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Importantly, overexpression of keap1a or knockdown of hmox1a partially rescued the blood clot formation, suggesting that the disrupted Keap1-Nrf2 signaling is responsible for the venous thrombosis-like phenotypes in smarca5 mutants
The effects of exogenous Myr on the conversion efficiency of GR to SF was compared to gut microbial Myr-like activity
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