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huMSTN(GDF8)
製品ID :
C001636
系統:
C57BL/6NCya
状況:
説明:
The MSTN gene, also known as myostatin or growth differentiation factor 8 (GDF8), encodes a secreted protein belonging to the transforming growth factor-beta (TGF-β) superfamily [1]. Primarily expressed in skeletal muscle, with minor expression in mitochondria, myocardium, and brain tissue, MSTN encodes the myostatin protein, a key negative regulator of skeletal muscle development [1]. Myostatin, through autocrine and paracrine signaling, inhibits muscle cell proliferation and differentiation, thereby limiting excessive skeletal muscle growth and maintaining muscle mass homeostasis [1-4]. Thus, MSTN plays a critical role in regulating body muscle development and maintaining normal muscle mass [3]. Furthermore, myostatin is implicated in adipogenesis regulation, exerting an inhibitory effect on fat cell differentiation [2]. Mutations in MSTN are associated with myostatin-related muscle hypertrophy, characterized by significant increases in muscle volume and strength, typically without severe medical consequences [5]. Consequently, inhibitors targeting myostatin are considered potential therapeutic targets for diseases such as muscular dystrophy and sarcopenia, and have shown promise in improving metabolic syndrome [1-5].
The huMSTN(GDF8) mouse is a humanized model constructed using gene editing technology, where the mouse Mstn genomic DNA was replaced with the human MSTN genomic DNA . The murine signal peptide was preserved. This model can be used for studying the pathological mechanisms and therapeutic approaches of muscular dystrophy, sarcopenia and metabolic syndrome, and for the development of MSTN-targeted drugs.
The MSTN gene, also known as myostatin or growth differentiation factor 8 (GDF8), encodes a secreted protein belonging to the transforming growth factor-beta (TGF-β) superfamily [1]. Primarily expressed in skeletal muscle, with minor expression in mitochondria, myocardium, and brain tissue, MSTN encodes the myostatin protein, a key negative regulator of skeletal muscle development [1]. Myostatin, through autocrine and paracrine signaling, inhibits muscle cell proliferation and differentiation, thereby limiting excessive skeletal muscle growth and maintaining muscle mass homeostasis [1-4]. Thus, MSTN plays a critical role in regulating body muscle development and maintaining normal muscle mass [3]. Furthermore, myostatin is implicated in adipogenesis regulation, exerting an inhibitory effect on fat cell differentiation [2]. Mutations in MSTN are associated with myostatin-related muscle hypertrophy, characterized by significant increases in muscle volume and strength, typically without severe medical consequences [5]. Consequently, inhibitors targeting myostatin are considered potential therapeutic targets for diseases such as muscular dystrophy and sarcopenia, and have shown promise in improving metabolic syndrome [1-5].
The huMSTN(GDF8) mouse is a humanized model constructed using gene editing technology, where the mouse Mstn genomic DNA was replaced with the human MSTN genomic DNA . The murine signal peptide was preserved. This model can be used for studying the pathological mechanisms and therapeutic approaches of muscular dystrophy, sarcopenia and metabolic syndrome, and for the development of MSTN-targeted drugs.
huGDF8/huINHBE
製品ID :
C002074
系統:
C57BL/6NCya
状況:
説明:
The huGDF8/huINHBE mouse is a dual-gene humanized model obtained by crossing the huMSTN(GDF8) mouse (Catalog No.: C001636) with the huINHBE mouse (Catalog No.: C001533). The huGDF8/huINHBE mouse is a dual-target humanized model that integrates skeletal muscle growth regulation with lipid metabolism control. Co-expressing humanized MSTN and INHBE genes, this model can be utilized for the screening, pharmacodynamic evaluation, safety assessment, and mechanism of action studies of dual-target therapeutics targeting MSTN and INHBE. It serves as an ideal preclinical research platform for developing innovative therapies for diseases including obesity, sarcopenic obesity, and metabolic syndrome.
The huGDF8/huINHBE mouse is a dual-gene humanized model obtained by crossing the huMSTN(GDF8) mouse (Catalog No.: C001636) with the huINHBE mouse (Catalog No.: C001533). The huGDF8/huINHBE mouse is a dual-target humanized model that integrates skeletal muscle growth regulation with lipid metabolism control. Co-expressing humanized MSTN and INHBE genes, this model can be utilized for the screening, pharmacodynamic evaluation, safety assessment, and mechanism of action studies of dual-target therapeutics targeting MSTN and INHBE. It serves as an ideal preclinical research platform for developing innovative therapies for diseases including obesity, sarcopenic obesity, and metabolic syndrome.
huGDF8/huALK7
製品ID :
C002075
系統:
C57BL/6NCya
状況:
説明:
The huGDF8/huALK7 mouse is a dual-gene humanized model obtained by crossing the huMSTN(GDF8) mouse (Catalog No.: C001636) with the huALK7(ACVR1C) mouse (Catalog No.: C001911). The huGDF8/huALK7 mouse is a dual-target humanized model that integrates skeletal muscle growth regulation with lipid metabolism control. Co-expressing humanized MSTN and ACVR1C genes, this model can be utilized for the screening, pharmacodynamic evaluation, safety assessment, and mechanism of action studies of dual-target therapeutics targeting MSTN and ACVR1C. It serves as an ideal preclinical research platform for developing innovative therapies for combination strategies aimed at muscle gain and fat loss, as well as diseases including sarcopenic obesity and metabolic syndrome.
The huGDF8/huALK7 mouse is a dual-gene humanized model obtained by crossing the huMSTN(GDF8) mouse (Catalog No.: C001636) with the huALK7(ACVR1C) mouse (Catalog No.: C001911). The huGDF8/huALK7 mouse is a dual-target humanized model that integrates skeletal muscle growth regulation with lipid metabolism control. Co-expressing humanized MSTN and ACVR1C genes, this model can be utilized for the screening, pharmacodynamic evaluation, safety assessment, and mechanism of action studies of dual-target therapeutics targeting MSTN and ACVR1C. It serves as an ideal preclinical research platform for developing innovative therapies for combination strategies aimed at muscle gain and fat loss, as well as diseases including sarcopenic obesity and metabolic syndrome.
B6-huGDF8/huTFRC
製品ID :
C001794
系統:
C57BL/6NCya
状況:
説明:
The B6-huGDF8/huTFRC mouse is a dual-gene humanized model obtained by mating B6-huMSTN (huGDF8) mice (catalog No.: C001636) with B6-huTFRC mice (catalog No.: C001860). Transferrin receptor 1 (TFR1 or TFRC) is highly expressed in brain endothelial cells and muscle cells. It can be used as a target for receptor-mediated transcytosis (RMT) to achieve efficient transport of macromolecular drugs across the blood-brain barrier (BBB) and into muscle tissues. This model can be used for research on the pathological mechanisms and treatment methods of muscular atrophy, sarcopenia, metabolic syndrome, and iron metabolism diseases, as well as for the development of MSTN/TFRC targeted drugs.
The B6-huGDF8/huTFRC mouse is a dual-gene humanized model obtained by mating B6-huMSTN (huGDF8) mice (catalog No.: C001636) with B6-huTFRC mice (catalog No.: C001860). Transferrin receptor 1 (TFR1 or TFRC) is highly expressed in brain endothelial cells and muscle cells. It can be used as a target for receptor-mediated transcytosis (RMT) to achieve efficient transport of macromolecular drugs across the blood-brain barrier (BBB) and into muscle tissues. This model can be used for research on the pathological mechanisms and treatment methods of muscular atrophy, sarcopenia, metabolic syndrome, and iron metabolism diseases, as well as for the development of MSTN/TFRC targeted drugs.
huGDF8/huALK7/huINHBE
製品ID :
C002082
系統:
C57BL/6NCya
状況:
説明:
Growth differentiation factor 8 (GDF8) is a key negative regulator of skeletal muscle growth that inhibits the proliferation and differentiation of muscle cells and maintains muscle mass homeostasis [1-4]. Activin receptor-like kinase 7 (ALK7, ACVR1C) is a type I receptor of the transforming growth factor-β (TGF-β) superfamily. It is widely expressed in adipose tissue and metabolically active organs and participates in the regulation of adipogenesis, energy metabolism, and glucose homeostasis [5-6]. Inhibin beta E subunit (INHBE) is a liver-specific member of the TGF-β superfamily. The Activin E encoded by INHBE functions as a hepatokine that plays an important role in maintaining metabolic homeostasis by regulating lipid storage, adipose tissue function, and systemic energy metabolism [7]. Recent studies have further demonstrated that the INHBE-ALK7 signaling axis participates in the metabolic regulation between the liver and adipose tissue, and its dysregulation is closely associated with metabolic diseases, including obesity, type 2 diabetes (T2D), and metabolic dysfunction-associated steatotic liver disease (MASLD) [8]. Meanwhile, GDF8-mediated regulation of skeletal muscle mass is extensively interconnected with adipose and hepatic metabolism [9-10]. GDF8, INHBE, and ALK7 each participate in the metabolic regulation among these tissues and collectively influence whole-body energy homeostasis, fat distribution, and glucose metabolism, providing new insights into combination intervention strategies for promoting muscle growth, reducing adiposity, and improving metabolic health.
The huGDF8/huALK7/huINHBE mouse is a triple-gene humanized model that can be generated by intercrossing the huMSTN(GDF8) mouse (Catalog No.: C001636), the huALK7(ACVR1C) mice (Catalog No.: C001911) and the huINHBE mice (Catalog No.: C001533). This model simultaneously carries the humanized GDF8, ACVR1C, and INHBE genes and can be used for the screening, pharmacodynamic evaluation, safety assessment, and mechanism of action studies of therapeutics targeting GDF8, ACVR1C, and INHBE, as well as studies on body composition remodeling, regulation of the muscle-adipose-liver metabolic axis, and energy metabolic reprogramming. It also serves as a preclinical research platform for developing combination therapeutic strategies for promoting muscle growth, reducing adiposity, and improving metabolic health, as well as innovative therapies for metabolic diseases, including obesity, type 2 diabetes (T2D), and metabolic dysfunction-associated steatotic liver disease (MASLD).
Growth differentiation factor 8 (GDF8) is a key negative regulator of skeletal muscle growth that inhibits the proliferation and differentiation of muscle cells and maintains muscle mass homeostasis [1-4]. Activin receptor-like kinase 7 (ALK7, ACVR1C) is a type I receptor of the transforming growth factor-β (TGF-β) superfamily. It is widely expressed in adipose tissue and metabolically active organs and participates in the regulation of adipogenesis, energy metabolism, and glucose homeostasis [5-6]. Inhibin beta E subunit (INHBE) is a liver-specific member of the TGF-β superfamily. The Activin E encoded by INHBE functions as a hepatokine that plays an important role in maintaining metabolic homeostasis by regulating lipid storage, adipose tissue function, and systemic energy metabolism [7]. Recent studies have further demonstrated that the INHBE-ALK7 signaling axis participates in the metabolic regulation between the liver and adipose tissue, and its dysregulation is closely associated with metabolic diseases, including obesity, type 2 diabetes (T2D), and metabolic dysfunction-associated steatotic liver disease (MASLD) [8]. Meanwhile, GDF8-mediated regulation of skeletal muscle mass is extensively interconnected with adipose and hepatic metabolism [9-10]. GDF8, INHBE, and ALK7 each participate in the metabolic regulation among these tissues and collectively influence whole-body energy homeostasis, fat distribution, and glucose metabolism, providing new insights into combination intervention strategies for promoting muscle growth, reducing adiposity, and improving metabolic health.
The huGDF8/huALK7/huINHBE mouse is a triple-gene humanized model that can be generated by intercrossing the huMSTN(GDF8) mouse (Catalog No.: C001636), the huALK7(ACVR1C) mice (Catalog No.: C001911) and the huINHBE mice (Catalog No.: C001533). This model simultaneously carries the humanized GDF8, ACVR1C, and INHBE genes and can be used for the screening, pharmacodynamic evaluation, safety assessment, and mechanism of action studies of therapeutics targeting GDF8, ACVR1C, and INHBE, as well as studies on body composition remodeling, regulation of the muscle-adipose-liver metabolic axis, and energy metabolic reprogramming. It also serves as a preclinical research platform for developing combination therapeutic strategies for promoting muscle growth, reducing adiposity, and improving metabolic health, as well as innovative therapies for metabolic diseases, including obesity, type 2 diabetes (T2D), and metabolic dysfunction-associated steatotic liver disease (MASLD).
Lrig1-KO
製品ID :
S-KO-02660
系統:
C57BL/6JCya
状況:
説明:
Lrig1 is located on chromosome 6 of mice. Nuclease Technology was used to design sgRNA; Lrig1 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Lrig1 is located on chromosome 6 of mice. Nuclease Technology was used to design sgRNA; Lrig1 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
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