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hCD38
製品ID :
C002047
系統:
C57BL/6NCya
状況:
説明:
The CD38 gene, located on human chromosome 4, encodes a multifunctional type II transmembrane glycoprotein (also known as ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase 1) that acts both as an ectoenzyme and a receptor. It is widely expressed on immune cells, including plasma cells, activated T and B lymphocytes, natural killer cells, monocytes, and dendritic cells, with variable expression depending on cell activation and differentiation states; it is also found in various tissues and can exist in soluble forms [1]. The encoded protein primarily functions as a potent NADase, catalyzing the hydrolysis of NAD⁺ to ADP-ribose (ADPR) and nicotinamide while also synthesizing cyclic ADP-ribose (cADPR), a second messenger involved in intracellular calcium mobilization, cell adhesion (via CD31 interaction), signal transduction, and metabolic regulation [2-4]. High CD38 expression labels malignant plasma cells in multiple myeloma and serves as a prognostic marker in chronic lymphocytic leukemia (CLL), while its role in NAD⁺ depletion links it to inflammation, aging, immune modulation, and metabolic diseases [5-6]. In drug development, CD38 has emerged as a major target, with approved monoclonal antibodies like daratumumab (and isatuximab) demonstrating efficacy in multiple myeloma through mechanisms such as antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct apoptosis induction, with ongoing studies exploring broader applications in hematologic malignancies and autoimmune conditions [7].
The hCD38 mice were a humanized mouse model generated via gene editing. The mouse Cd38 endogenous splice acceptor (SA) of intron 1 was replaced with the human CD38 SA of intron 1-Human CD38 exon 2~8 CDS-WPRE-BGH pA cassette. This model is primarily indicated for mechanistic studies and therapeutic development in hematologic malignancies such as multiple myeloma (MM) and chronic lymphocytic leukemia (CLL), as well as for the development of CD38-targeted agents. Furthermore, given the pivotal role of CD38 in NAD⁺ metabolism, this model is also suitable for evaluating the efficacy of CD38-targeted therapies in ameliorating age-related metabolic decline, neurodegenerative diseases, and enhancing NAD⁺ levels.
The CD38 gene, located on human chromosome 4, encodes a multifunctional type II transmembrane glycoprotein (also known as ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase 1) that acts both as an ectoenzyme and a receptor. It is widely expressed on immune cells, including plasma cells, activated T and B lymphocytes, natural killer cells, monocytes, and dendritic cells, with variable expression depending on cell activation and differentiation states; it is also found in various tissues and can exist in soluble forms [1]. The encoded protein primarily functions as a potent NADase, catalyzing the hydrolysis of NAD⁺ to ADP-ribose (ADPR) and nicotinamide while also synthesizing cyclic ADP-ribose (cADPR), a second messenger involved in intracellular calcium mobilization, cell adhesion (via CD31 interaction), signal transduction, and metabolic regulation [2-4]. High CD38 expression labels malignant plasma cells in multiple myeloma and serves as a prognostic marker in chronic lymphocytic leukemia (CLL), while its role in NAD⁺ depletion links it to inflammation, aging, immune modulation, and metabolic diseases [5-6]. In drug development, CD38 has emerged as a major target, with approved monoclonal antibodies like daratumumab (and isatuximab) demonstrating efficacy in multiple myeloma through mechanisms such as antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct apoptosis induction, with ongoing studies exploring broader applications in hematologic malignancies and autoimmune conditions [7].
The hCD38 mice were a humanized mouse model generated via gene editing. The mouse Cd38 endogenous splice acceptor (SA) of intron 1 was replaced with the human CD38 SA of intron 1-Human CD38 exon 2~8 CDS-WPRE-BGH pA cassette. This model is primarily indicated for mechanistic studies and therapeutic development in hematologic malignancies such as multiple myeloma (MM) and chronic lymphocytic leukemia (CLL), as well as for the development of CD38-targeted agents. Furthermore, given the pivotal role of CD38 in NAD⁺ metabolism, this model is also suitable for evaluating the efficacy of CD38-targeted therapies in ameliorating age-related metabolic decline, neurodegenerative diseases, and enhancing NAD⁺ levels.
Fgfr3-Y367C(neo-del)
製品ID :
C001952
系統:
C57BL/6NCya
状況:
説明:
The FGFR3 gene encodes Fibroblast Growth Factor Receptor 3, a transmembrane receptor tyrosine kinase that plays a crucial role in regulating cell growth, differentiation, and apoptosis. It is widely expressed in various tissues, including the brain, kidney, testis, lung, small intestine, and liver, but is particularly important in cells forming bones, especially within the growth plate of cartilage [1]. The Fgfr3*Y367C mutation, which corresponds to the human Y373C mutation (a gain-of-function mutation), leads to constitutive activation of the FGFR3 protein. This overactivity disrupts normal chondrocyte proliferation and differentiation, impairing endochondral ossification and linear bone growth [2]. As a result, this mutation is significantly associated with severe skeletal dysplasias, including Thanatophoric Dysplasia type I (TDI) and Achondroplasia (ACH), the most common form of short-limbed dwarfism, characterized by disproportionate short stature, macrocephaly, and other skeletal deformities [3]. Y373C is one of the common activating mutations of FGFR3, accounting for approximately 50% of patients with thanatophoric dysplasia (TD-type I), but a lower proportion in the more prevalent achondroplasia (ACH) (ACH is primarily dominated by the G380R mutation). In reported literature, the Fgfr3*Y367C mutation is typically used to construct mouse models in a heterozygous form, which corresponds to the heterozygous nature of this mutation in human clinical patients. Its dominant-negative effect is sufficient to cause the disease [4].
Fgfr3-Y367C(neo-del) mice are a neo‑free disease model generated by crossing Fgfr3‑neoY367C mice (catalog No.: C001745) with Flpo mice. Internal data indicate that these double-heterozygous offspring begin to die at postnatal day 11 (P11) and exhibit typical dwarfism phenotypes, characterized by reduced overall body size, shortened long bones, craniofacial skeletal abnormalities, and decreased trunk and rib dimensions. This model can be utilized to investigate the pathogenesis and therapeutic strategies for achondroplasia (ACH) and thanatophoric dysplasia (TD).
The FGFR3 gene encodes Fibroblast Growth Factor Receptor 3, a transmembrane receptor tyrosine kinase that plays a crucial role in regulating cell growth, differentiation, and apoptosis. It is widely expressed in various tissues, including the brain, kidney, testis, lung, small intestine, and liver, but is particularly important in cells forming bones, especially within the growth plate of cartilage [1]. The Fgfr3*Y367C mutation, which corresponds to the human Y373C mutation (a gain-of-function mutation), leads to constitutive activation of the FGFR3 protein. This overactivity disrupts normal chondrocyte proliferation and differentiation, impairing endochondral ossification and linear bone growth [2]. As a result, this mutation is significantly associated with severe skeletal dysplasias, including Thanatophoric Dysplasia type I (TDI) and Achondroplasia (ACH), the most common form of short-limbed dwarfism, characterized by disproportionate short stature, macrocephaly, and other skeletal deformities [3]. Y373C is one of the common activating mutations of FGFR3, accounting for approximately 50% of patients with thanatophoric dysplasia (TD-type I), but a lower proportion in the more prevalent achondroplasia (ACH) (ACH is primarily dominated by the G380R mutation). In reported literature, the Fgfr3*Y367C mutation is typically used to construct mouse models in a heterozygous form, which corresponds to the heterozygous nature of this mutation in human clinical patients. Its dominant-negative effect is sufficient to cause the disease [4].
Fgfr3-Y367C(neo-del) mice are a neo‑free disease model generated by crossing Fgfr3‑neoY367C mice (catalog No.: C001745) with Flpo mice. Internal data indicate that these double-heterozygous offspring begin to die at postnatal day 11 (P11) and exhibit typical dwarfism phenotypes, characterized by reduced overall body size, shortened long bones, craniofacial skeletal abnormalities, and decreased trunk and rib dimensions. This model can be utilized to investigate the pathogenesis and therapeutic strategies for achondroplasia (ACH) and thanatophoric dysplasia (TD).
Ager-KO
製品ID :
S-KO-00952
系統:
C57BL/6NCya
状況:
説明:
Ager is located on chromosome 17 of mice. Nuclease Technology was used to design sgRNA; Ager knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Ager is located on chromosome 17 of mice. Nuclease Technology was used to design sgRNA; Ager knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Gm4952-KO
製品ID :
S-KO-07201
系統:
C57BL/6JCya
状況:
説明:
Gm4952 is located on chromosome 19 of mice. Nuclease Technology was used to design sgRNA; Gm4952 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Gm4952 is located on chromosome 19 of mice. Nuclease Technology was used to design sgRNA; Gm4952 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Acaa1a-flox
製品ID :
S-CKO-00952
系統:
C57BL/6JCya
状況:
説明:
Acaa1a is located on chromosome 9 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Acaa1a conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Acaa1a is located on chromosome 9 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Acaa1a conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Gm4952-flox
製品ID :
S-CKO-08266
系統:
C57BL/6JCya
状況:
説明:
Gm4952 is located on chromosome 19 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Gm4952 conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Gm4952 is located on chromosome 19 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Gm4952 conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Zfp952-KO
製品ID :
S-KO-07156
系統:
C57BL/6JCya
状況:
説明:
Zfp952 is located on chromosome 17 of mice. Nuclease Technology will be used to design sgRNA; Zfp952 knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Zfp952 is located on chromosome 17 of mice. Nuclease Technology will be used to design sgRNA; Zfp952 knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Zfp952-flox
製品ID :
S-CKO-08219
系統:
C57BL/6JCya
状況:
説明:
Zfp952 is located on chromosome 17 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Zfp952 conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Zfp952 is located on chromosome 17 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Zfp952 conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
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