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The Kraus 2014 study reported that adipocyte-specific NNMT knockdown in mice increased adipocyte energy expenditure through a mechanism interpreted as elevated methyl-donor availability for polyamine biosynthesis and for histone methylation that modulates adipocyte gene-expression programs [2]

Dieser Genmodulationseffekt erstreckt sich auf Wege im Zusammenhang mit der Wundreaktion, Wachstumsfaktoren und antifibrotischen Mechanismen, was das Interesse in der regenerativen Biologie steigert

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