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TG-hAPOC3
製品ID :
C001588
系統:
C57BL/6NCya
状況:
説明:
Apolipoprotein C-III (ApoC-III), encoded by the APOC3 gene, is a 79-amino acid glycoprotein primarily synthesized in the liver, with minor production in the intestine. ApoC-III is a key component of triglyceride-rich lipoproteins (TRLs), including chylomicrons and very low-density lipoprotein (VLDL). Its primary functions include inhibiting lipoprotein lipase (LPL)-mediated hydrolysis of triglycerides within TRLs and modulating hepatic uptake of TRL remnants, thereby elevating plasma triglyceride levels. Consequently, ApoC-III is crucial in regulating plasma triglyceride levels [1-2]. Elevated APOC3 expression leads to increased ApoC-III levels, which is associated with hypertriglyceridemia (a risk factor for cardiovascular disease) and conditions such as familial hypertriglyceridemia, metabolic syndrome, and type 2 diabetes. Therefore, targeting the reduction of APOC3 expression or blocking its protein function offers a therapeutic avenue for hypertriglyceridemia and mitigating cardiovascular disease risk [3].
The TG-hAPOC3 mouse is a humanized model generated by integrating the human APOC3 gene sequence, encompassing the upstream and downstream untranslated regions (UTRs), into the mouse genome, enabling the expression of human ApoC-III protein in vivo. This model is valuable for developing therapeutics targeting human APOC3, such as small interfering RNA (siRNA) and antisense oligonucleotides (ASOs), for the treatment of hypertriglyceridemia.
Apolipoprotein C-III (ApoC-III), encoded by the APOC3 gene, is a 79-amino acid glycoprotein primarily synthesized in the liver, with minor production in the intestine. ApoC-III is a key component of triglyceride-rich lipoproteins (TRLs), including chylomicrons and very low-density lipoprotein (VLDL). Its primary functions include inhibiting lipoprotein lipase (LPL)-mediated hydrolysis of triglycerides within TRLs and modulating hepatic uptake of TRL remnants, thereby elevating plasma triglyceride levels. Consequently, ApoC-III is crucial in regulating plasma triglyceride levels [1-2]. Elevated APOC3 expression leads to increased ApoC-III levels, which is associated with hypertriglyceridemia (a risk factor for cardiovascular disease) and conditions such as familial hypertriglyceridemia, metabolic syndrome, and type 2 diabetes. Therefore, targeting the reduction of APOC3 expression or blocking its protein function offers a therapeutic avenue for hypertriglyceridemia and mitigating cardiovascular disease risk [3].
The TG-hAPOC3 mouse is a humanized model generated by integrating the human APOC3 gene sequence, encompassing the upstream and downstream untranslated regions (UTRs), into the mouse genome, enabling the expression of human ApoC-III protein in vivo. This model is valuable for developing therapeutics targeting human APOC3, such as small interfering RNA (siRNA) and antisense oligonucleotides (ASOs), for the treatment of hypertriglyceridemia.
B6-hPCSK9/TG-hAPOC3
製品ID :
C001744
系統:
C57BL/6NCya
状況:
説明:
Proprotein convertase subtilisin/kexin 9 (PCSK9) is a serine protease primarily produced in the liver but expressed in other tissues, including the intestine, heart, and neurons. The N-terminal domain of the PCSK9 protein is responsible for protein localization and stability, while the C-terminal domain is responsible for protein enzymatic activity [1]. The Low-density lipoprotein receptor (LDLR) is a receptor that is responsible for clearing low-density lipoprotein cholesterol (LDL-C) from the blood. PCSK9 cleaves the intracellular domain of LDLR on the cell surface, causing it to detach from the cell membrane and be transported to the lysosome for degradation, promoting LDLR degradation, and increasing plasma LDL-C. Overexpression or gain-of-function mutations of the PCSK9 gene can lead to LDL-C accumulation by reducing LDLR levels. This can cause hypercholesterolemia, which increases the risk of cardiovascular diseases, such as atherosclerosis and coronary heart disease, and neurodegenerative diseases, such as Alzheimer's disease [2]. PCSK9 has become an important target for the development of lipid-lowering drugs. Several PCSK9-targeted antibodies or small nucleic acid drugs have been approved for marketing worldwide, including evolocumab from Amgen, alirocumab from Sanofi and Regeneron, and inclisiran from Novartis. These drugs primarily work by inhibiting PCSK9 activity or preventing PCSK9 protein from binding to LDLR, lowering LDL-C levels in the blood to treat hypercholesterolemia [3-4]. In addition, PCSK9 can promote tumor growth and development by regulating cell proliferation, migration, and invasion. It can also regulate the expression of inflammatory factors that contribute to inflammation. Therefore, targeting the expression of PCSK9 has been investigated in tumor immunotherapy and autoimmune disease therapy [5-6].
Apolipoprotein C-III (ApoC-III), encoded by the APOC3 gene, is a 79-amino acid glycoprotein primarily synthesized in the liver, with minor production in the intestine. ApoC-III is a key component of triglyceride-rich lipoproteins (TRLs), including chylomicrons and very low-density lipoprotein (VLDL). Its primary functions include inhibiting lipoprotein lipase (LPL)-mediated hydrolysis of triglycerides within TRLs and modulating hepatic uptake of TRL remnants, thereby elevating plasma triglyceride levels. Consequently, ApoC-III is crucial in regulating plasma triglyceride levels [7-8]. Elevated APOC3 expression leads to increased ApoC-III levels, which is associated with hypertriglyceridemia (a risk factor for cardiovascular disease) and conditions such as familial hypertriglyceridemia, metabolic syndrome, and type 2 diabetes. Therefore, targeting the reduction of APOC3 expression or blocking its protein function offers a therapeutic avenue for hypertriglyceridemia and mitigating cardiovascular disease risk [9].
B6-hPCSK9/TG-hAPOC3 mice are humanized models generated by crossing B6-hPCSK9 mice (Catalog No.: C001617) with TG-hAPOC3 mice (Catalog No.: C001588), enabling systemic expression of human PCSK9 and ApoC-Ⅲ proteins. This model is suitable for developing drugs targeting human APOC3/PCSK9, such as small interfering RNA (siRNA) and antisense oligonucleotides (ASO), for treating hypertriglyceridemia and other metabolic disorders, as well as for research on neurodegenerative diseases, tumorigenesis, and autoimmune diseases.
Proprotein convertase subtilisin/kexin 9 (PCSK9) is a serine protease primarily produced in the liver but expressed in other tissues, including the intestine, heart, and neurons. The N-terminal domain of the PCSK9 protein is responsible for protein localization and stability, while the C-terminal domain is responsible for protein enzymatic activity [1]. The Low-density lipoprotein receptor (LDLR) is a receptor that is responsible for clearing low-density lipoprotein cholesterol (LDL-C) from the blood. PCSK9 cleaves the intracellular domain of LDLR on the cell surface, causing it to detach from the cell membrane and be transported to the lysosome for degradation, promoting LDLR degradation, and increasing plasma LDL-C. Overexpression or gain-of-function mutations of the PCSK9 gene can lead to LDL-C accumulation by reducing LDLR levels. This can cause hypercholesterolemia, which increases the risk of cardiovascular diseases, such as atherosclerosis and coronary heart disease, and neurodegenerative diseases, such as Alzheimer's disease [2]. PCSK9 has become an important target for the development of lipid-lowering drugs. Several PCSK9-targeted antibodies or small nucleic acid drugs have been approved for marketing worldwide, including evolocumab from Amgen, alirocumab from Sanofi and Regeneron, and inclisiran from Novartis. These drugs primarily work by inhibiting PCSK9 activity or preventing PCSK9 protein from binding to LDLR, lowering LDL-C levels in the blood to treat hypercholesterolemia [3-4]. In addition, PCSK9 can promote tumor growth and development by regulating cell proliferation, migration, and invasion. It can also regulate the expression of inflammatory factors that contribute to inflammation. Therefore, targeting the expression of PCSK9 has been investigated in tumor immunotherapy and autoimmune disease therapy [5-6].
Apolipoprotein C-III (ApoC-III), encoded by the APOC3 gene, is a 79-amino acid glycoprotein primarily synthesized in the liver, with minor production in the intestine. ApoC-III is a key component of triglyceride-rich lipoproteins (TRLs), including chylomicrons and very low-density lipoprotein (VLDL). Its primary functions include inhibiting lipoprotein lipase (LPL)-mediated hydrolysis of triglycerides within TRLs and modulating hepatic uptake of TRL remnants, thereby elevating plasma triglyceride levels. Consequently, ApoC-III is crucial in regulating plasma triglyceride levels [7-8]. Elevated APOC3 expression leads to increased ApoC-III levels, which is associated with hypertriglyceridemia (a risk factor for cardiovascular disease) and conditions such as familial hypertriglyceridemia, metabolic syndrome, and type 2 diabetes. Therefore, targeting the reduction of APOC3 expression or blocking its protein function offers a therapeutic avenue for hypertriglyceridemia and mitigating cardiovascular disease risk [9].
B6-hPCSK9/TG-hAPOC3 mice are humanized models generated by crossing B6-hPCSK9 mice (Catalog No.: C001617) with TG-hAPOC3 mice (Catalog No.: C001588), enabling systemic expression of human PCSK9 and ApoC-Ⅲ proteins. This model is suitable for developing drugs targeting human APOC3/PCSK9, such as small interfering RNA (siRNA) and antisense oligonucleotides (ASO), for treating hypertriglyceridemia and other metabolic disorders, as well as for research on neurodegenerative diseases, tumorigenesis, and autoimmune diseases.
Ighj-KO(BALB/c)
製品ID :
C001345
系統:
BALB/cAnCya
状況:
説明:
Immunoglobulins recognize foreign antigens and initiate immune responses such as phagocytosis and the complement system. Each immunoglobulin molecule consists of two identical heavy chains and two identical light chains. The immunoglobulin heavy locus, also known as IGH, is a region that contains a gene for the heavy chains of human antibodies (or immunoglobulins). This locus includes V (variable), D (diversity), J (joining), and C (constant) segments. During B-cell development, a recombination event at the DNA level joins a single D segment with a J segment; the fused D-J exon of this partially rearranged D-J region is then joined to a V segment. The rearranged V-D-J region containing a fused V-D-J exon is then transcribed and fused at the RNA level to the IGHM constant region; this transcript encodes a mu-heavy chain. Later in development B cells generate V-D-J-Cmu-Cdelta pre-messenger RNA, which is alternatively spliced to encode either a mu or a delta-heavy chain. Mature B cells in the lymph nodes undergo switch recombination so that the fused V-D-J gene segment is brought in proximity to one of the IGHG, IGHA, or IGHE gene segments, and each cell expresses either the gamma, alpha, or epsilon heavy chain.
This strain is an Ighj-deletion model. In the homozygous Ighj-KO(BALB/c) mice, the J-segment of the Ig heavy chain locus is completely deleted, resulting in the inability of the cell to produce a recombinant version of the complete heavy chain variable region. The B cells of Ighj-KO(BALB/c) mice have undergone dramatic changes in the developmental process and cell number, which can be used as an animal model of B cell immune deficiency. Ighj-KO(BALB/c) mice retain other immune cells except for B cells, so the presence of other immune cells can be detected in Ighj-KO(BALB/c) mice.
Immunoglobulins recognize foreign antigens and initiate immune responses such as phagocytosis and the complement system. Each immunoglobulin molecule consists of two identical heavy chains and two identical light chains. The immunoglobulin heavy locus, also known as IGH, is a region that contains a gene for the heavy chains of human antibodies (or immunoglobulins). This locus includes V (variable), D (diversity), J (joining), and C (constant) segments. During B-cell development, a recombination event at the DNA level joins a single D segment with a J segment; the fused D-J exon of this partially rearranged D-J region is then joined to a V segment. The rearranged V-D-J region containing a fused V-D-J exon is then transcribed and fused at the RNA level to the IGHM constant region; this transcript encodes a mu-heavy chain. Later in development B cells generate V-D-J-Cmu-Cdelta pre-messenger RNA, which is alternatively spliced to encode either a mu or a delta-heavy chain. Mature B cells in the lymph nodes undergo switch recombination so that the fused V-D-J gene segment is brought in proximity to one of the IGHG, IGHA, or IGHE gene segments, and each cell expresses either the gamma, alpha, or epsilon heavy chain.
This strain is an Ighj-deletion model. In the homozygous Ighj-KO(BALB/c) mice, the J-segment of the Ig heavy chain locus is completely deleted, resulting in the inability of the cell to produce a recombinant version of the complete heavy chain variable region. The B cells of Ighj-KO(BALB/c) mice have undergone dramatic changes in the developmental process and cell number, which can be used as an animal model of B cell immune deficiency. Ighj-KO(BALB/c) mice retain other immune cells except for B cells, so the presence of other immune cells can be detected in Ighj-KO(BALB/c) mice.
Nt5m-flox
製品ID :
S-CKO-00345
系統:
C57BL/6JCya
状況:
説明:
Nt5m is located on chromosome 11 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Nt5m conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Nt5m is located on chromosome 11 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Nt5m conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.
Zfp120-KO
製品ID :
S-KO-00345
系統:
C57BL/6JCya
状況:
説明:
Zfp120 is located on chromosome 2 of mice. Nuclease Technology will be used to design sgRNA; Zfp120 knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Zfp120 is located on chromosome 2 of mice. Nuclease Technology will be used to design sgRNA; Zfp120 knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Gm19345-KO
製品ID :
S-KO-00113
系統:
C57BL/6JCya
状況:
説明:
Gm19345 is located on chromosome 7 of mice. Nuclease Technology will be used to design sgRNA; Gm19345 knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.
Gm19345 is located on chromosome 7 of mice. Nuclease Technology will be used to design sgRNA; Gm19345 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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