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We hypothesize that integrating these agents with innate immune modulators could enhance durability, as innate pathways may perpetuate low-level inflammation even after adaptive immunity is suppressed

Given that YAP1 and TAZ are homologues with overlapping functions as downstream effectors of the Hippo pathway [4], we also observed that co-knockdown of CDK4/6, treatment with Abemaciclib or DUB3 depletion could reduce TAZ protein levels, likely due to increased TAZ polyubiquitination (Figs

2017;12(3):e0173722

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Low-shear stress promotes atherosclerosis via inducing endothelial cell pyroptosis mediated by IKK/STAT1/NLRP3 Pathway

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