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Increased ASK1 expression level inhibited cell migration and proliferation of gastric cancer cells.
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LATS2 interacts with ASK1 and increases ASK1-mediated signaling to promote apoptosis and activate the JNK mitogen-activated protein kinase (MAPK).
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Data show greater expression of apoptosis signal-regulating kinase 1 (ASK1) in airway smooth muscle (ASM) bundles of chronic obstructive pulmonary disease (COPD) lung when compared with non-COPD.
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Study in human dopaminergic neuroblastoma SH-SY5Y cells revealed that CIB1 physically associates with ASK1, and thereby prevents ASK1 activation induced by 1-methyl-4-phenylpyrinidium (MPP+). CIB1 binds to the region containing amino acid residues 378-648 of ASK1. CIB1 depletion by RNA interference potentiates MPP+-induced dopaminergic neuronal death.
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SOCS-1 relieves smoke inhalation-induced lung injury by repressing ASK-1 and DISC-mediated epithelium apoptosis.
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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
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upregulation of miR-199 could inhibit Human nucleus pulposus cells injury through downregulation of MAP3K5 expression
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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.
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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.
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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.
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ASK1 transcriptional upregulation molecularly defines a metabolically-detrimental obese sub-phenotype.
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Knockdown of miR-20a enhanced sensitivity of colorectal cancer cells to cisplatin through the ROS/ASK1/JNK pathway.
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Findings offer insight into positive regulation of Akt signaling through P2Y12 phosphorylation as well as MAPK signaling in platelets by ASK1.
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Cold stress-induced ferroptosis involves the ASK1-p38 pathway.
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TRIM48 Promotes ASK1 Activation and Cell Death through Ubiquitination-Dependent Degradation of the ASK1-Negative Regulator PRMT1
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These findings indicate that chaetocin arrests the cell cycle and induces apoptosis by regulating the reactive oxygen species-mediated ASK-1/JNK signaling pathways.
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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.
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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.
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The anti-cancer mechanism for the AgNPs may be involved in activating the ASK1-JNK/p38-Caspase-3 pathway.
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TRAF1 functions as a positive regulator of insulin resistance, inflammation, and hepatic steatosis dependent on the activation of ASK1-P38/JNK axis.