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hALK7(ACVR1C)
製品ID :
C001709
系統:
C57BL/6NCya
状況:
説明:
The activin A receptor type 1C (ACVR1C), also known as activin receptor-like kinase 7 (ALK7), is a crucial type I serine/threonine kinase receptor belonging to the transforming growth factor-β (TGF-β) superfamily signaling pathway. Upon binding ligands such as activin AB, activin B, and NODAL, ACVR1C initiates intracellular signaling cascades by phosphorylating downstream SMAD2 and SMAD3 transcription factors, thereby regulating diverse cellular processes including cell differentiation, proliferation, apoptosis, and metabolic homeostasis [1]. ACVR1C exhibits a broad expression profile across various tissues, with notable enrichment in adipose tissue, pancreas, heart, and specific brain regions, suggesting its pleiotropic roles in maintaining tissue function [2]. Dysregulation of ACVR1C signaling has been implicated in a range of metabolic disorders, including obesity and type 2 diabetes, as well as in the pathogenesis of certain cancers like retinoblastoma, highlighting its significance as a potential therapeutic target for these conditions [3].
The hALK7(ACVR1C) 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 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 activin A receptor type 1C (ACVR1C), also known as activin receptor-like kinase 7 (ALK7), is a crucial type I serine/threonine kinase receptor belonging to the transforming growth factor-β (TGF-β) superfamily signaling pathway. Upon binding ligands such as activin AB, activin B, and NODAL, ACVR1C initiates intracellular signaling cascades by phosphorylating downstream SMAD2 and SMAD3 transcription factors, thereby regulating diverse cellular processes including cell differentiation, proliferation, apoptosis, and metabolic homeostasis [1]. ACVR1C exhibits a broad expression profile across various tissues, with notable enrichment in adipose tissue, pancreas, heart, and specific brain regions, suggesting its pleiotropic roles in maintaining tissue function [2]. Dysregulation of ACVR1C signaling has been implicated in a range of metabolic disorders, including obesity and type 2 diabetes, as well as in the pathogenesis of certain cancers like retinoblastoma, highlighting its significance as a potential therapeutic target for these conditions [3].
The hALK7(ACVR1C) 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 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.
huALK7(ACVR1C)
製品ID :
C001911
系統:
C57BL/6NCya
状況:
説明:
The activin A receptor type 1C (ACVR1C), also known as activin receptor-like kinase 7 (ALK7), is a crucial type I serine/threonine kinase receptor belonging to the transforming growth factor-β (TGF-β) superfamily signaling pathway. Upon binding ligands such as activin AB, activin B, and NODAL, ACVR1C initiates intracellular signaling cascades by phosphorylating downstream SMAD2 and SMAD3 transcription factors, thereby regulating diverse cellular processes including cell differentiation, proliferation, apoptosis, and metabolic homeostasis [1]. ACVR1C exhibits a broad expression profile across various tissues, with notable enrichment in adipose tissue, pancreas, heart, and specific brain regions, suggesting its pleiotropic roles in maintaining tissue function [2]. Dysregulation of ACVR1C signaling has been implicated in a range of metabolic disorders, including obesity and type 2 diabetes, as well as in the pathogenesis of certain cancers like retinoblastoma, highlighting its significance as a potential therapeutic target for these conditions [3].
The huALK7(ACVR1C) mouse is a humanized model constructed through gene-editing technology, in which the sequence from the 5'UTR to the downstream of the 3'UTR of the mouse Acvr1c gene is replaced with the sequence from the 5'UTR to the downstream of the 3'UTR of the human ACVR1C gene. This model can be used for the research on the pathological mechanisms and treatment methods of metabolic diseases such as obesity and type 2 diabetes (T2D) and malignant tumors such as retinoblastoma, as well as the development of ACVR1C-targeted drugs.
The activin A receptor type 1C (ACVR1C), also known as activin receptor-like kinase 7 (ALK7), is a crucial type I serine/threonine kinase receptor belonging to the transforming growth factor-β (TGF-β) superfamily signaling pathway. Upon binding ligands such as activin AB, activin B, and NODAL, ACVR1C initiates intracellular signaling cascades by phosphorylating downstream SMAD2 and SMAD3 transcription factors, thereby regulating diverse cellular processes including cell differentiation, proliferation, apoptosis, and metabolic homeostasis [1]. ACVR1C exhibits a broad expression profile across various tissues, with notable enrichment in adipose tissue, pancreas, heart, and specific brain regions, suggesting its pleiotropic roles in maintaining tissue function [2]. Dysregulation of ACVR1C signaling has been implicated in a range of metabolic disorders, including obesity and type 2 diabetes, as well as in the pathogenesis of certain cancers like retinoblastoma, highlighting its significance as a potential therapeutic target for these conditions [3].
The huALK7(ACVR1C) mouse is a humanized model constructed through gene-editing technology, in which the sequence from the 5'UTR to the downstream of the 3'UTR of the mouse Acvr1c gene is replaced with the sequence from the 5'UTR to the downstream of the 3'UTR of the human ACVR1C gene. This model can be used for the research on the pathological mechanisms and treatment methods of metabolic diseases such as obesity and type 2 diabetes (T2D) and malignant tumors such as retinoblastoma, as well as the development of ACVR1C-targeted drugs.
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.
huALK7/huINHBE
製品ID :
C001994
系統:
C57BL/6NCya
状況:
説明:
The huALK7/huINHBE mice are a dual-gene humanized model obtained by mating the huALK7(ACVR1C) mice (catalog number: C001911) with the huINHBE mice (catalog number: C001533). This model can be used for the research on pathological mechanisms and treatment methods of metabolic diseases such as obesity and type 2 diabetes (T2D), as well as malignant tumors such as retinoblastoma. It can also be used for the screening, development, and safety evaluation of ACVR1C/INHBE-targeted drugs.
The huALK7/huINHBE mice are a dual-gene humanized model obtained by mating the huALK7(ACVR1C) mice (catalog number: C001911) with the huINHBE mice (catalog number: C001533). This model can be used for the research on pathological mechanisms and treatment methods of metabolic diseases such as obesity and type 2 diabetes (T2D), as well as malignant tumors such as retinoblastoma. It can also be used for the screening, development, and safety evaluation of ACVR1C/INHBE-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).
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