B6-Fgfr3*Y367C mice are obtained by introducing the Y367C mutation into the mouse Fgfr3 gene using gene editing technology. Internal preliminary data show that homozygous B6-Fgfr3*Y367C mice die at 3 weeks. This model can be used to study the mechanisms and therapeutic approaches for diseases such as achondroplasia (ACH) and thanatophoric dysplasia (TD).

This strain is a mouse Atp7b gene humanized model and can be used for HLD. The homozygous B6-hATP7B mice are viable and fertile.

This strain is a mouse Cftr gene humanized model and can be used for research on CF. The homozygous B6-hCFTR mice are viable and fertile.

This strain is a mouse Col7a1 gene humanized model and can be used for research on DEB. The homozygous B6-hCOL7A1 mice are viable and fertile.

This strain represents a mouse Lmna gene humanized model, in which the mouse Lmna gene is replaced by the human LMNA gene, including the 3'UTR. It can be employed to investigate the pathogenesis of neuromuscular diseases, heart disease, HGPS, and other disorders, as well as for preclinical evaluation of therapeutic drugs. Homozygous B6-hLMNA mice are viable and fertile.

This strain is a humanized model of the mouse Scn2a gene, useful for epilepsy research. The homozygous B6-hSCN2A mice are viable and fertile.

The B6-hSCN9A mouse is a mouse Scn9a humanized model, generated by replacing the mouse Scn9a gene (including the 5' UTR and 3' UTR) with the corresponding human SCN9A gene sequence using gene editing technology. This model can be used for studying the pathogenic mechanisms of neurological diseases such as erythromelalgia, Dravet syndrome, small fiber neuropathy, and congenital insensitivity to pain, as well as for screening analgesic drug candidates.

The B6-hTTN mouse is a humanized model, constructed by replacing the coding sequences of the endogenous mouse Ttn gene with the coding sequences of the human TTN gene. B6-hTTN mice can be used for research into the pathogenesis of genetic muscle diseases such as familial dilated cardiomyopathy (DCM), early-onset myopathy, and muscular dystrophy. They are also useful for the screening, development, and safety evaluation of TTN-targeted drugs.

Col7a1 knockout (KO) mice, constructed by using gene editing technology to knock out the homologous gene Col7a1 of human COL7A1 in mice, serve as a research model for Dystrophic Epidermolysis Bullosa (DEB). Homozygous Col7a1 KO mice lack the expression of the Col7a1 gene and COL7A1 protein, and exhibit symptoms of skin redness and blistering on the palms of the fore and hind paws on the first day after birth, and die within three days after birth. Histological examination results show that the skin of Col7a1 KO mice exhibits significant subcutaneous edema, and there is a separation between the epidermis and dermis, which is roughly the same as the pathogenesis and pathological characteristics of human Dystrophic Epidermolysis Bullosa (DEB) in the clinic. Therefore, Col7a1 KO mice can be used for the mechanistic study of Dystrophic Epidermolysis Bullosa (DEB), as well as the development, screening, and evaluation of therapeutic drugs.

This strain is an MDR1 knockout model, in which the human ABCB1 gene's homologous genes, Abcb1a and Abcb1b, were knocked out in mice using gene editing technology. This model lacks the expression of MDR1 protein and can be used for research in areas such as blood-brain barrier permeability-related diseases and multidrug resistance of anti-tumor drugs.