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MAP3K11 as a candidate gene for left ventricular hypertrophy
High MLK3 phosphorylation promotes invasion of colorectal cancer.
This study identified two distinct peptide-binding sites in the SH3 domain of MLK3, providing critical insights into mechanisms of ligand binding by the mixed-lineage kinase family of kinases.
These results suggest that in the early response to stressful stimuli, MLK4beta-MLK3 binding is important for regulating MLK3 activity and MAPK signalling, and after prolonged periods of stress exposure, MLK4beta and MLK3 proteins decline via CHIP-dependent degradation.
In summary, this investigation identifies an EGFR-DOCK180-RAC1-MLK3-JNK signaling axis that drives glioblastoma cell migration and dissemination.IMPLICATIONS: On the basis of these findings, MLK3 emerges as a potential therapeutic target for the treatment of glioblastoma
chronic hypoxia can reduce MLK3 expression in a posttranscriptional regulatory manner.
In lipotoxic hepatocytes, MLK3 activates a MAPK signaling cascade, resulting in the activating phosphorylation of STAT1, and CXCL10 transcriptional upregulation.
Data indicate that BTG2, MAP3K11, RPS6KA1 and PRDM1 as putative targets of microRNA miR-125b.
Increased expression of MAP3K11 is associated with esophageal cancer.
During hepatocyte lipotoxicity, activated MLK3 induces the release of CXCL10-bearing vesicles from hepatocytes, which are chemotactic for macrophages.
MLK3 serves as a common upstream kinase of AMPK and JNK and functions as a direct upstream kinase for AMPK independent of LKB1
MLK3 represents a newly recognized integral component of HER2 biology in HER2+ 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
NS5A targets MLK3 with multiple downstream consequences for both apoptosis and K(+) homeostasis.
Lysine 63-linked ubiquitination modulates mixed lineage kinase-3 interaction with JIP1 scaffold protein in cytokine-induced pancreatic beta cell death
High MAP3K11 expression is associated with prostate cancer.
MAP3K11 might function as an important tumor suppressor neutralized by oncomiR-125b in B-cell leukemia.
TRB3(-/-) islets show a decrease in both the amplitude and duration of cytokine-stimulated MLK3 induction and JNK activation.
MLK3 limits RhoA activation and injury-induced neointima formation by binding to and inhibiting the activation of p63Rho guanine nucleotide exchange factor, a RhoA activator.
Genetic or pharmacologic inhibition of MLK3 blocks fMLP-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 signaling; MLK3 appears to be involved in pathogenesis of obesity, adipose tissue in fl ammation, insulin resistance, and fatty liver disease.
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.
mice with a targeted deletion of Mlk3 displayed multiple skeletal defects, including dental abnormalities, deficient calvarial mineralization, and reduced bone mass
MLK3 ablation does not protect against hair cell death following acoustic trauma or exposure to aminoglycoside antibiotics, suggesting that MLK3 is not the major upstream regulator of JNK-mediated hair cell death following these stresses.
MLK3 mediates its effects via the pseudokinase TRB3, a mammalian homolog of Drosophila Tribbles.
Although, cellular and humoral immune responses were similar between wild-type and MLK3-/- hosts, the viral load in the lungs was comparatively higher in MLK3-/- mice at day 8 post-infection.
Hence, our data show that the direct interaction between TRAF2 and MLK3 is required for TNF-alpha-induced activation of MLK3 and its downstream target, JNK.
MLK3 functions to limit IKK activity, and depleting MLK3 helps protect cells from etoposide-induced cell death through activation of IKK-dependent signaling.
MLK3 contributes to the TNF signaling pathway that activates JNK.
MLK3 is involved in C-EBP beta regulated, IFN-gamma signaling
These data raise the possibility that CRISP2 is a MAP3K11-modifying protein or, alternatively, that MAP3K11 acts to phosphorylate CRISP2 during acrosome development.
a direct link between GSK-3beta and MLK3 activation in a neuronal cell death pathway and identify MLK3 as a direct downstream target of GSK-3beta.
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