|
Chemical and Drug Induced Liver Injury
|
0.300 |
Biomarker
|
disease |
CTD_human |
Deletion of apoptosis signal-regulating kinase 1 attenuates acetaminophen-induced liver injury by inhibiting c-Jun N-terminal kinase activation.
|
18700144 |
2008 |
|
Chemically-Induced Liver Toxicity
|
0.300 |
Biomarker
|
disease |
CTD_human |
Deletion of apoptosis signal-regulating kinase 1 attenuates acetaminophen-induced liver injury by inhibiting c-Jun N-terminal kinase activation.
|
18700144 |
2008 |
|
Cerebral Infarction
|
0.240 |
Biomarker
|
disease |
BEFREE |
Many experimental studies have shown the association of apoptosis signal-regulating kinase 1 (ASK1) with cellular pathomechanisms after cerebral ischemia.
|
29743976 |
2018 |
|
Cerebral Infarction
|
0.240 |
Biomarker
|
disease |
BEFREE |
The objective of the present study was to evaluate the role of ASK1 in controlling NLRP2 inflammasomes in astrocytes after cerebral ischemia.
|
30172704 |
2018 |
|
Cerebral Infarction
|
0.240 |
Biomarker
|
disease |
BEFREE |
Herein, we focus on apoptosis signal-regulating kinase 1 (ASK1), which is involved in apoptotic cell death, brain infarction, and production of inflammatory mediators after cerebral ischemia.
|
28855861 |
2017 |
|
Cerebral Infarction
|
0.240 |
AlteredExpression
|
disease |
BEFREE |
Here we reported ASK1 was activated by nitric oxide (NO) through S-nitrosylation during cerebral ischemia-reperfusion.
|
23137546 |
2013 |
|
Cerebral Infarction
|
0.240 |
Therapeutic
|
disease |
RGD |
As a result of RNAi, corresponding mRNA was distinctly degraded, expression of Ask1 protein was obviously suppressed, apoptotic cell death was apparently decreased and cerebral infarct area was significantly reduced.
|
23968852 |
2013 |
|
Transient Ischemic Attack
|
0.200 |
Biomarker
|
disease |
RGD |
Endogenous nitric oxide induces activation of apoptosis signal-regulating kinase 1 via S-nitrosylation in rat hippocampus during cerebral ischemia-reperfusion.
|
23137546 |
2013 |
|
Myocardial Infarction
|
0.200 |
Therapeutic
|
disease |
RGD |
A small molecule inhibitor of ASK1 was shown for the first time to reduce apoptosis and myocardial infarct size in a rat model of ischemia/reperfusion.
|
22635076 |
2012 |
|
Hypoxia-Ischemia, Brain
|
0.200 |
Biomarker
|
disease |
RGD |
Blocking Daxx trafficking attenuates neuronal cell death following ischemia/reperfusion in rat hippocampus CA1 region.
|
21843499 |
2011 |
|
Membranous glomerulonephritis
|
0.200 |
Biomarker
|
disease |
RGD |
Role of apoptosis signal-regulating kinase 1 in complement-mediated glomerular epithelial cell injury.
|
18178252 |
2008 |
|
Visual seizure
|
0.200 |
Biomarker
|
disease |
RGD |
Formation of a tumour necrosis factor receptor 1 molecular scaffolding complex and activation of apoptosis signal-regulating kinase 1 during seizure-induced neuronal death.
|
12786973 |
2003 |
|
Neointima
|
0.200 |
Therapeutic
|
disease |
RGD |
Activation of apoptosis signal-regulating kinase 1 in injured artery and its critical role in neointimal hyperplasia.
|
14638553 |
2003 |
|
Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Conclusion: These results suggest that Lys6-linked polyubiquitination of ASK1 by TRAF6 represents a mechanism underlying ASK1 activation in hepatocytes and a key driving force of proinflammatory and profibrogenic responses in NASH.
|
31222801 |
2020 |
|
White Blood Cell Count procedure
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Eosinophil count procedure
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
|
30595370 |
2019 |
|
Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
FBXW5 is the central component of the SCF complex (SCF<sup>Fbxw5</sup> ) that directly interacts with and ubiquitinates ASK1 in hepatocytes during NASH development.
|
30703849 |
2019 |
|
Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Conclusion: Hepatocyte Dusp9 prevents NAFLD and NASH progression in mice, including lipid accumulation, glucose metabolism disorders, and enhanced inflammation and liver fibrosis, in an ASK1-dependent manner; these findings suggest that Dusp9 may be a promising therapeutic target for the treatment of NAFLD and NASH.
|
30063256 |
2019 |
|
Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here we demonstrate that overexpression of Cxcl1 in the liver alone promotes steatosis-to-NASH progression in HFD-fed mice by inducing neutrophil infiltration, oxidative stress, and stress kinase (such as ASK1 and p38MAPK) activation.
|
31705800 |
2019 |
|
Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Apoptosis signal-regulating Kinase 1 (ASK1) has been confirmed as a potential therapeutic target for the treatment of non-alcoholic steatohepatitis (NASH) disorder and the discovery of ASK1 inhibitors has attracted increasing attention.
|
31612792 |
2019 |
|
Fatty Liver Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In human livers of lean and obese subjects, ASK1 expression correlated negatively with liver fat content and NASH scores, but positively with markers for autophagy.
|
31595673 |
2019 |
|
Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Selonsertib, a serine/threonine kinase inhibitor, targets apoptosis signal-regulating kinase 1 (ASK1) and is now in phase III clinical trial for the treatment of non-alcoholic steatohepatitis (NASH).
|
30315846 |
2019 |
|
Fatty Liver Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In human livers of lean and obese subjects, ASK1 expression correlated negatively with liver fat content and NASH scores, but positively with markers for autophagy.
|
31171651 |
2019 |
|
High density lipoprotein measurement
|
0.100 |
GeneticVariation
|
phenotype |
GWASCAT |
Genetics of blood lipids among ~300,000 multi-ethnic participants of the Million Veteran Program.
|
30275531 |
2018 |
|
Fatty Liver Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results implicate TNFAIP3 as a functionally important endogenous suppressor of ASK1 hyperactivation in the pathogenesis of NASH and identify it as a potential new molecular target for NASH therapy.
|
29227477 |
2018 |