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In conclusion, we show that SR-B1 deficiency alters the metabolic environment of obese mice through modulation of liver and adipose tissue lipid accumulation. Our findings provide the basis for further elucidation of SR-B1's role in obesity and fatty liver, two major public health issues that increase the risk of advanced chronic diseases and overall mortality.The design of hybrid nucleic acid nanomaterials capitalizes on the partitioning of architectural and functional roles between structurally diverse RNA modules and chemically robu