During axon degeneration, NAD+ levels are largely controlled by two enzymes: nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) and sterile alpha and toll interleukin motif containing protein 1 (SARM1). NMNAT2, which catalyzes the formation of NAD+ from NMN and ATP, is actively degraded leading to decreased NAD+ levels. SARM1 activity further decreases the concentration of NAD+ by catalyzing its hydrolysis to form nicotinamide and a mixture of ADPR and cADPR. Notably, SARM1 knockout mice show decreased neurodegeneration in animal models of axon degeneration, highlighting the therapeutic potential of targeting this novel NAD+ hydrolase. This review discusses recent advances in the SARM1 field, including SARM1 structure, regulation, and catalysis as well as the identification of the first SARM1 inhibitors.
Nicotinamide Mononucleotide Adenylyltransferase 2 Neurodegeneration In Animal Models Axon Degeneration SARM1 Activity Sterile Alpha Sterile Alpha Motif Models Of Degeneration Concentration Of NAD Toll Interleukin Nicotinamide Mononucleotide
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Round-ups are the summaries of handpicked papers around trending topics published every week. These would enable you to scan through a collection of papers and decide if the paper is relevant to you before actually investing time into reading it.
Climate change Research Articles published between Sep 12, 2022 to Sep 18, 2022
Sep 19, 2022
Articles Included: 5
Rainfall projections from the Coupled Model Intercomparison Project (CMIP) models are strongly tied to projected sea surface temperature (SST) spatial...Read More
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