Citations 2
Development of a Hepatocyte‐Specific Temporal Genetic Mouse Model Using Albumin Promoter‐Driven FlpER2 Expression
Wang, Bin , Wang, Jiale , Liu, Yang , He, Gordon, Jahan‐mihan, Yasmin , Hu, Jie , Li, Audrey , Bi, Yan , Ji, Baoan , Wang, Yuxi, Muhammad, Faheem, Wang, Jiale , Wang, Bin , He, Gordon, Wang, Di , Faheem, Muhammad
genesis | July 9, 2025 | Volume: 63 | Issue: 4 | Pages: No page available
ABSTRACTTissue‐specific gene manipulation using Cre/loxP or Flp/frt recombination systems is a cornerstone of genetically engineered mouse models. In this study, we aim to develop a novel hepatocyte‐specific, tamoxifen‐inducible Flp mouse line. BAC (bacterial artificial chromosome)‐Alb(albumin)‐FlpER2(estrogen receptor ligan binding domain) was developed by inserting IRES‐FlpER2 cDNA between the translation stop codon and 3′‐UTR of the mouse albumin gene in a bacterial artificial chromosome. Upon tamoxifen induction in mice crossed with reporter lines, western blotting, immunohistochemistry, immunofluorescence staining, and X‐gal staining (5‐bromo‐4‐chloro‐3‐indolyl‐β‐D‐galactopyranoside Staining) were used to verify the recombination efficiency and specificity of this mouse model. Recombination was highly efficient and specific in hepatocytes, with no recombination detected in intrahepatic cholangiocytes or other organs in this mouse model. We generated a new tamoxifen‐induced hepatocyte‐specific mouse model with highly efficient recombination specifically in hepatocytes, and this model can be used to generate tumor model lines.
A novel mouse model of diverse tumors derived from epithelial cells
Wang, Lingxiang, Liu, Yang, Jahan‐mihan, Yasmin , He, Gordon, Hu, Jie , Bi, Yan , Ji, Baoan , Jahan-mihan, Yasmin, Wang, Yuxi, Ji, Baoan , Wang, Bin , Liu, Yang, He, Gordon, Wang, Di , Wang, Jiale
Physiological Reports | March 30, 2025 | Volume: 13 | Issue: 7 | Pages: No page available
AbstractA deeper understanding of pathophysiology, from the initiation of tumors of epithelial cells to the outcomes associated with it, is imperative to test potential interventions for these diseases. However, few models can accomplish this because of the complexity of origin cells and their transformation. We established an epithelial cell original tumor mouse model by conditional KrasG12D activation and tumor suppressor gene p53 deletion specifically in epithelial cells of the whole body using Cytokeratin 19 (CK19) promoter via Cre‐ERT mediation. Multiple tumors derived from epithelial cells developed in this novel model. This model can recapitulate the progress of intestinal, pancreatic, liver, lung, and subcutaneous tumors which derive from epithelial cells. This model is suitable for studying the pathophysiology of tumors derived from epithelial cells and may have the potential to test interventions.