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Cardiac HMGB1 knockout led to a series of changes in PGC-1α, UCP3 and GyK, which were the cause of metabolic changes and further impacted cardiac function. Ckmm-Cre Hmgb1fl/fl mice did not show a specific phenotype, which was consistent with the reported negative result of cardiomyocyte-specific Hmgb1 deletion via MHC-Cre. We concluded that HMGB1 plays essential roles in maintaining normal cardiac growth, and different phenotype from cardiac-specific HMGB1-deficient mice may be caused by the cross with mice of different Cre strains. Resto
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