免疫相关

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.

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.

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.

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。

药物代谢

该模型利用CRISPR/Cas9技术构建完成。

药物代谢

该模型利用CRISPR/Cas9技术构建完成。

药物代谢相关

该模型利用CRISPR/Cas9技术构建完成

药物代谢相关

该模型利用CRISPR/Cas9技术构建完成

药物代谢

该模型利用CRISPR/Cas9技术构建完成。

药物代谢研究

该模型利用CRISPR/Cas9技术构建完成

代谢病

该模型利用CRISPR/Cas9技术构建完成。

代谢病

该模型利用CRISPR/Cas9技术构建完成。