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Shanghai Model Organisms Center alb cre transgenic mice
Alb Cre Transgenic Mice, supplied by Shanghai Model Organisms Center, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/alb+cre+transgenic+mice/alb+cre+mice/pm42235328-47-11-14
Average 86 stars, based on 1 article reviews
alb cre transgenic mice - by Bioz Stars, 2026-10
86/100 stars

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Related Articles

Transgenic Assay:

Article Title: Loss of hepatic ME1 ameliorates MASLD by Suppressing peroxisomal β-Oxidation and Activating Lipophagy/Lipolysis.
Article Snippet: .. The Me1-floxed mice, LyzM-Cre, and Alb-Cre transgenic mice were produced by Shanghai Model Organisms Center. ..

Article Title: Hepatic Senp2 deletion resolves the angiogenic switch in fibrosis via β-catenin/LECT2.
Article Snippet: Liver fibrosis can arise from diverse etiologies, including metabolic stress and nutritional deficiencies.. The methionineand choline-deficient (MCD) diet induces liver fibrosis independent of metabolic syndrome, offering a model to study non-metabolic drivers of hepatic fibrogenesis.. SUMO-specific protease 2 (SENP2) has been implicated in metabolic liver disease, but its role in nutritionally induced fibrosis remains unknown.

Produced:

Article Title: Loss of hepatic ME1 ameliorates MASLD by Suppressing peroxisomal β-Oxidation and Activating Lipophagy/Lipolysis.
Article Snippet: .. The Me1-floxed mice, LyzM-Cre, and Alb-Cre transgenic mice were produced by Shanghai Model Organisms Center. ..

Generated:

Article Title: Hepatic Senp2 deletion resolves the angiogenic switch in fibrosis via β-catenin/LECT2.
Article Snippet: Liver fibrosis can arise from diverse etiologies, including metabolic stress and nutritional deficiencies.. The methionineand choline-deficient (MCD) diet induces liver fibrosis independent of metabolic syndrome, offering a model to study non-metabolic drivers of hepatic fibrogenesis.. SUMO-specific protease 2 (SENP2) has been implicated in metabolic liver disease, but its role in nutritionally induced fibrosis remains unknown.



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