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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
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"Regenerative and protective actions of the GHK-Cu peptide in the light of the new gene data." International Journal of Molecular Sciences, 19(7), 1987
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