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Their proliferation, activation, and fusion directly determine repair efficiency
The source of WS is the Werner (WRN) DNA helicase gene, which regulates the transcription of the essential NAD+ biosynthetic enzyme Nicotinamide Nucleotide Adenylyltransferase 1 (24,25). NAD+ depletion through disruption of mitochondrial homeostasis is a substantial contributor to the metabolic dysfunction in WS, according to a 2019 study (25)
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