Cell Signaling Technology

Phospho-AMPK beta1 (Ser108) (E8N3N) Rabbit Monoclonal Antibody

#23021 · $176

28
Citing papers
476
Combined citations
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Research areas

Adipose Tissue and Metabolism4Metabolism, Diabetes, and Cancer4Muscle Physiology and Disorders3Autophagy in Disease and Therapy3Advanced Glycation End Products research3Mesenchymal stem cell research3Cancer, Hypoxia, and Metabolism3Protein Kinase Regulation and GTPase Signaling3

Papers citing this product

1
Cisplatin prevents high mobility group box 1 release and is protective in a murine model of hepatic ischemia/reperfusion injury†
Hepatology·2009·76 cit.·DOI
2
Carbon black suppresses the osteogenesis of mesenchymal stem cells: the role of mitochondria
Particle and Fibre Toxicology·2018·74 cit.·DOI
3
HIF1α overexpression enhances diabetic wound closure in high glucose and low oxygen conditions by promoting adipose-derived stem cell paracrine function and survival
Stem Cell Research & Therapy·2020·58 cit.·DOI
4
miR-5591-5p regulates the effect of ADSCs in repairing diabetic wound via targeting AGEs/AGER/JNK signaling axis
Cell Death and Disease·2018·45 cit.·DOI
5
<p>PINK1 mediates spinal cord mitophagy in neuropathic pain</p>
Journal of Pain Research·2019·29 cit.·DOI
6
Phospholipase C-ε signaling mediates endothelial cell inflammation and barrier disruption in acute lung injury
American Journal of Physiology-Lung Cellular and Molecular Physiology·2016·28 cit.·DOI
7
Antioxidants inhibit advanced glycosylation end-product-induced apoptosis by downregulation of miR-223 in human adipose tissue-derived stem cells
Scientific Reports·2016·27 cit.·DOI
8
SLFN11-mediated ribosome biogenesis impairment induces TP53-independent apoptosis
Molecular Cell·2025·25 cit.·DOI
9
Epithelial NAD+ depletion drives mitochondrial dysfunction and contributes to intestinal inflammation
Frontiers in Immunology·2023·20 cit.·DOI
10
Chinese Herbal Preparation Xuebijing Potently Inhibits Inflammasome Activation in Hepatocytes and Ameliorates Mouse Liver Ischemia-Reperfusion Injury
PLoS ONE·2015·18 cit.·DOI

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