anti-MAP3K5 (MAP3K5) Antikörper

Human Mitogen-Activated Protein Kinase Kinase Kinase 5 (MAP3K5) Interaktionspartner

1. SOCS-1 relieves smoke inhalation-induced lung injury by repressing ASK-1 and DISC-mediated epithelium apoptosis.

2. results implicate TNFAIP3 as a functionally important endogenous suppressor of ASK1 hyperactivation in the pathogenesis of nonalcoholic steatohepatitis (NASH) and identify it as a potential new molecular target for NASH therapy

3. upregulation of miR-199 could inhibit Human nucleus pulposus cells injury through downregulation of MAP3K5 expression

4. Nine tag SNPs (rs13203080, rs2076262, rs2237268, rs6914406, rs1009709, rs911182, rs9285484, rs6941553, and rsrs4896219) of the human MAP3K5 gene were selected, and genotyped. Conclusively, our case-control association study indicated an association between MAP3K5 gene polymorphisms and schizophrenia.

5. beta-TrCP was identified as a novel interacting partner of ASK1, capable of ubiquitinating and degrading ASK1 through the ubiquitin-proteasome system. These findings suggest that beta-TrCP is capable of suppressing oxidative stress-induced caspase 3-dependent apoptosis by suppressing ASK1.

6. 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.

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

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

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

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

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

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

13. 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.

14. 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.

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

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

17. 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

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

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

20. 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

Arabidopsis thaliana Mitogen-Activated Protein Kinase Kinase Kinase 5 (MAP3K5) Interaktionspartner

1. Results indicate that brassinosteroid-signaling kinase 1 (BSK1) regulates plant immunity by phosphorylating MAPK Kinase Kinase 5 (MAPKKK5).

2. 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) Interaktionspartner

1. the ASK1/2 complex is a regulator of NLRP3 activation

2. interaction between Ask1 and Card6 absolutely required for Card6 function in vivo

3. Study shownd that apoptosis signal-regulating kinase 1 (ASK1) silencing and ASK1 inhibition reduced ischemic injury-induced nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 2 inflammasomes in the brain and astrocyte cell line, respectively.

4. Data show that miR-23b could inhibit inflammation to promote wound healing by targeting apoptotic signal-regulating kinase 1 (ASK1).

5. beta-TrCP was identified as a novel interacting partner of ASK1 that is capable of ubiquitinating and degrading ASK1 through the ubiquitin-proteasome system. These findings suggest that beta-TrCP is capable of suppressing oxidative stress-induced caspase 3-dependent apoptosis through suppression of ASK1.

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

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

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

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

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

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

12. 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.

13. 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.

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

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

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

17. ASK1 signalling regulates brown and beige adipocyte function.

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

19. 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

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

Pig (Porcine) Mitogen-Activated Protein Kinase Kinase Kinase 5 (MAP3K5) Interaktionspartner

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.