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The potential association between psychiatric AEs and GLP-1 RAs was assessed by comparing the psychiatric AE reports for GLP-1 RAs with the complete FAERS database, performing a disproportionality analysis, and calculating the ROR
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Experimental studies have shown that BHB suppresses NLRP3 inflammasome activation in response to defined inflammatory stimuli (urate crystals, ATP and lipotoxic fatty acids), suggesting that this effect depends on the cellular activation state and the inflammatory context [21]
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While CBP/p300 is a well-validated direct interaction partner of NRF2 with prominent functions at enhancers, we report that this interaction is not required for NRF2-dependent NSCLC cell growth, indicating that NRF2 can sustain sufficient transcriptional activity in the absence of CBP/p300 coactivation
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