标识符 | 资源中文名称 | 资源英文名称 | 疾病概述 | 制作方法 | 相关文章 |
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CSTR:16397.09.0G01000579 | Man2c1基因沉默小鼠 | B6.U6-hMan2c1SiRNA-GC/ILAS | 利用u6启动子系统表达人Man2c1基因SiRNA的转基因小鼠可以抑制Man2c1的表达60%,是研究Man2c1基因与免疫调节机制的小鼠模型。 |
pXSN-U6-man2c1-3 RNAi-3靶点GGGTAGAAATGGATGGGAACC pSilencer-U6-man2c1-3 RNAi-4靶点GTTTGACCAAAGAAGGCGAAA pSilencer-U6-man2c1-4 |
1. Li B, Wang ZZ, Ma FR, et al. Cloning expression and characterization of a cDNA (6A8) encoding a new human a-mannosidase. Europ J Biochem, 2000, 267:7176-7182 2. 岳玮,史耕先, 王壮志等 转导反向6A8α-甘露糖苷酶cDNA 对抗Fas 抗体诱导J urkat 细胞凋亡的影响.基础医学与临床,2001,21(2):136-140 3. 曲莉 向志光 史耕先 等6A8α2甘露糖苷酶表达抑制使Jurkat细胞间的黏附性增强[J]。中华微生物学和免疫学杂志,2004,24(6):456-461 4.Jun Diao, Erin Winter, Wenhao Chen, Characterization of Distinct Conventional and Plasmacytoid Dendritic Cell-Committed Precursors in Murine Bone Marrow . The Journal of Immunology 2004, 1826-1833 5. Moremen KW. Golgi α-mannosidase II deficiency in vertebrate systems: implications for asparagine-linked oligosaccharide processing in mammals . Biochim Biophys Acta, 2002, 1573: 225-235. |
CSTR:16397.09.0G01000577 | 全身性表达hMan2c1转基因小鼠 | B6.Tg(CMV-h-Man2c1)-GC/ILAS | 免疫相关 |
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1. Li B, Wang ZZ, Ma FR, et al. Cloning expression and characterization of a cDNA (6A8) encoding a new human a-mannosidase. Europ J Biochem, 2000, 267:7176-7182 2. 岳玮,史耕先, 王壮志等 转导反向6A8α-甘露糖苷酶cDNA 对抗Fas 抗体诱导J urkat 细胞凋亡的影响.基础医学与临床,2001,21(2):136-140 3. 曲莉 向志光 史耕先 等6A8α2甘露糖苷酶表达抑制使Jurkat细胞间的黏附性增强[J]。中华微生物学和免疫学杂志,2004,24(6):456-461 4. Jun Diao, Erin Winter, Wenhao Chen, Characterization of Distinct Conventional and Plasmacytoid Dendritic Cell-Committed Precursors in Murine Bone Marrow . The Journal of Immunology 2004, 1826-1833 5. Moremen KW. Golgi α-mannosidase II deficiency in vertebrate systems: implications for asparagine-linked oligosaccharide processing in mammals . Biochim Biophys Acta, 2002, 1573: 225-235. |
CSTR:16397.09.0G01000573 | Trim32基因敲除小鼠 | B6.Trim32(tm) | TRIM32 基因坐落在染色体9q33.1,编码653氨基酸,分子量72 kD的蛋白质,N-末端局具有一个C3HC4锌指结构,TRIM32是活化Tat蛋白的重要因子,和HIV病毒的复制感染相关。TRIM32基因剔除小鼠不仅是研究该基因功能的重要模型,也是研究HIV和宿主相互作用的动物模型。 |
基因敲除 |
1. Chiang, A. P. Beck, J. S. Yen, H.-J. eat la. Homozygosity mapping with SNP arrays identifies TRIM32, an E3 ubiquitin ligase, as a Bardet-Biedl syndrome gene (BBS11). Proc. Nat. Acad. Sci. 103: 6287-6292, 2006. 2. Fridell, R. A. Harding, L. S. Bogerd, H. P. Cullen, B. R. Identification of a novel human zinc finger protein that specifically interacts with the activation domain of lentiviral Tat proteins. Virology 209: 347-357, 1995. 3. Frosk, P. Del Bigio, M. R. Wrogemann, K. Greenberg, C. R. Hutterite brothers both affected with two forms of limb girdle muscular dystrophy: LGMD2H and LGMD2I. Europ. J. Hum. Genet. 13: 978-982, 2005. 4. Frosk, P. Weiler, T. Nylen, E. Et al. Limb-girdle muscular dystrophy type 2H associated with mutation in TRIM32, a putative E3-ubiquitin-ligase gene. Am. J. Hum. Genet. 70: 663-672, 2002. 5. Jerusalem, F. Engel, A. G. Gomez, M. R. : Sarcotubular myopathy. Neurology 23: 897-906, 1973. |
CSTR:16397.09.0G01000571 | Rag2基因敲除小鼠 | B6.Rag2(tm) | 免疫缺陷动物模型 |
敲除第三外显子 |
1. Adams, J. Kelso, R. Cooley, L. The kelch repeat superfamily of proteins: propellers of cell function. Trends Cell Biol. 10: 17-24, 2000. 2. Callebaut, I. Mornon, J.-P. The V(D)J recombination activating protein RAG2 consists of a six-bladed propeller and a PHD fingerlike domain, as revealed by sequence analysis. Cell. Molec. Life Sci. 54: 880-891, 1998. 3. Corneo, B. Moshous, D. Gungor, T. et al. Identical mutations in RAG1 or RAG2 genes leading to defective V(D)J recombinase activity can cause either T-B-severe combined immune deficiency or Omenn syndrome. Blood 97: 2772-2776, 2001. 4. Corneo, B. Wendland, R. L. Deriano, L. et al. Rag mutations reveal robust alternative end joining. Nature 449: 483-486, 2007. 5. Hikida, M. Mori, M. Takai, T. Tomochika, K. et al. Reexpression of RAG-1 and RAG-2 genes in activated mature mouse B cells. Science 274: 2091-2093, 1996. |
CSTR:16397.09.0F02000606 | CYP3A-A9基因敲除大鼠 | SD.CYP3A9(tm)-GC/ILAS | 药物代谢 |
该模型利用CRISPR/Cas9技术构建完成,此品系为polypeptide 9单独被敲除。 |
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CSTR:16397.09.0F02000605 | CYP3A-A9-A62基因敲除大鼠 | SD.Cyp3A(a9-a62)(tm)-GC/ILAS | 药物代谢 |
该模型利用CRISPR/Cas9技术构建完成。 |
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CSTR:16397.09.0F02000604 | CYP3A-A1-A2基因敲除大鼠 | SD.Cyp3A(a1-a2)(tm)-GC/ILAS | 药物代谢 |
该模型利用CRISPR/Cas9技术构建完成。 |
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CSTR:16397.09.0F02000603 | CYP3A-A1-A18基因敲除大鼠 | SD.Cyp3A(a1-a18)-22(tm)-GC/ILAS | 药物代谢相关 |
该模型利用CRISPR/Cas9技术构建完成 |
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CSTR:16397.09.0F02000602 | CYP3A-A1-A18基因敲除大鼠 | SD.Cyp3A(a1-a18)-2(tm)-GC/ILAS | 药物代谢相关 |
该模型利用CRISPR/Cas9技术构建完成 |
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CSTR:16397.09.0F02000601 | CYP3A-A1/A2基因敲除大鼠 | SD.CYP3A(a1/a2) (tm)-GC/ILAS | 药物代谢 |
该模型利用CRISPR/Cas9技术构建完成。 |
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CSTR:16397.09.0F02000600 | AHR基因敲除大鼠 | SD.Ahr(tm)-GC/ILAS | 药物代谢研究 |
该模型利用CRISPR/Cas9技术构建完成 |
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CSTR:16397.09.0F02000598 | UCP1基因敲除大鼠 | SD.UCP1(tm)-GC/ILAS | 代谢病 |
该模型利用CRISPR/Cas9技术构建完成。 |