Logo
홈페이지
모델 살펴보기
장바구니
연락처
구독하기
연구 모델
HUGO Series 🌟
HUGO-GT™(유전자 치료를 위한 인간화 게놈 Ortholog)
HUGO-Ab™(항체 개발을 위한 인간화 게놈 Ortholog)
MouseAtlas 모델 라이브러리
번개 세일
연구용 동물 모델
Cre 마우스
인간화 타겟 유전자 모델
대사 질환 모델
안과 질환 모델
신경질환 모델
자가면역 질환 모델
면역결핍 마우스 모델
인간화 면역계 마우스 모델
종양 및 면역 항암 모델
Covid-19 마우스 모델
세포주 모델
Knockout 세포주 제품 카탈로그
종양 세포주 제품 카탈로그
유도만능줄기세포(iPSC) 카탈로그
AAV 표준 제품 카탈로그
서비스
전임상 효능 평가
신경과학
알츠하이머병(AD)
혈액-뇌 장벽(BBB)
파킨슨병(PD)
헌팅턴병(HD)
안과학
녹내장
연령관련 황반변성(AMD)
종양학
PBMC 인간화 마우스 모델
면역항암 연구를 위한 인간 면역 시스템(HIS) 마우스
대사 및 심혈관 질환
자가면역 및 염증
유전자 변형 동물
Knockout 마우스
Transgenic 마우스
Knock-in 마우스
Knockout Rat
Knock-in(KI) Rat
Transgenic Rat
모델 제작 기술
Turboknockout™ 유전자 타겟팅
타겟 유전자 편집
일반 Transgenic
PiggyBac Transgenesis
BAC Transgenic
ES 세포 유전자 타겟팅
브리딩 및 지원 서비스
브리딩 서비스
동결 보존 및 복원
Phenotyping 서비스
BAC 변형 서비스
바이러스 패키징
AAV 패키징
렌티바이러스(Lentivirus) 패키징
아데노바이러스(Adenovirus ) 패키징
맞춤형 세포주 서비스
유도만능줄기세포(iPSCs)
Knockout(KO) 세포주
Knock-in(KI) 세포주
Point Mutation 세포주
과발현 세포주
모달리티
유전자 치료
AI 기반 AAV 발굴
Oligonucleotide 치료
세포 면역치료
Resource
프로모션
이벤트 및 웨비나
뉴스
블로그 및 인사이트
자료실
참고 데이터베이스
Peer-Reviewed 인용
희귀질환 데이터센터
AbSeek
Cell iGeneEditor™ System
OriCell 세포 배양
회사 소개
회사 소개
시설 개요
동물 건강 및 복지
건강 보고서
대리점
인재채용
문의하기
Login
필터
필터
KO/cKO Mouse Models
Flash Sales
HUGO-GT™ Platform
Full-Gene Humanized Models
Humanized Target Gene Models
Immune Target Humanized ModelsTumor Target Humanized ModelsMetabolic Target Humanized ModelsCytokine Humanized ModelsOther Target Humanized Models
Immune System Mouse Models
Immunodeficient Mouse ModelsHumanized Immune System Models
Genetic Tool Mouse Models
Cre Driver LinesReporter Mouse LinesOther Genetic Tool Lines
Specialized Disease Models
Ophthalmic Disease ModelsNeurological Disease ModelsMetabolic Disease ModelsOncology & Immuno-oncology ModelsAutoimmune Disease ModelsRare Disease ModelsInfectious Disease ModelsOther Disease Models
“345” 에 대한 검색 결과 6 건
필터
정렬 기준:
알파벳순 (A-Z)
베스트셀러
TG-hAPOC3
제품 ID:
C001588
계통(Strain):
C57BL/6NCya
상태:
Live Mouse
설명:
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
제품 ID:
C001744
계통(Strain):
C57BL/6NCya
상태:
Live Mouse
설명:
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)
제품 ID:
C001345
계통(Strain):
BALB/cAnCya
상태:
Live Mouse
설명:
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
제품 ID:
S-CKO-00345
계통(Strain):
C57BL/6JCya
상태:
Research and Development
설명:
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
제품 ID:
S-KO-00345
계통(Strain):
C57BL/6JCya
상태:
Research and Development
설명:
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
제품 ID:
S-KO-00113
계통(Strain):
C57BL/6JCya
상태:
Research and Development
설명:
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.
Items: 1 to 6 of 6
1
더보기
전체 필터
Strain Type
Mouse
Rat
Modification Type
Knockout
Conditional Knockout
Knockin
Point Mutation
Transgenic
Conditional Knockin
Others
Status
Live Mice
R&D
Frozen Sperm
Validation Data
Verified
In Progress
초기화
확인
모델 라이브러리
모델 라이브러리
리소스
리소스
동물 품질
동물 품질
고객 지원
고객 지원
주소:
2255 Martin Avenue, Suite E Santa Clara, CA 95050-2709, US
전화:
800-921-8930 (8-6pm PST)
+1408-963-0306 (lnt’l)
팩스:
408-969-0336
이메일:
[email protected]
연구 모델
HUGO-Ab™(항체 개발을 위한 인간화 게놈 Ortholog)HUGO-GT™(유전자 치료를 위한 인간화 게놈 Ortholog)MouseAtlas 모델 라이브러리연구용 동물 모델
서비스
신경과학안과학종양학대사 및 심혈관 질환자가면역 및 염증
회사 소개
회사 소개시설 개요동물 건강 및 복지건강 보고서대리점인재채용문의하기
소셜 미디어
면책 조항: Cyagen의 제품 및 서비스 가격과 제공 여부는 지역에 따라 다를 수 있습니다. 명표시된 가격은 특정 국가에만 적용됩니다. 자세한 내용은 Cyagen으로 문의해 주시기 바랍니다.
Copyright © 2025 Cyagen. All rights reserved.
개인정보 처리방침
사이트 맵
Cyagen 최신 소식 받아보기
연구 모델, CRO 서비스, 과학 자료 및 특별 혜택에 대한 최신 소식을 연구 니즈에 맞춰 이메일로 받아보세요.
성명
이메일
조직
관심 분야
주요 연구 분야