vivo and suggest that MLK3 may be an important target for the regulation of intestinal mucosal healing.
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