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B6-huAPRIL (huTNFSF13)
製品ID :
C001852
系統:
C57BL/6NCya
状況:
説明:
The TNFSF13 gene, also known as APRIL (a proliferation-inducing ligand), encodes a critical member of the tumor necrosis factor (TNF) superfamily. Its expression is detected in various cell types within the immune and stromal compartments, including monocytes, macrophages, dendritic cells, and bone marrow precursors [1]. The encoded cytokine functions by binding to specific receptors, namely TNFRSF17/BCMA and TNFRSF13B/TACI, thereby regulating key aspects of B cell and plasma cell biology, including their development and long-term survival. TNFSF13 is instrumental in the adaptive immune response, facilitating antibody class switching and providing essential survival cues to antibody-secreting cells [2]. Dysregulated TNFSF13 expression has been etiologically linked to various pathologies. Aberrant TNFSF13 signaling contributes to the pathogenesis of multiple myeloma and chronic lymphocytic leukemia (CLL) by promoting the proliferation and survival of malignant cells [3]. Furthermore, its dysregulation is also implicated in the progression of several autoimmune disorders, such as rheumatoid arthritis (RA), IgA nephropathy, and systemic lupus erythematosus (SLE) [4].
The B6-huAPRIL (huTNFSF13) mouse is a humanized model constructed via gene-editing technology. The sequence from the ATG start codon to the TGA stop codon of mouse Tnfsf13 is replaced with the sequence from the ATG start codon to the TGA stop codon of human TNFSF13. B6-huAPRIL (huTNFSF13) mice can be used for research into the pathogenesis of autoimmune disorders like rheumatoid arthritis (RA), IgA nephropathy, and systemic lupus erythematosus (SLE), as well as some cancers, and for the development of TNFSF13-targeted drugs.
The TNFSF13 gene, also known as APRIL (a proliferation-inducing ligand), encodes a critical member of the tumor necrosis factor (TNF) superfamily. Its expression is detected in various cell types within the immune and stromal compartments, including monocytes, macrophages, dendritic cells, and bone marrow precursors [1]. The encoded cytokine functions by binding to specific receptors, namely TNFRSF17/BCMA and TNFRSF13B/TACI, thereby regulating key aspects of B cell and plasma cell biology, including their development and long-term survival. TNFSF13 is instrumental in the adaptive immune response, facilitating antibody class switching and providing essential survival cues to antibody-secreting cells [2]. Dysregulated TNFSF13 expression has been etiologically linked to various pathologies. Aberrant TNFSF13 signaling contributes to the pathogenesis of multiple myeloma and chronic lymphocytic leukemia (CLL) by promoting the proliferation and survival of malignant cells [3]. Furthermore, its dysregulation is also implicated in the progression of several autoimmune disorders, such as rheumatoid arthritis (RA), IgA nephropathy, and systemic lupus erythematosus (SLE) [4].
The B6-huAPRIL (huTNFSF13) mouse is a humanized model constructed via gene-editing technology. The sequence from the ATG start codon to the TGA stop codon of mouse Tnfsf13 is replaced with the sequence from the ATG start codon to the TGA stop codon of human TNFSF13. B6-huAPRIL (huTNFSF13) mice can be used for research into the pathogenesis of autoimmune disorders like rheumatoid arthritis (RA), IgA nephropathy, and systemic lupus erythematosus (SLE), as well as some cancers, and for the development of TNFSF13-targeted drugs.
B6-hBAFF/huAPRIL
製品ID :
C001802
系統:
C57BL/6NCya
状況:
説明:
The TNFSF13B gene encodes B cell-activating factor (BAFF), a critical cytokine for B cell survival and maturation, primarily expressed by monocytes, macrophages, dendritic cells, and T cells [1]. BAFF, a member of the tumour necrosis factor (TNF) superfamily, functions through binding to receptors on B cells, including BAFF-R, TACI, and BCMA. Activation of these receptors initiates the NF-κB and MAPK signaling cascades, leading to B cell survival, proliferation, and immunoglobulin production [1-2]. This cytokine is essential for humoral immunity and the development of lymphoid tissues [1]. Aberrant BAFF expression and signaling are implicated in the pathogenesis of autoimmune diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis. BAFF overexpression can drive B cell hyperactivity and the production of autoantibodies, contributing to these conditions [2-3]. Clinically, monoclonal antibodies targeting BAFF, such as belimumab, are employed in the treatment of SLE [4]. In the tumor microenvironment, BAFF exhibits a complex role, supporting B cell lymphomas and influencing the immune response to solid tumours, exhibiting context-dependent pro- and anti-tumourigenic effects [5]. This multifaceted role highlights BAFF as a key therapeutic target in autoimmune diseases and specific B cell malignancies [1-5].
The TNFSF13 gene, also known as APRIL (a proliferation-inducing ligand), encodes a critical member of the tumor necrosis factor (TNF) superfamily. Its expression is detected in various cell types within the immune and stromal compartments, including monocytes, macrophages, dendritic cells, and bone marrow precursors [6]. The encoded cytokine functions by binding to specific receptors, namely TNFRSF17/BCMA and TNFRSF13B/TACI, thereby regulating key aspects of B cell and plasma cell biology, including their development and long-term survival. TNFSF13 is instrumental in the adaptive immune response, facilitating antibody class switching and providing essential survival cues to antibody-secreting cells [7]. Dysregulated TNFSF13 expression has been etiologically linked to various pathologies. Aberrant TNFSF13 signaling contributes to the pathogenesis of multiple myeloma and chronic lymphocytic leukemia (CLL) by promoting the proliferation and survival of malignant cells [8]. Furthermore, its dysregulation is also implicated in the progression of several autoimmune disorders, such as rheumatoid arthritis (RA), IgA nephropathy, and systemic lupus erythematosus (SLE) [9].
The B6-hBAFF/huAPRIL mouse is a dual-gene humanized model generated by crossing B6-hBAFF (hTNFSF13B) mice (Catalog No.: C001621) with B6-huAPRIL (huTNFSF13) mice (Catalog No.: C001852). This model can be used for the study of autoimmune disorders, such as rheumatoid arthritis (RA), IgA nephropathy, and systemic lupus erythematosus (SLE) and B cell malignancies, as well as for the development of related targeted therapeutics.
The TNFSF13B gene encodes B cell-activating factor (BAFF), a critical cytokine for B cell survival and maturation, primarily expressed by monocytes, macrophages, dendritic cells, and T cells [1]. BAFF, a member of the tumour necrosis factor (TNF) superfamily, functions through binding to receptors on B cells, including BAFF-R, TACI, and BCMA. Activation of these receptors initiates the NF-κB and MAPK signaling cascades, leading to B cell survival, proliferation, and immunoglobulin production [1-2]. This cytokine is essential for humoral immunity and the development of lymphoid tissues [1]. Aberrant BAFF expression and signaling are implicated in the pathogenesis of autoimmune diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis. BAFF overexpression can drive B cell hyperactivity and the production of autoantibodies, contributing to these conditions [2-3]. Clinically, monoclonal antibodies targeting BAFF, such as belimumab, are employed in the treatment of SLE [4]. In the tumor microenvironment, BAFF exhibits a complex role, supporting B cell lymphomas and influencing the immune response to solid tumours, exhibiting context-dependent pro- and anti-tumourigenic effects [5]. This multifaceted role highlights BAFF as a key therapeutic target in autoimmune diseases and specific B cell malignancies [1-5].
The TNFSF13 gene, also known as APRIL (a proliferation-inducing ligand), encodes a critical member of the tumor necrosis factor (TNF) superfamily. Its expression is detected in various cell types within the immune and stromal compartments, including monocytes, macrophages, dendritic cells, and bone marrow precursors [6]. The encoded cytokine functions by binding to specific receptors, namely TNFRSF17/BCMA and TNFRSF13B/TACI, thereby regulating key aspects of B cell and plasma cell biology, including their development and long-term survival. TNFSF13 is instrumental in the adaptive immune response, facilitating antibody class switching and providing essential survival cues to antibody-secreting cells [7]. Dysregulated TNFSF13 expression has been etiologically linked to various pathologies. Aberrant TNFSF13 signaling contributes to the pathogenesis of multiple myeloma and chronic lymphocytic leukemia (CLL) by promoting the proliferation and survival of malignant cells [8]. Furthermore, its dysregulation is also implicated in the progression of several autoimmune disorders, such as rheumatoid arthritis (RA), IgA nephropathy, and systemic lupus erythematosus (SLE) [9].
The B6-hBAFF/huAPRIL mouse is a dual-gene humanized model generated by crossing B6-hBAFF (hTNFSF13B) mice (Catalog No.: C001621) with B6-huAPRIL (huTNFSF13) mice (Catalog No.: C001852). This model can be used for the study of autoimmune disorders, such as rheumatoid arthritis (RA), IgA nephropathy, and systemic lupus erythematosus (SLE) and B cell malignancies, as well as for the development of related targeted therapeutics.
Gsg1l-KO
製品ID :
S-KO-08741
系統:
C57BL/6JCya
状況:
説明:
Gsg1l is located on chromosome 7 of mice. Nuclease Technology will be used to design sgRNA; Gsg1l knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Gsg1l is located on chromosome 7 of mice. Nuclease Technology will be used to design sgRNA; Gsg1l knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
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