Results 21 to 30 of about 10,661 (224)

Conditional knockout of ASK1 in microglia/macrophages attenuates epileptic seizures and long-term neurobehavioural comorbidities by modulating the inflammatory responses of microglia/macrophages

Journal of Neuroinflammation, 2022
Background Apoptosis signal-regulating kinase 1 (ASK1) not only causes neuronal programmed cell death via the mitochondrial pathway but also is an essential component of the signalling cascade during microglial activation.
Yiying Zhang, Zhangyang Wang, Rongrong Wang, Lu Xia, Yiying Cai, Fangchao Tong, Yanqin Gao, Jing Ding, Xin Wang   +8 more
doaj   +1 more source

The Reciprocal Causation of the ASK1-JNK1/2 Pathway and Endoplasmic Reticulum Stress in Diabetes-Induced Cognitive Decline

Frontiers in Cell and Developmental Biology, 2020
Diabetes significantly induces cognitive dysfunction. Neuronal apoptosis is the main cause of diabetes-induced cognitive decline (DICD). Apoptosis signal-regulating kinase 1 (ASK1) and endoplasmic reticulum (ER) stress are remarkably activated by ...
Yanqing Wu, Yanqing Wu, Yuan Yuan, Chengbiao Wu, Ting Jiang, Beini Wang, Jun Xiong, Peipei Zheng, Yiyang Li, Jingyu Xu, Ke Xu, Yaqian Liu, Xiaokun Li, Jian Xiao   +13 more
doaj   +1 more source

Ischemia/Reperfusion Injury of Fatty Liver Is Protected by A2AR and Exacerbated by A1R Stimulation through Opposite Effects on ASK1 Activation

Cells, 2021
Hepatic ischemia/reperfusion injury (IRI) is aggravated by steatosis and is a main risk factor in fatty liver transplantation. Adenosine receptors (ARs) are emerging as therapeutic targets in liver diseases.
Elisa Alchera, Bangalore R. Chandrashekar, Nausicaa Clemente, Ester Borroni, Renzo Boldorini, Rita Carini   +5 more
doaj   +1 more source

Targeting apoptosis signalling kinase-1 (ASK-1) does not prevent the development of neuropathy in streptozotocin-induced diabetic mice. [PDF]

PLoS ONE, 2014
Apoptosis signal-regulating kinase-1 (ASK1) is a mitogen-activated protein 3 kinase (MAPKKK/MAP3K) which lies upstream of the stress-activated MAPKs, JNK and p38. ASK1 may be activated by a variety of extracellular and intracellular stimuli.
Victoria L Newton, Sumia Ali, Graham Duddy, Alan J Whitmarsh, Natalie J Gardiner   +4 more
doaj   +1 more source

AIP1 Recruits Phosphatase PP2A to ASK1 in Tumor Necrosis Factor–Induced ASK1-JNK Activation [PDF]

Circulation Research, 2008
Previously we have shown that AIP1 (apoptosis signal-regulating kinase [ASK]1-interacting protein 1), a novel member of the Ras-GAP protein family, facilitates dephosphorylation of ASK1 at pSer967 and subsequently 14-3-3 release from ASK1, leading to enhanced ASK1-JNK signaling.
Wang, Min, Yan, Lin, Shibo, Tang, Luyang, Yu, Haifeng, Zhang, Ting, Wan, Tricia, Luhn, Haian, Fu, Hong, Chen   +8 more
openaire   +2 more sources

Microcystin-LR induces ovarian injury and apoptosis in mice via activating apoptosis signal-regulating kinase 1-mediated P38/JNK pathway

Ecotoxicology and Environmental Safety, 2021
As an emerging pollutant in the aquatic environment, microcystin-LR (MC-LR) can enter the body through multiple pathways, and then induce apoptosis and gonadal damage, affecting reproductive function.
Xingde Du, Haohao Liu, Xiaohui Liu, Xinghai Chen, Le Yuan, Ya Ma, Hui Huang, Yueqin Wang, Rui Wang, Shiyu Zhang, Zhihui Tian, Linjia Shi, Huizhen Zhang   +12 more
doaj   +1 more source

ASK1 (MAP3K5) is transcriptionally upregulated by E2F1 in adipose tissue in obesity, molecularly defining a human dys-metabolic obese phenotype

Molecular Metabolism, 2017
Objective: Obesity variably disrupts human health, but molecular-based patients' health-risk stratification is limited. Adipose tissue (AT) stresses may link obesity with metabolic dysfunction, but how they signal in humans remains poorly-characterized ...
Yulia Haim, Matthias Blüher, Daniel Konrad, Nir Goldstein, Nora Klöting, Ilana Harman-Boehm, Boris Kirshtein, Doron Ginsberg, Tanya Tarnovscki, Yftach Gepner, Iris Shai, Assaf Rudich   +11 more
doaj   +1 more source

SOCS1 Inhibits Tumor Necrosis Factor-induced Activation of ASK1-JNK Inflammatory Signaling by Mediating ASK1 Degradation [PDF]

Journal of Biological Chemistry, 2006
We have previously shown that ASK1 undergoes ubiquitination and degradation in resting endothelial cells (EC) and that proinflammatory cytokine tumor necrosis factor (TNF) induces deubiquitination and stabilization, leading to ASK1 activation. However, the mechanism for the regulation of ASK1 stability is not known.
Yun, He, Wei, Zhang, Rong, Zhang, Haifeng, Zhang, Wang, Min   +4 more
openaire   +2 more sources

Kuoxin Decoction Alleviated Left Ventricular Remodeling by Inhibiting Cardiomyocyte Apoptosis Through ASK1/JNK/Cx43 Signaling Pathway in cTnTR141W Transgenic Mice and in vitro [PDF]

Drug Des Devel Ther
Ma M, Fan H, Dong Y, Feng T, Peng L, Zhou M, Liu F, Lee R, Wu R, Wu Q, Wang Y.   +10 more
europepmc   +3 more sources

ASK1 Negatively Regulates the 26 S Proteasome [PDF]

Journal of Biological Chemistry, 2010
The 26 S proteasome, composed of the 20 S core and 19 S regulatory particle, plays a central role in ubiquitin-dependent proteolysis. Disruption of this process contributes to the pathogenesis of the various diseases; however, the mechanisms underlying the regulation of 26 S proteasome activity remain elusive.
Ji Won, Um, Eunju, Im, Joongkyu, Park, Yohan, Oh, Boram, Min, Hyun Jung, Lee, Jong Bok, Yoon, Kwang Chul, Chung   +7 more
openaire   +2 more sources