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B6-hGIPR
製品ID :
C001858
系統:
C57BL/6NCya
状況:
説明:
The GIPR gene encodes the gastric inhibitory polypeptide receptor (GIPR), a G protein-coupled receptor with notable expression in pancreatic β-cells, and also detected in the gastrointestinal tract, adipose tissue, and brain [1-2]. The GIPR protein acts as the cognate receptor for gastric inhibitory polypeptide (GIP), a key incretin hormone that potentiates glucose-dependent insulin secretion, thereby regulating systemic glucose homeostasis [2]. While prominently expressed in pancreatic β-cells, GIPR is also present in tissues including the stomach and small intestine [3]. Dysregulation of GIPR function and genetic variants within GIPR have been implicated in metabolic disorders such as type 2 diabetes and obesity, and potentially in the pathogenesis of endocrine tumors and retinoblastoma [4-5]. Emerging evidence suggests a role for GIPR signaling in immunomodulation and inflammation within the gut, highlighting its potential relevance in inflammatory bowel diseases [3]. Currently, therapeutic monoclonal antibodies targeting GIPR are being explored for the treatment of diabetes and obesity. Intriguingly, GIPR may exhibit context-dependent roles within tumor microenvironments, with some evidence suggesting tumor-suppressive functions in specific cancers such as retinoblastoma [4-5]. This multifaceted nature positions GIPR as a compelling therapeutic target for metabolic and inflammatory diseases and potentially selected malignancies.
B6-hGIPR mouse is a humanized model generated using gene editing technology, in which the Exon 3~14 of the coding sequence (CDS) encoding the human GIPR protein and the 3'UTR of mouse Gipr gene are integrated into a specific site within the mouse Gipr gene, while retaining the endogenous gene sequence encoding the murine signal peptide (aa.1~18) and aa.19. This model can be used for studying the pathological mechanisms and therapeutic approaches of metabolic and inflammatory diseases and potentially selected malignancies, as well as for the development of GIPR-targeted drugs.
The GIPR gene encodes the gastric inhibitory polypeptide receptor (GIPR), a G protein-coupled receptor with notable expression in pancreatic β-cells, and also detected in the gastrointestinal tract, adipose tissue, and brain [1-2]. The GIPR protein acts as the cognate receptor for gastric inhibitory polypeptide (GIP), a key incretin hormone that potentiates glucose-dependent insulin secretion, thereby regulating systemic glucose homeostasis [2]. While prominently expressed in pancreatic β-cells, GIPR is also present in tissues including the stomach and small intestine [3]. Dysregulation of GIPR function and genetic variants within GIPR have been implicated in metabolic disorders such as type 2 diabetes and obesity, and potentially in the pathogenesis of endocrine tumors and retinoblastoma [4-5]. Emerging evidence suggests a role for GIPR signaling in immunomodulation and inflammation within the gut, highlighting its potential relevance in inflammatory bowel diseases [3]. Currently, therapeutic monoclonal antibodies targeting GIPR are being explored for the treatment of diabetes and obesity. Intriguingly, GIPR may exhibit context-dependent roles within tumor microenvironments, with some evidence suggesting tumor-suppressive functions in specific cancers such as retinoblastoma [4-5]. This multifaceted nature positions GIPR as a compelling therapeutic target for metabolic and inflammatory diseases and potentially selected malignancies.
B6-hGIPR mouse is a humanized model generated using gene editing technology, in which the Exon 3~14 of the coding sequence (CDS) encoding the human GIPR protein and the 3'UTR of mouse Gipr gene are integrated into a specific site within the mouse Gipr gene, while retaining the endogenous gene sequence encoding the murine signal peptide (aa.1~18) and aa.19. This model can be used for studying the pathological mechanisms and therapeutic approaches of metabolic and inflammatory diseases and potentially selected malignancies, as well as for the development of GIPR-targeted drugs.
B6-hGIPR/hGLP-1R
製品ID :
C001599
系統:
C57BL/6NCya
状況:
説明:
The Glucagon-like peptide 1 receptor (GLP1R) gene encodes a protein that belongs to the glucagon receptor subfamily of the G protein-coupled receptor B cluster [1]. This cell surface receptor protein is widely expressed in tissues such as the brain, small intestine, heart, and lungs, and plays a crucial role in insulin secretion signaling cascades by responding to GLP-1 and GLP-1 analogs. Animal model data also suggest that it has neuroprotective effects. Polymorphisms of this gene are closely associated with diabetes, making the GLP-1R protein an important drug target for the treatment of type 2 diabetes and stroke [2-3]. Glucagon-like peptide-1 receptor agonists (GLP-1RA) are novel anti-diabetic drugs that activate GLP-1R to enhance insulin secretion, inhibit glucagon secretion, delay gastric emptying, and reduce food intake through central appetite suppression, thereby achieving blood sugar reduction and weight loss [4].
The GIPR gene encodes a G-protein-coupled receptor for gastric inhibitory polypeptide (GIP), secreted by intestinal K cells after food intake. GIP was initially discovered in intestinal extracts to inhibit gastric acid secretion and gastrin release, but it was later found to stimulate insulin release in the presence of elevated glucose levels. GIPR activation stimulates pancreatic β-cells to secrete insulin and mediates fat deposition by increasing lipoprotein lipase activity, adipogenesis, and fatty acid and glucose uptake in adipocytes. GIPR is primarily expressed in EBV-transformed lymphocytes, the stomach, and visceral adipose tissue [6]. Knockout mice for this gene exhibit elevated blood glucose levels and impaired initial insulin response following oral glucose load. Mice with disrupted Gipr expression show resistance to diet-induced obesity [7]. A deficiency in the GIPR gene is associated with type 2 diabetes and obesity. Research suggests that one of the core strategies for the next generation of T2D drugs is the production of single-peptide agonists, targeting both GLP-1R activity and the glucose-dependent insulinotropic polypeptide receptor (GIPR). GIPR involvement enhances the weight-loss effects of GLP-1-based therapies. This approach improves glycemic control and weight loss in T2D patients, highlighting the GIPR signaling axis as a promising and effective co-target [8].
The B6-hGIPR/hGLP-1R mouse is a dual humanized model for the Gipr and Glp1r genes. Using gene-editing technology, a partial coding sequence (CDS) of the human GIPR gene was inserted into the mouse Gipr gene sequence in B6-hGLP-1R mice (Catalog No.: C001421). This model expresses the functional region of the human GIPR protein while preserving the mouse signal peptide. It can be used to study the pathogenic mechanisms of metabolic diseases such as obesity and type 2 diabetes, and the development of GIPR/GLP-1R dual agonist drugs. The homozygotes are viable and fertile.
The Glucagon-like peptide 1 receptor (GLP1R) gene encodes a protein that belongs to the glucagon receptor subfamily of the G protein-coupled receptor B cluster [1]. This cell surface receptor protein is widely expressed in tissues such as the brain, small intestine, heart, and lungs, and plays a crucial role in insulin secretion signaling cascades by responding to GLP-1 and GLP-1 analogs. Animal model data also suggest that it has neuroprotective effects. Polymorphisms of this gene are closely associated with diabetes, making the GLP-1R protein an important drug target for the treatment of type 2 diabetes and stroke [2-3]. Glucagon-like peptide-1 receptor agonists (GLP-1RA) are novel anti-diabetic drugs that activate GLP-1R to enhance insulin secretion, inhibit glucagon secretion, delay gastric emptying, and reduce food intake through central appetite suppression, thereby achieving blood sugar reduction and weight loss [4].
The GIPR gene encodes a G-protein-coupled receptor for gastric inhibitory polypeptide (GIP), secreted by intestinal K cells after food intake. GIP was initially discovered in intestinal extracts to inhibit gastric acid secretion and gastrin release, but it was later found to stimulate insulin release in the presence of elevated glucose levels. GIPR activation stimulates pancreatic β-cells to secrete insulin and mediates fat deposition by increasing lipoprotein lipase activity, adipogenesis, and fatty acid and glucose uptake in adipocytes. GIPR is primarily expressed in EBV-transformed lymphocytes, the stomach, and visceral adipose tissue [6]. Knockout mice for this gene exhibit elevated blood glucose levels and impaired initial insulin response following oral glucose load. Mice with disrupted Gipr expression show resistance to diet-induced obesity [7]. A deficiency in the GIPR gene is associated with type 2 diabetes and obesity. Research suggests that one of the core strategies for the next generation of T2D drugs is the production of single-peptide agonists, targeting both GLP-1R activity and the glucose-dependent insulinotropic polypeptide receptor (GIPR). GIPR involvement enhances the weight-loss effects of GLP-1-based therapies. This approach improves glycemic control and weight loss in T2D patients, highlighting the GIPR signaling axis as a promising and effective co-target [8].
The B6-hGIPR/hGLP-1R mouse is a dual humanized model for the Gipr and Glp1r genes. Using gene-editing technology, a partial coding sequence (CDS) of the human GIPR gene was inserted into the mouse Gipr gene sequence in B6-hGLP-1R mice (Catalog No.: C001421). This model expresses the functional region of the human GIPR protein while preserving the mouse signal peptide. It can be used to study the pathogenic mechanisms of metabolic diseases such as obesity and type 2 diabetes, and the development of GIPR/GLP-1R dual agonist drugs. The homozygotes are viable and fertile.
B6-hGIPR/huGCGR/hGLP-1R
製品ID :
C001939
系統:
C57BL/6NCya
状況:
説明:
The B6-hGIPR/huGCGR/hGLP-1R mouse is a triple-gene humanized model obtained by mating B6-hGIPR/hGLP-1R mice (catalog No.: C001599) with B6-huGCGR mice (catalog No.: C001723). This model can be used for studying the pathogenic mechanisms and developing treatment methods for glucose-related metabolic diseases such as obesity, type 2 diabetes (T2D), and steatohepatitis, as well as for the development of GIPR/GLP-1R/GCGR-targeted drugs.
The B6-hGIPR/huGCGR/hGLP-1R mouse is a triple-gene humanized model obtained by mating B6-hGIPR/hGLP-1R mice (catalog No.: C001599) with B6-huGCGR mice (catalog No.: C001723). This model can be used for studying the pathogenic mechanisms and developing treatment methods for glucose-related metabolic diseases such as obesity, type 2 diabetes (T2D), and steatohepatitis, as well as for the development of GIPR/GLP-1R/GCGR-targeted drugs.
Itgam-KO
製品ID :
S-KO-02696
系統:
C57BL/6JCya
状況:
説明:
Itgam is located on chromosome 7 of mice. Nuclease Technology will be used to design sgRNA; Itgam knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Itgam is located on chromosome 7 of mice. Nuclease Technology will be used to design sgRNA; Itgam knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Gng8-flox
製品ID :
S-CKO-02696
系統:
C57BL/6JCya
状況:
説明:
Gng8 is located on chromosome 7 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Gng8 conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Gng8 is located on chromosome 7 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Gng8 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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