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Gm11437-EGFP
製品ID :
C001659
系統:
C57BL/6JCya
状況:
説明:
The TGA stop codon was replaced with "3xEAAAK-EGFP" cassette. Enhanced green fluorescent protein (EGFP) is expressed under the regulatory control of Gm11437 gene elements. This model enables EGFP fluorescence protein tracing studies.
The TGA stop codon was replaced with "3xEAAAK-EGFP" cassette. Enhanced green fluorescent protein (EGFP) is expressed under the regulatory control of Gm11437 gene elements. This model enables EGFP fluorescence protein tracing studies.
NKG-SGM3
製品ID :
I001177
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.
In immunology research, direct studies on mice may not fully represent the human immune system due to physiological and immune system differences. However, by transplanting human peripheral blood mononuclear cells (PBMCs) or hematopoietic stem cells (HSCs) into immunodeficient mice, we can partially or completely replace the mouse immune system with a human counterpart. This approach enables in vivo simulation of human immune system function, providing an effective model for studying human immunity. In practical human-mouse xenotransplantation, using standard immunodeficient mice for transplantation may lead to differences in transplant efficiency due to the absence of specific human growth factors and supportive stromal cells within the mouse. Genetically modifying immunodeficient mice through gene editing techniques is a common strategy to enhance xenotransplantation efficiency.
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) [1], supporting stable engraftment of myeloid lineages and regulatory T cell populations [2]. NKG-SGM3 mice constructed by integrating human KITLG, CSF2, and IL3 genes into the genome of NKG mice can effectively enhance myeloid differentiation and improve the transplantation efficiency of hematopoietic and acute myeloid leukemia cells and thus are valuable 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.
In immunology research, direct studies on mice may not fully represent the human immune system due to physiological and immune system differences. However, by transplanting human peripheral blood mononuclear cells (PBMCs) or hematopoietic stem cells (HSCs) into immunodeficient mice, we can partially or completely replace the mouse immune system with a human counterpart. This approach enables in vivo simulation of human immune system function, providing an effective model for studying human immunity. In practical human-mouse xenotransplantation, using standard immunodeficient mice for transplantation may lead to differences in transplant efficiency due to the absence of specific human growth factors and supportive stromal cells within the mouse. Genetically modifying immunodeficient mice through gene editing techniques is a common strategy to enhance xenotransplantation efficiency.
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) [1], supporting stable engraftment of myeloid lineages and regulatory T cell populations [2]. NKG-SGM3 mice constructed by integrating human KITLG, CSF2, and IL3 genes into the genome of NKG mice can effectively enhance myeloid differentiation and improve the transplantation efficiency of hematopoietic and acute myeloid leukemia cells and thus are valuable for immuno-oncology, immunology, and infectious disease research.
B6-hIGHMBP2
製品ID :
C001437
系統:
C57BL/6NCya
状況:
説明:
The IGHMBP2 (Immunoglobulin mu binding protein 2) gene encodes an ATP-dependent helicase that is expressed throughout the body and contains a helicase structural domain, a single-stranded nucleic acid binding domain, and one zinc finger motif. It is involved in the regulation of DNA replication, mRNA splicing, transcription, and translation. Mutations in IGHMBP2 can lead to two different types of diseases: spinal muscular atrophy with respiratory distress type 1 (SMARD1) and Charcot-Marie-Tooth disease type 2S (CMT2S).
Spinal muscular atrophy with respiratory distress type 1 (SMARD1) is a rare autosomal recessive motor neuron disease, with its main clinical symptom being diaphragmatic paralysis leading to respiratory distress, occurring mostly in infants aged 6 to 12 months. In addition, SMARD1 can also cause severe muscle atrophy that progresses from the distal to the proximal limbs, intrauterine growth retardation, weak crying, and sensory and autonomic nervous system defects [1]. Restrictive cardiomyopathy may be one of the phenotypes of SMARD1 [2]. Charcot-Marie-Tooth disease type 2S (CMT2S) is a rare hereditary neurological disease and is a subtype of Charcot-Marie-Tooth disease type 2 (CMT2). CMT2 is a group of hereditary peripheral neuropathies characterized by abnormal fibers or axons extending from the nerve cell body to muscles or sensory organs, reducing the strength of nerve impulses. The clinical characteristics of CMT2S include symmetrical distal limb weakness and muscle atrophy, with severe peripheral nerve damage.
Currently, ASO drugs and AAV-based gene therapy have emerged in the IGHMBP2-targeted drug pipeline for the treatment of SMARD1 and CMT2. Gene therapy is expected to become one of the most promising treatments for these diseases. However, since most ASO, AAV-based gene therapy, etc., act on the human IGHMBP2 gene, considering the differences between animals and humans in genes, humanizing the mouse gene will help promote the further clinical translation of therapies targeting IGHMBP2. This strain is a mouse Ighmbp2 gene humanized model and can be used for research on SMARD1 and CMT2S. The homozygous B6-hIGHMBP2 mice are viable and fertile. In addition, based on the independently developed TurboKnockout fusion BAC recombination technology, Cyagen can also generate hot mutation models based on this strain and provide customized services for specific mutations to meet the experimental needs in pharmacology and other fields related to SMARD1 and CMT2S.
The IGHMBP2 (Immunoglobulin mu binding protein 2) gene encodes an ATP-dependent helicase that is expressed throughout the body and contains a helicase structural domain, a single-stranded nucleic acid binding domain, and one zinc finger motif. It is involved in the regulation of DNA replication, mRNA splicing, transcription, and translation. Mutations in IGHMBP2 can lead to two different types of diseases: spinal muscular atrophy with respiratory distress type 1 (SMARD1) and Charcot-Marie-Tooth disease type 2S (CMT2S).
Spinal muscular atrophy with respiratory distress type 1 (SMARD1) is a rare autosomal recessive motor neuron disease, with its main clinical symptom being diaphragmatic paralysis leading to respiratory distress, occurring mostly in infants aged 6 to 12 months. In addition, SMARD1 can also cause severe muscle atrophy that progresses from the distal to the proximal limbs, intrauterine growth retardation, weak crying, and sensory and autonomic nervous system defects [1]. Restrictive cardiomyopathy may be one of the phenotypes of SMARD1 [2]. Charcot-Marie-Tooth disease type 2S (CMT2S) is a rare hereditary neurological disease and is a subtype of Charcot-Marie-Tooth disease type 2 (CMT2). CMT2 is a group of hereditary peripheral neuropathies characterized by abnormal fibers or axons extending from the nerve cell body to muscles or sensory organs, reducing the strength of nerve impulses. The clinical characteristics of CMT2S include symmetrical distal limb weakness and muscle atrophy, with severe peripheral nerve damage.
Currently, ASO drugs and AAV-based gene therapy have emerged in the IGHMBP2-targeted drug pipeline for the treatment of SMARD1 and CMT2. Gene therapy is expected to become one of the most promising treatments for these diseases. However, since most ASO, AAV-based gene therapy, etc., act on the human IGHMBP2 gene, considering the differences between animals and humans in genes, humanizing the mouse gene will help promote the further clinical translation of therapies targeting IGHMBP2. This strain is a mouse Ighmbp2 gene humanized model and can be used for research on SMARD1 and CMT2S. The homozygous B6-hIGHMBP2 mice are viable and fertile. In addition, based on the independently developed TurboKnockout fusion BAC recombination technology, Cyagen can also generate hot mutation models based on this strain and provide customized services for specific mutations to meet the experimental needs in pharmacology and other fields related to SMARD1 and CMT2S.
Cd84-KO
製品ID :
S-KO-01437
系統:
C57BL/6JCya
状況:
説明:
Cd84 is located on chromosome 1 of mice. Nuclease Technology was used to design sgRNA; Cd84 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Cd84 is located on chromosome 1 of mice. Nuclease Technology was used to design sgRNA; Cd84 knockout mice were obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Bmp7-flox
製品ID :
S-CKO-01437
系統:
C57BL/6JCya
状況:
説明:
Bmp7 is located on chromosome 2 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Bmp7 conditional knockout mice were obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Bmp7 is located on chromosome 2 of mice. SgRNA and ssDNA were designed using Nuclease Technology; Bmp7 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.
Gm11437-KO
製品ID :
S-KO-11320
系統:
C57BL/6JCya
状況:
説明:
Gm11437 is located on chromosome 11 of mice. Nuclease Technology will be used to design sgRNA; Gm11437 knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Gm11437 is located on chromosome 11 of mice. Nuclease Technology will be used to design sgRNA; Gm11437 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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