These findings suggest that MUTYH does not rely upon the wedge residue for damage site recognition but this residue stabilizes the lesion recognition complex.
results suggested that MYH which interacts with TRADD inhibits TNF-alpha necroptotic signaling. Therefore MYH inactivation is essential for necroptosis via the downregulation of caspase-8.
Ogg1 and Mutyh regulate hippocampal gene expression related to cognition and behavior suggesting a role for the glycosylases in regulating adaptive behavior.
MUTYH loss is associated with an increase in inflammation associated colorectal cancer risk which involves immunosuppression and altered inflammatory response.
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