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hITGA4
製品ID :
C002091
系統:
C57BL/6NCya
状況:
説明:
The ITGA4 gene encodes the integrin α4 subunit, which associates with the integrin β7 subunit (ITGB7) to form the heterodimeric transmembrane protein α4β7, an important member of the integrin family [1,2]. The α4β7 integrin is expressed in a variety of cells and tissues and is highly expressed in immune tissues such as lymph nodes, bone marrow, spleen, and blood, as well as in multiple immune cell types including T lymphocytes, B lymphocytes, monocytes, granulocytes, and natural killer cells [3]. Its primary functions are to mediate cell adhesion and migration, thereby regulating the tissue homing of immune cells and inflammatory responses. By binding to vascular cell adhesion molecule-1 (VCAM-1) and mucosal addressin cell adhesion molecule-1 (MAdCAM-1), α4β7 promotes the migration of lymphocytes to inflamed tissues and gut-associated lymphoid tissues [1,2,4]. Studies have shown that the ITGA4 gene is closely linked to the pathogenesis and progression of multiple diseases, including autoimmune disorders such as inflammatory bowel disease (IBD), Crohn’s disease, ulcerative colitis, and multiple sclerosis (MS) [1,2,5]. Furthermore, high expression of ITGA4 in gastric cancer is associated with poor prognosis, cell proliferation and migration, as well as immune infiltration; its downregulation inhibits migration and promotes apoptosis [3]. Given the critical role of α4β7 integrin in inflammation and immune responses, targeting α4β7 has become an important research direction for the treatment of inflammatory and autoimmune diseases.
The hITGA4 mouse is a humanized model generated by gene-editing technology. The coding sequences of exon 2 plus partial intron 2 of mouse Itga4 were replaced with Chimeric ITGA4 CDS-WPRE-BGH pA cassette. The murine signal peptide was retained. hITGA4 mice can be used to investigate the pathological mechanisms and therapeutic strategies of inflammatory and autoimmune diseases, as well as for the screening, development, and preclinical efficacy and safety evaluation of ITGA4-targeted drugs.
The ITGA4 gene encodes the integrin α4 subunit, which associates with the integrin β7 subunit (ITGB7) to form the heterodimeric transmembrane protein α4β7, an important member of the integrin family [1,2]. The α4β7 integrin is expressed in a variety of cells and tissues and is highly expressed in immune tissues such as lymph nodes, bone marrow, spleen, and blood, as well as in multiple immune cell types including T lymphocytes, B lymphocytes, monocytes, granulocytes, and natural killer cells [3]. Its primary functions are to mediate cell adhesion and migration, thereby regulating the tissue homing of immune cells and inflammatory responses. By binding to vascular cell adhesion molecule-1 (VCAM-1) and mucosal addressin cell adhesion molecule-1 (MAdCAM-1), α4β7 promotes the migration of lymphocytes to inflamed tissues and gut-associated lymphoid tissues [1,2,4]. Studies have shown that the ITGA4 gene is closely linked to the pathogenesis and progression of multiple diseases, including autoimmune disorders such as inflammatory bowel disease (IBD), Crohn’s disease, ulcerative colitis, and multiple sclerosis (MS) [1,2,5]. Furthermore, high expression of ITGA4 in gastric cancer is associated with poor prognosis, cell proliferation and migration, as well as immune infiltration; its downregulation inhibits migration and promotes apoptosis [3]. Given the critical role of α4β7 integrin in inflammation and immune responses, targeting α4β7 has become an important research direction for the treatment of inflammatory and autoimmune diseases.
The hITGA4 mouse is a humanized model generated by gene-editing technology. The coding sequences of exon 2 plus partial intron 2 of mouse Itga4 were replaced with Chimeric ITGA4 CDS-WPRE-BGH pA cassette. The murine signal peptide was retained. hITGA4 mice can be used to investigate the pathological mechanisms and therapeutic strategies of inflammatory and autoimmune diseases, as well as for the screening, development, and preclinical efficacy and safety evaluation of ITGA4-targeted drugs.
B6-hα4β7/hTL1A
製品ID :
C001795
系統:
C57BL/6Cya
状況:
説明:
The ITGA4 gene encodes the integrin α4 subunit, which pairs with the integrin β7 subunit, encoded by the ITGB7 gene, to form the heterodimeric transmembrane protein α4β7, a key member of the integrin protein family [1]. α4β7 is prominently expressed in immune tissues, including lymph nodes, bone marrow, spleen, and blood, as well as in diverse immune cell populations, such as T lymphocytes, B lymphocytes, monocytes, granulocytes, and natural killer cells [1]. Functionally, α4β7 mediates cell adhesion and migration, critically regulating immune cell trafficking and inflammatory processes. Specifically, α4β7 facilitates lymphocyte migration to sites of inflammation and intestinal lymphoid tissues through interactions with vascular cell adhesion molecule-1 (VCAM-1) and mucosal addressin cell adhesion molecule-1 (MAdCAM-1) [2]. Notably, ITGA4 and ITGB7 have been implicated in the pathogenesis of autoimmune diseases, including inflammatory bowel disease (IBD), Crohn's disease, ulcerative colitis, and multiple sclerosis [2-4]. Consequently, the targeting of α4β7 has emerged as a key therapeutic strategy for inflammatory and autoimmune disorders.
TNF-like ligand 1A (TL1A), also known as TNF superfamily member 15 (TNFSF15), is a member of the tumor necrosis factor (TNF) family encoded by the TNFSF15 gene in humans. TL1A acts as a ligand for death receptor 3 (DR3) and decoy receptor 3 (DcR3), providing a stimulatory signal for downstream pathways. It regulates the proliferation, activation, and apoptosis of effector cells, as well as cytokine and chemokine production. TL1A is expressed in various immune cells, including monocytes, macrophages, dendritic cells, and T cells, as well as in non-immune cells such as synovial fibroblasts and endothelial cells. It plays a crucial role in modulating immune responses by promoting the differentiation and survival of T cells, particularly Th17 cells involved in inflammatory processes [5]. TL1A enhances IL-2 responses in anti-CD3/CD28-stimulated T cells and synergizes with IL-12 and IL-18 to augment IFN-γ release in human T and NK cells, biasing T cell differentiation toward a Th1 phenotype [6]. Dysregulation of TL1A expression is implicated in autoimmune diseases, including inflammatory bowel disease (IBD), rheumatoid arthritis (RA), primary biliary cholangitis (PBC), systemic lupus erythematosus (SLE), and ankylosing spondylitis (AS) [5]. TL1A has emerged as a promising therapeutic target, with ongoing research focused on developing monoclonal antibodies and other biologics to neutralize TL1A and reduce inflammation in autoimmune disorders. Clinical trial results suggest that TL1A inhibition can be used in the treatment of various autoimmune diseases, particularly IBD [7-9].
B6-hα4β7/hTL1A mouse is a triple-gene humanized model for ITGA4, ITGB7, and TNFSF15, generated by crossing B6-hα4β7 mice with B6-hTL1A (TNFSF15) mice (Catalog No.: C001603). This model serves as a valuable tool for researching immune-related diseases, applicable to studies on T cell differentiation and survival, immune response regulation, and autoimmune diseases. It provides a robust preclinical research platform for the screening, development, and safety evaluation of α4β7/TL1A-targeted drugs.
The ITGA4 gene encodes the integrin α4 subunit, which pairs with the integrin β7 subunit, encoded by the ITGB7 gene, to form the heterodimeric transmembrane protein α4β7, a key member of the integrin protein family [1]. α4β7 is prominently expressed in immune tissues, including lymph nodes, bone marrow, spleen, and blood, as well as in diverse immune cell populations, such as T lymphocytes, B lymphocytes, monocytes, granulocytes, and natural killer cells [1]. Functionally, α4β7 mediates cell adhesion and migration, critically regulating immune cell trafficking and inflammatory processes. Specifically, α4β7 facilitates lymphocyte migration to sites of inflammation and intestinal lymphoid tissues through interactions with vascular cell adhesion molecule-1 (VCAM-1) and mucosal addressin cell adhesion molecule-1 (MAdCAM-1) [2]. Notably, ITGA4 and ITGB7 have been implicated in the pathogenesis of autoimmune diseases, including inflammatory bowel disease (IBD), Crohn's disease, ulcerative colitis, and multiple sclerosis [2-4]. Consequently, the targeting of α4β7 has emerged as a key therapeutic strategy for inflammatory and autoimmune disorders.
TNF-like ligand 1A (TL1A), also known as TNF superfamily member 15 (TNFSF15), is a member of the tumor necrosis factor (TNF) family encoded by the TNFSF15 gene in humans. TL1A acts as a ligand for death receptor 3 (DR3) and decoy receptor 3 (DcR3), providing a stimulatory signal for downstream pathways. It regulates the proliferation, activation, and apoptosis of effector cells, as well as cytokine and chemokine production. TL1A is expressed in various immune cells, including monocytes, macrophages, dendritic cells, and T cells, as well as in non-immune cells such as synovial fibroblasts and endothelial cells. It plays a crucial role in modulating immune responses by promoting the differentiation and survival of T cells, particularly Th17 cells involved in inflammatory processes [5]. TL1A enhances IL-2 responses in anti-CD3/CD28-stimulated T cells and synergizes with IL-12 and IL-18 to augment IFN-γ release in human T and NK cells, biasing T cell differentiation toward a Th1 phenotype [6]. Dysregulation of TL1A expression is implicated in autoimmune diseases, including inflammatory bowel disease (IBD), rheumatoid arthritis (RA), primary biliary cholangitis (PBC), systemic lupus erythematosus (SLE), and ankylosing spondylitis (AS) [5]. TL1A has emerged as a promising therapeutic target, with ongoing research focused on developing monoclonal antibodies and other biologics to neutralize TL1A and reduce inflammation in autoimmune disorders. Clinical trial results suggest that TL1A inhibition can be used in the treatment of various autoimmune diseases, particularly IBD [7-9].
B6-hα4β7/hTL1A mouse is a triple-gene humanized model for ITGA4, ITGB7, and TNFSF15, generated by crossing B6-hα4β7 mice with B6-hTL1A (TNFSF15) mice (Catalog No.: C001603). This model serves as a valuable tool for researching immune-related diseases, applicable to studies on T cell differentiation and survival, immune response regulation, and autoimmune diseases. It provides a robust preclinical research platform for the screening, development, and safety evaluation of α4β7/TL1A-targeted drugs.
Prkch-KO
製品ID :
S-KO-03676
系統:
C57BL/6NCya
状況:
説明:
Prkch is located on chromosome 12 of mice. Nuclease Technology was used to design sgRNA; Prkch knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Prkch is located on chromosome 12 of mice. Nuclease Technology was used to design sgRNA; Prkch knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Mc5r-flox
製品ID :
S-CKO-03676
系統:
C57BL/6JCya
状況:
説明:
Mc5r is located on chromosome 18 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Mc5r conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Mc5r is located on chromosome 18 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Mc5r 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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