Browse our anti-MAP3K5 (MAP3K5) Antibodies

Human Mitogen-Activated Protein Kinase Kinase Kinase 5 (MAP3K5) interaction partners

1. Advanced glycation end products significantly activated ASK1, MKK3, and MKK6, which led to activation of p38 MAPK, resulting in upregulated fibrotic response in human coronary smooth muscle cells.

2. ASK1 transcriptional upregulation molecularly defines a metabolically-detrimental obese sub-phenotype.

3. Knockdown of miR-20a enhanced sensitivity of colorectal cancer cells to cisplatin through the ROS/ASK1/JNK pathway.

4. Findings offer insight into positive regulation of Akt signaling through P2Y12 phosphorylation as well as MAPK signaling in platelets by ASK1.

5. Cold stress-induced ferroptosis involves the ASK1-p38 pathway.

6. TRIM48 Promotes ASK1 Activation and Cell Death through Ubiquitination-Dependent Degradation of the ASK1-Negative Regulator PRMT1

7. These findings indicate that chaetocin arrests the cell cycle and induces apoptosis by regulating the reactive oxygen species-mediated ASK-1/JNK signaling pathways.

8. Findings provide evidence that ASK-1 expression is regulated by SLC35F2 which exerts its oncogenic effect on papillary thyroid carcinoma progression through activation of TGFBR-1 and ASK-1.

9. Co-administration of acetaminophen and 5'-AMP significantly ameliorated APAP-induced hepatotoxicity in mice. This was triggered by attenuating apoptosis signal-regulated kinase 1(ASK1) methylation and increasing ubiquitination-mediated ASK1 protein degradation.

10. The anti-cancer mechanism for the AgNPs may be involved in activating the ASK1-JNK/p38-Caspase-3 pathway.

11. TRAF1 functions as a positive regulator of insulin resistance, inflammation, and hepatic steatosis dependent on the activation of ASK1-P38/JNK axis.

12. LRRK2-induced apoptosis was suppressed by ASK1 inhibition in neuronal stem cells derived from patients with Parkinson's disease (PD). These results clearly indicate that LRRK2 acts as an upstream kinase in the ASK1 pathway and plays an important role in the pathogenesis of PD

13. Apoptosis signal-regulating kinase 1 (ASK1) expression was dramatically suppressed and correlated with hepatocyte nuclear factor 4alpha (HNF4alpha) levels in hepatocellular carcinoma (HCC) tissues.

14. ASK1 phosphorylated and stabilized TLX, which led induction of HIF-1alpha, and its downstream VEGF-A in an Akt dependent manner.

15. CD40 activation resulted in down-regulation of Thioredoxin (Trx)-1 to permit ASK1 activation and apoptosis. Although soluble receptor agonist alone could not induce death, combinatorial treatment incorporating soluble CD40 agonist and pharmacological inhibition of Trx-1 was functionally equivalent to the signal triggered by mCD40L

16. These results suggest that the platelet Ask1 plays an important role in regulation of hemostasis and thrombosis.

17. from the two catalytic cysteines of TRX1 the residue C32 is responsible for the high-affinity binding of TRX1 to the ASK1-TRX-binding domain in reducing conditions

18. Shotgun mass spectrometry and manual validation identified 12 distinct ASK1 phosphosites. Targeted parallel reaction monitoring assays were used to track the phosphorylation dynamics of each confirmed site in response to treatment.

19. phosphorus NMR and time-resolved tryptophan fluorescence measurements suggest that 14-3-3zeta interacts with the kinase domain of ASK1 in close proximity to its active site, thus indicating this interaction might block its accessibility and/or affect its conformation.

20. ASK1 MAP kinase signaling cascade is an important regulator of chondrocyte terminal differentiation.

Arabidopsis thaliana Mitogen-Activated Protein Kinase Kinase Kinase 5 (MAP3K5) interaction partners

1. PBL27 interacts with both CERK1 and the MAPK kinase kinase MAPKKK5 at the plasma membrane and knockout of MAPKKK5 compromise chitin-induced MAPK kinase activation and disease resistance to Alternaria brassicicola.

Mouse (Murine) Mitogen-Activated Protein Kinase Kinase Kinase 5 (MAP3K5) interaction partners

1. Findings offer insight into positive regulation of Akt signaling through P2Y12 phosphorylation as well as MAPK signaling in platelets by ASK1.

2. This study demonstrated that the first evidence suggesting that ASK1 may play some role in the pathophysiology of Alzheimer's Disease and brain aging.

3. Oxidative and endoplasmic reticulum stress-dependent ASK1 activation in steatotic hepatocytes and Kupffer cells sensitizes mice fatty liver to ischemia/reperfusion injury.

4. The results of this investigation indicate ASK1 inhibition prolongs keratinocyte and blastemal cell activation leading to ear regeneration.

5. These results suggest that the platelet Ask1 plays an important role in regulation of hemostasis and thrombosis.

6. Lysine 29-linkage of ASK1 by Skp1-Cullin 1-Fbxo21 ubiquitin ligase complex is required for antiviral innate response.

7. These results demonstrate that trans-fatty acids promote extracellular ATP-induced apoptosis by targeting ASK1 and indicate novel TFA-associated pathways leading to inflammatory signal transduction and cell death that underlie the pathogenesis and progression of trans-fatty acids-induced atherosclerosis.

8. Conversely, treatment with LY294002 (a selective inhibitor of Akt1) reversed the effects of quercetin. In conclusion, these findings highlight the important role of quercetin in protecting against cognitive deficits and inhibiting neuronal apoptosis via the Akt signaling pathway. We believe that quercetin might prove to be a useful therapeutic component in treating cerebral I/R diseases in the near future.

9. ASK1 MAP kinase signaling cascade is an important regulator of chondrocyte terminal differentiation.

10. ASK1 mediates astrocyte activation and leads to glial scar formation after cerebral ischaemia.

11. ASK1 mediates 3-NP toxicity and regulates C1q level through the astrocyte TGF-beta.

12. ASK1 signalling regulates brown and beige adipocyte function.

13. blocking MPTP-mediated TNF signaling through intrathecal administration of TNF-neutralizing antibody prevented Trx1 oxidation and downstream ASK1-p38 MAPK activation

14. ASK1 deletion in vivo significantly suppresses hyperoxia-induced elevation of inflammatory cytokines (i.e. IL-1beta and TNF-alpha), cell apoptosis in the lung, and recruitment of immune cells

15. data highlight the importance of ASK1/p38 MAPK pathway in the brain and identify Klotho as a possible anti-oxidant effector

16. Data show that deletion of either MAPKKK5 ASK1 or MAPKKK6 ASK2 in mice promoted the replication of influenza A virus in the lung.

17. Our results provided the evidence that high-fat diet itself causes cognitive impairment and ASK1 participates in such cognitive impairment.

18. ASK1 may mediate the teratogenicity of diabetes through activating the JNK1/2-ER stress pathway and inhibiting cell cycle progression, thereby impeding the cardiogenesis pathways essential for ventricular septation and outflow tract development.

19. Study demonstrates that ASK1 is not involved in beta-cell function and dysfunction but controls stress-induced beta-cell death.

20. ASK1 in sensitized CD41 T cells appears to play a major role in CHS by facilitating IL-17 production.

Pig (Porcine) Mitogen-Activated Protein Kinase Kinase Kinase 5 (MAP3K5) interaction partners

1. PP2A and AIP1 cooperatively induce activation of ASK1-JNK signaling and vascular endothelial cell apoptosis.

2. These results indicate an important regulatory role of ASK1 in porcine circovirus type 2-induced apoptotic responses.

3. MAP3K5 is expressed in the heart, liver, spleen, lung, kidney, muscle, fat, pancrea, ileum, and stomach tissues of pigs.