iNOS/NO is required for IRF1 activation in response to liver ischemia-reperfusion in mice.

Qiang DuJing LuoMu-Qing YangQuan LiuCaroline HeresYi-He YanDonna StolzDavid A Geller

Published in: Molecular medicine (Cambridge, Mass.) (2020)

This study demonstrates a novel mechanism that iNOS/NO is required for IRF1/PUMA signaling through a positive-feedback loop between iNOS and IRF1, in which HDAC2-mediated histone modification is involved to up-regulate IRF1 in response to I/R in mice.

Keyphrases

dendritic cells
nitric oxide synthase
high fat diet induced
dna methylation
nitric oxide
transcription factor
type diabetes
gene expression
metabolic syndrome
adipose tissue
insulin resistance
skeletal muscle