Acute PKD (inducible) mice represent an inducible conditional Pkd1 knockout model generated by crossing Pkd1-floxed mice with kidney-specific, tamoxifen-inducible Cre mice (Cdh16-MerCreMer). Offspring were induced with tamoxifen during lactation to achieve targeted deletion of Pkd1 within renal tubular epithelial cells. Preliminary observations at three weeks post-induction reveal pronounced polycystic kidney disease phenotypes, including the emergence of renal cysts, a marked increase in kidney volume, and elevated serum blood urea nitrogen (BUN) levels. We will continue to monitor this model to assess its late-stage phenotypes and overall disease progression.

The Agxt KO mouse is a gene knockout model created using gene-editing techniques to knock out the coding sequence of the Agxt gene (the homolog of the human AGXT gene) in mice. This model is used to research the pathogenic mechanisms of primary hyperoxaluria and develop related therapeutic strategies.

The Alpl KO mouse is a knockout (KO) model in which the exon 3~4 of the Alpl gene (homologous to the human ALPL gene) has been deleted via gene-editing technology. Preliminary validation data indicate that homozygous Alpl KO mice have a short lifespan, dying within four weeks when given a specialized diet. If they are not provided with this dietary support, no surviving homozygous individuals are obtained. This model can be used to study the pathogenic mechanisms of diseases such as hypophosphatasia (HPP), osteoporosis, and osteosarcoma (OS), and to provide a basis for developing related therapeutic strategies.

This strain is an Atp7b deletion mouse model, which uses gene editing technology to knock out Atp7b, the homolog of the human ATP7B gene in mice that lack the expression of ATP7B protein and can be used in the study of disorders related to copper metabolisms such as Wilson's disease, acute liver failure, and steatohepatitis. The heterozygous Atp7b KO mice are viable and fertile, and homozygous mice have a reduced life expectancy.

B6-Mmut*M698K/Mmut KO mice are a MMA disease model generated by crossing Mmut-knockout mice (with exon 3 deleted) with Mmut-mutant mice (carrying the p.M698K mutation in exon 12). Homozygous deletion of the gene results in embryonic lethality, and homozygous mutant mice die within 1 day of birth. The p.M698K (ATG to AAG) mutation carried by B6-Mmut*M698K/Mmut KO mice is equivalent to the p.M700K (ATG to AAG) mutation in the human MMUT gene. This model can be used to study the pathogenic mechanisms and therapeutic approaches for MMA.

B6-Pnpla3*I148M mice are obtained by introducing the I148M mutation into the mouse Pnpla3 gene using gene editing technology. Homozygous B6-Pnpla3*I148M mice are viable and fertile. This model can be used for research on the disease mechanisms and treatment methods of metabolism-associated fatty liver disease (MASLD), alcoholic liver disease, and liver fibrosis.

The B6-RCL-hLPA/Alb-cre/TG (APOB) mice express human LP(a) and ApoB, two risk factors for cardiovascular disease. It can be used in the study of hyperlipidemia, stroke, coronary heart disease, familial hypercholesterolemia (FH), and other atherosclerotic cardiovascular diseases (ASCVD). Internal data (not shown) indicates that, compared to the Cyagen strain B6-LPA (CKI) /Alb-Cre & Tg (APOB) mice (Catalog No. C001494), this model exhibits a more stable expression of human LPA protein at different ages. Please choose the model based on the experimental need for continuous stability of human LPA protein expression.

B6-hALB/Alpl KO mice are generated by crossing B6-hALB (HSA) mice (Catalog No.: C001492) with Alpl KO mice (Catalog No.: C001849). Among them, Alpl KO mice are a gene knockout (KO) model: homozygous Alpl KO mice have a short lifespan, dying within 4 weeks even when fed with special feed; without special feed, no viable homozygous individuals can be obtained. This model can be used for research on the pathogenic mechanisms of diseases such as hypophosphatasia (HPP), osteoporosis, and osteosarcoma (OS), as well as for the development of therapeutic drugs using human serum albumin (HSA) as a carrier, and studies on in vivo efficacy and pharmacokinetics.

The B6-hALK7 (hACVR1C) mouse is a humanized model constructed using gene editing technology, where the region from aa.27 in exon 2 to partial intron 2 of mouse Acvr1c was replaced with "ACVR1C chimeric CDS-WPRE-BGH pA" cassette. The murine signal peptide (aa.1~25) of Acvr1c was preserved. This model can be used for studying the pathological mechanisms and therapeutic approaches of metabolic disorders such as obesity and type 2 diabetes, and certain cancers like retinoblastoma, and for the development of ACVR1C-targeted drugs.

The B6-hCIDEB mouse is a humanized model, constructed by replacing the sequences from exon 1 to partial intron 2 of mouse Cideb with the Human CIDEB genomic region (exon 1 to exon 5)-rBG pA cassette. B6-hCIDEB mice can be used for research into the pathogenesis of various liver conditions such as metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction-associated steatohepatitis (MASH), cirrhosis, and viral hepatitis (HCV, HBV). They are also useful for the screening, development, and safety evaluation of CIDEB-targeted drugs.