Last update 01 Nov 2024

ASK1 x PKC

Last update 01 Nov 2024

Basic Info

Related Targets

ASK1PKC

Drugs associated with ASK1 x PKC

KC-459

Target

ASK1 x PKC

Mechanism

ASK1 inhibitors [+1]

Active Org.-

Originator Org.

SBI Biotech Co., Ltd.

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ASK1 x PKC

100 Translational Medicine associated with ASK1 x PKC

0 Patents (Medical) associated with ASK1 x PKC

Literatures (Medical) associated with ASK1 x PKC

01 May 2022·Ecotoxicology and Environmental SafetyQ2 · ENVIRONMENTAL SCIENCE & ECOLOGY

Lipid metabolism, immune and apoptosis transcriptomic responses of the hepatopancreas of Chinese mitten crab to the exposure to microcystin-LR

Q2 · ENVIRONMENTAL SCIENCE & ECOLOGY

Article

Author: Zhang, Ding Dong ; Liu, Yuan ; Liu, Wen Bin ; Chen, Bin Lin ; Gao, Xin ; Li, Xiang Fei ; Chi, Cheng ; Jiang, Guang Zhen ; Park, Se Chang ; Giri, Sib Sankar ; Yu, Xia Wei ; Chen, Ke Ke

Global warming is favouring the incidence, intensity and duration of harmful cyanobacterial blooms. Microcystin-LR (MC-LR), a hepatotoxic agent, is produced during cyanobacterial blooms. To understand the molecular mechanisms of acute hepatotoxic effect of low doses of MC-LR in crab, we examined differentially expressed genes in samples of the hepatopancreas of Chinese mitten crab (Eriocheir sinensis) collected in 48 h after injections of MC-LR at doses of 0, 25, 50, and 75 µg/kg. The results revealed that MC-LR induced changes in corresponding gene led to the accumulation of triglycerides. MC-LR exposure affected sterol metabolism. Apoptosis-related genes such as Fas-L, Bcl-XL, Cytc, AiF, p53, PERK, calpain, CASP2, CASP7, α-tubulin, PARP, GF, G12, and PKC were upregulated. Conversely, expression levels of CASP10 and ASK1 were downregulated. Genes related to the regulation of actin cytoskeleton (Rho, ROCK, MLCP, MLC, PAK, and PFN) were upregulated. Further, expression levels of genes encoding fatty acid elongation-related enzymes were upregulated, but the expression of genes related to fatty acid synthesis was slightly down regulated. Taken together, these results demonstrated the hepatic toxicity and molecular mechanisms of changes in lipid metabolism, immune and apoptosis in Chinese mitten crab under the MC-LR-induced stress, which is the first report on crabs and performs a comprehensive analysis and a new insight of the molecular toxicological responses in crabs.

01 Feb 2020·Arteriosclerosis, Thrombosis, and Vascular Biology

Letter by van der Vorst et al Regarding Article, “Anti-Inflammatory Effects of HDL (High-Density Lipoprotein) in Macrophages Predominate Over Proinflammatory Effects in Atherosclerotic Plaques”

Letter

Author: Biessen, Erik A.L. ; van der Vorst, Emiel P.C. ; Donners, Marjo M.P.C.

Proposes the induction of ER stress as a main trigger for the pro-inflammatory effects by activating the IRE1a/ASK1 /p38 MAPK axis and intriguingly this signaling pathway is upstream of NF-κΒ and could, therefore, be integrated in the signaling effects that were previously observed and confirmed in the present study and It would be interesting to validate the role of specific PKC isoforms in this signaling axis and evaluate a potential role for PKC in ER stress.The indication that CSL-1 1 1 and endogenous HDL/ApoA-I have very distinct properties was highlighted by.The fact that peritoneal macrophages isolated after in vivo rHDL (reconstituted HDL; CSL-111) injection demonstrated significant, albeit minor, reductions whereas those from ApoA-I transgenic mice showed strong upregulation of inflammatory cytokine expression.Finally HDL affects plaque macrophages, a relevant question left unanswered in previous studies and CD11b+ cells isolated from the aortic wall of atherogenic mice showed mild anti-inflammatory effects of (in vitro validated anti-inflammatory) CSL-111 treatment.The author concluded that role of HDL in macrophages, harmonizing the reported Janus-faced roles of HDL in macrophages into a single model.

01 Dec 2015·BMC GenomicsQ2 · BIOLOGY

Reorganization of metastamiRs in the evolution of metastatic aggressive neuroblastoma cells

Q2 · BIOLOGY

ArticleOA

Author: Aravindan, Natarajan ; Ramraj, Satishkumar ; Herman, Terence S ; Aravindan, Sheeja ; Pandian, Vijayabaskar ; Khan, Faizan H

BACKGROUNDMetastamiRs have momentous clinical relevance and have been correlated with disease progression in many tumors. In this study, we identified neuroblastoma metastamiRs exploiting unique mouse models of favorable and high-risk metastatic human neuroblastoma. Further, we related their deregulation to the modulation of target proteins and established their association with clinical outcomes.RESULTSWhole genome miRNA microarray analysis identified 74 metastamiRs across the manifold of metastatic tumors. RT-qPCR on select miRNAs validated profile expression. Results from bio-informatics across the ingenuity pathway, miRCancer, and literature data-mining endorsed the expression of these miRNAs in multiple tumor systems and showed their role in metastasis, identifying them as metastamiRs. Immunoblotting and TMA-IHC analyses revealed alterations in the expression/phosphorylation of metastamiRs' targets, including ADAMTS-1, AKT1/2/3, ASK1, AURKβ, Birc1, Birc2, Bric5, β-CATENIN, CASP8, CD54, CDK4, CREB, CTGF, CXCR4, CYCLIN-D1, EGFR, ELK1, ESR1, CFOS, FOSB, FRA, GRB10, GSK3β, IL1α, JUND, kRAS, KRTAP1, MCP1, MEGF10, MMP2, MMP3, MMP9, MMP10, MTA2, MYB, cMYC, NF2, NOS3, P21, pP38, PTPN3, CLEAVED PARP, PKC, SDF-1β, SEMA3D, SELE, STAT3, TLR3, TNFα, TNFR1, and VEGF in aggressive cells ex vivo and in a manifold of metastatic tumors in vivo. miRNA mimic (hsa-miR-125b, hsa-miR-27b, hsa-miR-93, hsa-miR-20a) and inhibitor (hsa-miR-1224-3p, hsa-miR-1260) approach for select miRNAs revealed the direct influence of the altered metastamiRs in the regulation of identified protein targets. Clinical outcome association analysis with the validated metastamiRs' targets corresponded strongly with poor overall and relapse-free survival.CONCLUSIONSFor the first time, these results identified a comprehensive list of neuroblastoma metastamiRs, related their deregulation to altered expression of protein targets, and established their association with poor clinical outcomes. The identified set of distinctive neuroblastoma metastamiRs could serve as potential candidates for diagnostic markers for the switch from favorable to high-risk metastatic disease.

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