Aperçu des produits pour anti-MAP3K12 (MAP3K12) Anticorps

Human Mitogen-Activated Protein Kinase Kinase Kinase 12 (MAP3K12) interaction partners

1. Aryl hydrocarbon receptor enhances the expression of miR-150-5p to suppress cell proliferation and invasion in prostate cancer by regulating MAP3K12

2. LZK cooperates with DLK to promote retinal ganglion cell death in response to axon injury.

3. REVIEW: Regulation of Beta-Cell Function and Mass by the Dual Leucine Zipper Kinase

4. miR-130a inhibited the JNK pathway by targeting MAP3K12, contributing to its anti-apoptotic effect and the maintenance of diabetic endothelial progenitor cell function.

5. Data suggest that specific pharmacological inhibition of dual leucine zipper kinase (DLK, MAP3K12) may have therapeutic potential in multiple indications of neuronal degeneration.

6. these findings indicate that DLK participates in cell proliferation and/or survival, at least in part, by modulating the expression of cell cycle regulatory proteins.

7. The results confirm the significance of apoptosis deregulation in CLL, and suggest a possible relationship between ZIPK expression and the clinical course of the disease.

8. the DLK-ERK signaling pathway may act as a regulator of the interaction that occurs between Hsp27 and the cytoskeleton during the formation of the cornified cell envelope, a process conferring to the skin its crucial barrier function

9. for the selective expression of ZPK gene, cell-specific negative regulatory element(s) which locate outside of the core promoter region repress the potent basic promoter activity

10. ZIPK is positively regulated by phosphorylation within its kinase domain and contains an inhibitory C-terminal domain that controls enzyme activity.

11. DLK is a signaling molecule implicated in the regulation of keratinocyte terminal differentiation and cornification

12. DAPK-ZIPK-L13a axis forms a unique regulatory module that first represses, then repermits inflammatory gene expression.

13. Src-dependent tyrosine phosphorylation recombinant human DLK was important for regulation of its activity. DLK may have a role in PDGF signaling.

Mouse (Murine) Mitogen-Activated Protein Kinase Kinase Kinase 12 (MAP3K12) interaction partners

1. Using a sensory neuron-conditional DLK knockout mouse model, we show a time course for the dependency of gene expression changes on the DLK pathway after sciatic nerve injury.

2. DLK is required for mechanical allodynia and microgliosis after nerve injury by controling a transcriptional program in somatosensory neurons regulating the expression of numerous genes implicated in pain pathogenesis, including Csf1.

3. These findings demonstrate that pathological activation of DLK is a conserved mechanism that regulates neurodegeneration.

4. These findings identify DLK as a central regulator of not only JNK but also PERK stress signaling in neurons, with both pathways contributing to neurodegeneration.

5. Results provide the first evidence that axon guidance genes are downstream targets of the dual leucine zipper kinase (DLK) signaling pathway, which through their regulation probably modulates neuronal cell development, structure and function.

6. LZK cooperates with DLK to promote retinal ganglion cell death in response to axon injury.

7. the prevention of the nuclear localization of DLK as induced by prediabetic signals with consecutive suppression of beta-cell apoptosis might constitute a novel target in the therapy of diabetes mellitus

8. Data assesses DLK's role in axons of adult, injured CNS neurons in vivo and shows that DLK does not appear to have a critical function in axonal degeneration; function appears restricted to soma

9. This study provides compelling evidence for the pivotal roles of the ZPK/DLK and MKK4/MAP2K4-dependent mechanism in axotomy-induced motoneuron death in neonates

10. DLK-inducible knockouts displayed a modest increase in basal synaptic transmission but had an attenuation of the JNK/c-Jun stress response pathway activation and significantly reduced neuronal degeneration after kainic acid-induced seizures.

11. Abundance of DLK in turn controlled the levels of downstream JNK signaling and apoptosis.

12. DLK is required for RGC JNK activation and cell death in a rodent model of optic neuropathy

13. The cell intrinsic factors that determine whether a neuron regenerates or undergoes apoptosis in response to axonal injury are not well defined. DLK is an essential upstream mediator of both of these divergent outcomes in the same cell type.

14. These data demonstrate that DLK enhances regeneration by promoting a retrograde injury signal that is required for the activation of the neuronal proregenerative program.

15. The mixed lineage kinase dual leucine zipper kinase (DLK) selectively regulates the JNK-based stress response pathway to mediate axon degeneration and neuronal apoptosis without influencing other aspects of JNK signaling.

16. ZPK/DLK plays a critical role in naturally occurring programmed cell death of motoneurons.

17. This study indicated that the DLK-JNK pathway facilitates axon formation in neocortical neurons via stage-specific regulation of microtubule stability.

18. Hepatic progenitors from DLK+ hepatocytes were maintained in long-term culture.

19. This protein kinase is tightly associated with the microtubules of neurond in the embryonic nervous system.

20. Hsp70 contributes to the regulation of activated DLK by promoting its CHIP-dependent proteasomal degradation