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Kit-LSL-T2A-DTR-P2A-Dre
製品ID :
I001102
系統:
C57BL/6JCya
状況:
説明:
The TGA stop codon of the mouse Kit gene is replaced with loxP-6*SV40 pA-loxP-T2A-DTR-P2A-Dre. When Kit-LSL-T2A-DTR-P2A-Dre mice are crossed with Cre mice, the 6*SV40 pA sequence in the offspring mice is deleted, and DTR (diphtheria toxin receptor) and Dre are expressed.
The TGA stop codon of the mouse Kit gene is replaced with loxP-6*SV40 pA-loxP-T2A-DTR-P2A-Dre. When Kit-LSL-T2A-DTR-P2A-Dre mice are crossed with Cre mice, the 6*SV40 pA sequence in the offspring mice is deleted, and DTR (diphtheria toxin receptor) and Dre are expressed.
NKG-Kit*V831M
製品ID :
I001175
系統:
NKG
状況:
説明:
NKG mice are a type of severe immunodeficient mouse developed by Cyagen by knocking out the Il2rg gene in the NOD-Scid background strain. This strain lacks mature T, B, and NK immune cells, has reduced complement activity, and weak phagocytic activity of macrophages against human cells. Therefore, NKG mice can efficiently engraft human hematopoietic stem cells (HSC), peripheral blood mononuclear cells (PBMC), patient-derived xenografts (PDX), or adult stem cells and tissues.
Significant physiological and immunological differences exist between humans and mice in immunological research, making direct extrapolation of murine data to humans challenging. However, by transplanting human PBMCs or HSCs into immunodeficient mice, human immune components can partially or fully replace the murine immune system, creating an in vivo model that facilitates the study of human immune functions. Typically, successful reconstitution of HSCs in severely immunodeficient mice requires myeloablative irradiation to deplete endogenous murine HSCs. This process creates a niche for human HSC engraftment while reducing the risk of host immune rejection. Nevertheless, myeloablative irradiation is associated with off-target damage to various tissues and organs, impacting the survival and functional integrity of engrafted cells [1-2]. Thus, genetic modification of murine HSC function to obviate the need for irradiation during HSC reconstitution represents a significant advancement in improving post-reconstitution survival and overall health of the mice.
The KIT gene encodes a receptor tyrosine kinase (c-Kit or CD117) that is activated by its ligand, stem cell factor (SCF). Activation of this receptor triggers phosphorylation of a variety of downstream intracellular proteins, governing essential cellular processes such as proliferation, differentiation, migration, and apoptosis across numerous cell types. The KIT gene plays a pivotal role in hematopoiesis, stem cell maintenance, gametogenesis, melanogenesis, and the development and function of mast cells. Mutations in KIT are implicated in a range of pathologies, including gastrointestinal stromal tumors, mastocytosis, and acute myeloid leukemia. Importantly, immunodeficient mice harboring the KIT W41 mutation (V831M) have demonstrated the ability to undergo human HSC transplantation without the need for irradiation, while maintaining high rates of engraftment [3-4]. The NKG-Kit*V831M mouse strain is generated by introducing the W41 mutation (V831M) into the KIT gene of the NKG mouse. Compared to standard NKG mice, these mice eliminate the need for irradiation during HSC reconstitution, thereby avoiding the deleterious effects of irradiation on the hematopoietic, gastrointestinal, and nervous systems. This feature renders NKG-Kit*V831M mice an invaluable tool for developing and evaluating tumor immunotherapies and conducting drug efficacy assessments.
NKG mice are a type of severe immunodeficient mouse developed by Cyagen by knocking out the Il2rg gene in the NOD-Scid background strain. This strain lacks mature T, B, and NK immune cells, has reduced complement activity, and weak phagocytic activity of macrophages against human cells. Therefore, NKG mice can efficiently engraft human hematopoietic stem cells (HSC), peripheral blood mononuclear cells (PBMC), patient-derived xenografts (PDX), or adult stem cells and tissues.
Significant physiological and immunological differences exist between humans and mice in immunological research, making direct extrapolation of murine data to humans challenging. However, by transplanting human PBMCs or HSCs into immunodeficient mice, human immune components can partially or fully replace the murine immune system, creating an in vivo model that facilitates the study of human immune functions. Typically, successful reconstitution of HSCs in severely immunodeficient mice requires myeloablative irradiation to deplete endogenous murine HSCs. This process creates a niche for human HSC engraftment while reducing the risk of host immune rejection. Nevertheless, myeloablative irradiation is associated with off-target damage to various tissues and organs, impacting the survival and functional integrity of engrafted cells [1-2]. Thus, genetic modification of murine HSC function to obviate the need for irradiation during HSC reconstitution represents a significant advancement in improving post-reconstitution survival and overall health of the mice.
The KIT gene encodes a receptor tyrosine kinase (c-Kit or CD117) that is activated by its ligand, stem cell factor (SCF). Activation of this receptor triggers phosphorylation of a variety of downstream intracellular proteins, governing essential cellular processes such as proliferation, differentiation, migration, and apoptosis across numerous cell types. The KIT gene plays a pivotal role in hematopoiesis, stem cell maintenance, gametogenesis, melanogenesis, and the development and function of mast cells. Mutations in KIT are implicated in a range of pathologies, including gastrointestinal stromal tumors, mastocytosis, and acute myeloid leukemia. Importantly, immunodeficient mice harboring the KIT W41 mutation (V831M) have demonstrated the ability to undergo human HSC transplantation without the need for irradiation, while maintaining high rates of engraftment [3-4]. The NKG-Kit*V831M mouse strain is generated by introducing the W41 mutation (V831M) into the KIT gene of the NKG mouse. Compared to standard NKG mice, these mice eliminate the need for irradiation during HSC reconstitution, thereby avoiding the deleterious effects of irradiation on the hematopoietic, gastrointestinal, and nervous systems. This feature renders NKG-Kit*V831M mice an invaluable tool for developing and evaluating tumor immunotherapies and conducting drug efficacy assessments.
Itgb5-KO
製品ID :
S-KO-16590
系統:
C57BL/6JCya
状況:
説明:
Itgb5 is located on chromosome 16 of mice. Nuclease Technology was used to design sgRNA; Itgb5 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Itgb5 is located on chromosome 16 of mice. Nuclease Technology was used to design sgRNA; Itgb5 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Kit-KO
製品ID :
S-KO-20974
系統:
C57BL/6JCya
状況:
説明:
Kit is located on chromosome 5 of mice. Nuclease Technology was used to design sgRNA; Kit knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Kit is located on chromosome 5 of mice. Nuclease Technology was used to design sgRNA; Kit knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Mettl15-flox
製品ID :
S-CKO-16590
系統:
C57BL/6JCya
状況:
説明:
Mettl15 is located on chromosome 2 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Mettl15 conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Mettl15 is located on chromosome 2 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Mettl15 conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Kit-flox
製品ID :
S-CKO-20889
系統:
C57BL/6NCya
状況:
説明:
Kit is located on chromosome 5 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Kit conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Kit is located on chromosome 5 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Kit conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Kit-flox
製品ID :
S-CKO-03276
系統:
C57BL/6JCya
状況:
説明:
Kit is located on chromosome 5 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Kit conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Kit is located on chromosome 5 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Kit conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
NKG-SGM3/hIL6/Kit*V831M
製品ID :
C001695
系統:
NKG
状況:
説明:
NKG mice are a type of severe immunodeficient mouse developed by Cyagen by deleting the Il2rg gene from the NOD-Scid strain. This strain lacks mature T, B, and NK cells, has reduced complement activity, and weak macrophage phagocytosis of human cells. As a result, NKG mice can efficiently engraft human hematopoietic stem cells (HSC), peripheral blood mononuclear cells (PBMC), patient-derived xenografts (PDX), or adult stem cells and tissues.
Interleukin-6 (IL-6) is a cytokine that plays a crucial role in inflammation and B cell maturation. It is primarily produced and secreted into the bloodstream at acute and chronic inflammatory sites. IL-6 induces transcriptional inflammatory responses through its receptor, IL6Rα. Research indicates that immunodeficient mice carrying the human IL6 gene effectively enhance the differentiation of human monocytes and macrophages during HSC reconstruction [1].
The KIT gene encodes a receptor tyrosine kinase (c-Kit or CD117) that is activated by its ligand, stem cell factor (SCF). Activation of this receptor triggers phosphorylation of a variety of downstream intracellular proteins, governing essential cellular processes such as proliferation, differentiation, migration, and apoptosis across numerous cell types. The KIT gene plays a pivotal role in hematopoiesis, stem cell maintenance, gametogenesis, melanogenesis, and the development and function of mast cells. Mutations in KIT are implicated in a range of pathologies, including gastrointestinal stromal tumors, mastocytosis, and acute myeloid leukemia. Importantly, immunodeficient mice harboring the KIT W41 mutation (V831M) have demonstrated the ability to undergo human HSC transplantation without the need for irradiation, while maintaining high rates of engraftment [2-3].
The SCF gene, also known as KITLG, encodes the receptor-type protein-tyrosine kinase KIT ligand. This gene is crucial for the development of germ cells and neurons during embryogenesis and plays a significant role in hematopoiesis. The GM-CSF gene, or CSF2, encodes a cytokine that orchestrates the production, differentiation, and function of granulocytes and macrophages. Meanwhile, the IL3 gene encodes a growth-promoting cytokine essential for the proliferation of various blood cell types, influencing cell growth, differentiation, and apoptosis. Research demonstrates that severe immunodeficient mice expressing human IL3, GM-CSF (CSF2), and SCF (KITLG) show markedly enhanced engraftment efficiency in the xenotransplantation of acute myeloid leukemia (AML) [4], supporting stable engraftment of myeloid lineages and regulatory T cell populations [5].
NKG-SGM3/hIL6/Kit*V831M mice are mouse models obtained by mating KIT W41 mutation (V831M) mouse models (Catalog Number: I001175) with IL6 humanized mouse models (Catalog Number: I001176) and IL3, KITLG and CSF2 triple humanized mouse models (Catalog Number: I001177). These mice express human IL6, IL3, KITLG, and CSF2 genomic sequences, as well as mouse KIT genomic sequences carrying the W41 mutation (V831M). This model is a valuable tool for immuno-oncology, immunology, and infectious disease research.
NKG mice are a type of severe immunodeficient mouse developed by Cyagen by deleting the Il2rg gene from the NOD-Scid strain. This strain lacks mature T, B, and NK cells, has reduced complement activity, and weak macrophage phagocytosis of human cells. As a result, NKG mice can efficiently engraft human hematopoietic stem cells (HSC), peripheral blood mononuclear cells (PBMC), patient-derived xenografts (PDX), or adult stem cells and tissues.
Interleukin-6 (IL-6) is a cytokine that plays a crucial role in inflammation and B cell maturation. It is primarily produced and secreted into the bloodstream at acute and chronic inflammatory sites. IL-6 induces transcriptional inflammatory responses through its receptor, IL6Rα. Research indicates that immunodeficient mice carrying the human IL6 gene effectively enhance the differentiation of human monocytes and macrophages during HSC reconstruction [1].
The KIT gene encodes a receptor tyrosine kinase (c-Kit or CD117) that is activated by its ligand, stem cell factor (SCF). Activation of this receptor triggers phosphorylation of a variety of downstream intracellular proteins, governing essential cellular processes such as proliferation, differentiation, migration, and apoptosis across numerous cell types. The KIT gene plays a pivotal role in hematopoiesis, stem cell maintenance, gametogenesis, melanogenesis, and the development and function of mast cells. Mutations in KIT are implicated in a range of pathologies, including gastrointestinal stromal tumors, mastocytosis, and acute myeloid leukemia. Importantly, immunodeficient mice harboring the KIT W41 mutation (V831M) have demonstrated the ability to undergo human HSC transplantation without the need for irradiation, while maintaining high rates of engraftment [2-3].
The SCF gene, also known as KITLG, encodes the receptor-type protein-tyrosine kinase KIT ligand. This gene is crucial for the development of germ cells and neurons during embryogenesis and plays a significant role in hematopoiesis. The GM-CSF gene, or CSF2, encodes a cytokine that orchestrates the production, differentiation, and function of granulocytes and macrophages. Meanwhile, the IL3 gene encodes a growth-promoting cytokine essential for the proliferation of various blood cell types, influencing cell growth, differentiation, and apoptosis. Research demonstrates that severe immunodeficient mice expressing human IL3, GM-CSF (CSF2), and SCF (KITLG) show markedly enhanced engraftment efficiency in the xenotransplantation of acute myeloid leukemia (AML) [4], supporting stable engraftment of myeloid lineages and regulatory T cell populations [5].
NKG-SGM3/hIL6/Kit*V831M mice are mouse models obtained by mating KIT W41 mutation (V831M) mouse models (Catalog Number: I001175) with IL6 humanized mouse models (Catalog Number: I001176) and IL3, KITLG and CSF2 triple humanized mouse models (Catalog Number: I001177). These mice express human IL6, IL3, KITLG, and CSF2 genomic sequences, as well as mouse KIT genomic sequences carrying the W41 mutation (V831M). This model is a valuable tool for immuno-oncology, immunology, and infectious disease research.
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