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c-Myc-driven glycolysis polarizes functional regulatory B cells that trigger pathogenic inflammatory responses
Specifically, CHAC1 provides neuroprotection during damage induced by subarachnoid or intracerebral hemorrhage ( CHAC1/BOTCH , which significantly reduced neuroinflammation by blocking NOTCH1 signaling ( The regulation of CHAC1/BOTCH involves additional molecular players: during intracerebral hemorrhage, inhibition of CHAC1/BOTCH by the androgen receptor (AR) and Jumonji-domain containing protein-3 (JMJD3) led to elevated NOTCH1 levels and exacerbated neuroinflammation ( ATF4 was most prominently upregulated, though other related genes were also significantly elevated (Yasuda et al., 2014)
Guan X, Li X, Yang X, Yan J, Shi P, Ba L, Cao Y, Wang P
Invest New Drugs 20:173-82, 2002
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