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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)
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This allows the intact tripeptide to safely reach the lower intestinal tract, where it is gradually released and absorbed over an extended period
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