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Mechanism research reveals that LONP1 participates in COPD and influenza virus infection-induced airway remodeling by precisely regulating the differentiation fate of progenitor cells

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CDK1 directly binds and phosphorylates the S447 site of ACSL4, promoting the ubiquitination degradation of ACSL4, while genetic and pharmacological blocking of CDK1 enhances ACSL4 activity, promoting ferroptosis of colon cancer cells and increasing their susceptibility to oxaliplatin

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