c-Jun N-terminal kinase (JNK)-mediated phosphorylation of SARM1 regulates NAD+ cleavage activity to inhibit mitochondrial respiration

Mitochondrial dysfunction is a key pathological feature of many different types of neurodegenerative disease. Sterile alpha and Toll/interleukin receptor motif-containing protein 1 (SARM1) has been attracting much attention as an important molecule for inducing axonal degeneration and neuronal cell...

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Bibliographic Details
Published in:	The Journal of biological chemistry Vol. 293; no. 49; pp. 18933 - 18943
Main Authors:	Murata, Hitoshi, Khine, Cho Cho, Nishikawa, Akane, Yamamoto, Ken-ichi, Kinoshita, Rie, Sakaguchi, Masakiyo
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 07-12-2018 American Society for Biochemistry and Molecular Biology
Subjects:	Adenosine Triphosphate - metabolism Armadillo Domain Proteins - chemistry Armadillo Domain Proteins - metabolism Cell Biology Cell Line, Tumor Cell Respiration Cytoskeletal Proteins - chemistry Cytoskeletal Proteins - metabolism HEK293 Cells Humans JNK Mitogen-Activated Protein Kinases - metabolism Mitochondria - metabolism NAD - metabolism NAD+ Nucleosidase - chemistry NAD+ Nucleosidase - metabolism Oxidative Stress Phosphorylation Serine - chemistry NAD cell death nicotinamide adenine dinucleotide (NAD) mitochondria SARM1 c-Jun N-terminal kinase (JNK) ATP
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