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RIPK1 (the recessive interaction of serine/suline protein kinase 1) is a key medium for regulating cell death and inflammation.
transition between the scaffolding function and kinase function of RIPK1 is regulated by (de) ubibinization and (de) phosphatization processes.
previous studies have shown that inhibiting RIPK1 expression can fundamentally improve the treatment of RIPK1-dependent organ damage in stroke, myocardial infarction, kidney failure, and systemic inflammatory response syndrome.
addition, in patients with COVID-19, it can improve or prevent multi-organ failure caused by cytokine release in the event of an excessive inflammatory response.
In a mouse model, the researchers identified the aromatic anti-epileptic drug and the FDA-approved drug liskantin as an effective inhibitor activated by RIPK1 in the study.
inhibition was validated in exo-experimental and TNF alpha-induced shock mouse models that simulated cytokine high inflammatory state release syndrome.
, the researchers tested for the first time the activation of RIPK1 in the respiratory upper corties of hospitalized patients who were positive for SARS-CoV-2 infection.
a comprehensive immunologic test of p-RIPK1 in respiratory endocyst cells in COVID-19 patients, the results provide a strong basis for evaluating the efficacy of the drug paracetones in over-inflammatory states.
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