运动失调性毛细血管扩张症

干细胞打靶

肿瘤

利用CRISPR/Cas9技术构建完成

乙肝

1．Ganem D，Prince AM. Hepatitis B virus infection – natural history and clinical consequence. N Engl J Med 2004;350;1118-1129 2．EE, Matzke B. High-level hepatitis B virus replication in transgenic miceJ Virol. 1995 Oct;69(10):6158-69 3．Moriyama T, Guilhot S. Immunobiology and pathogenesis of hepatocellular injury in hepatitis B virus transgenic mice. Science. 1990 Apr 20;248(4953):361-4. 4．Kakimi K, Guidotti LG,Natural killer T cell activation inhibits hepatitis B virus replication in vivo. J Exp Med. 2000 Oct 2;192(7):921-30 5．Chisari FV, Pinkert CA A transgenic mouse model of the chronic hepatitis B surfa ceantigencarrier state. Science. 1985Dec6;230 (4730):1157-60. 6．Chisari FV, Filippi P.Structural and pathological effects of synthesis of hepatitis B virus large envelope polypeptide in transgenic mice.Proc Natl Acad Sci U S A. 1987 Oct;84(19):6909-13 7．Tateno C, Yoshizane Y. Near completely humanized liver in mice shows human-type metabolic responses to drugs. Am J Pathol. 2004 Sep;165(3):901-12. 8．Huang LR, Wu HL, An immunocompetent mouse model for the tolerance of human chronic hepatitis B virus infection. Proc Natl Acad Sci U S A. 2006 Nov

癌症相关

干细胞打靶

1. Bernards, R. Wip-ing out cancer. Nature Genet. 36: 319-320, 2004. 2. Bulavin, D. V. Demidov, O. N. Saito, S. et al. Amplification of PPM1D in human tumors abrogates p53 tumor-suppressor activity. Nature Genet. 31: 210-215, 2002. 3. Bulavin, D. V. Phillips, C. Nannenga, B. et al. Inactivation of the Wip1 phosphatase inhibits mammary tumorigenesis through p38 MAPK-mediated activation of the p16(Ink4a)-p19(Arf) pathway. Nature Genet. 36: 343-350, 2004. 4. Choi, J. Nannenga, B. Demidov, O. N.et al. Mice deficient for the wild-type p53-induced phosphatase gene (Wip1) exhibit defects in reproductive organs, immune function, and cell cycle control. Molec. Cell. Biol. 22: 1094-1105, 2002. 5. Fiscella, M. Zhang, H. Fan, S. et al. Wip1, a novel human protein phosphatase that is induced in response to ionizing radiation in a p53-dependent manner. Proc. Nat. Acad. Sci. 94:

癌症相关

干细胞打靶

代谢相关疾病模型

该模型利用CRISPR/Cas9技术构建完成。

免疫相关疾病模型

干细胞打靶

Mombaerts P; Iacomini J; Johnson RS; Herrup K; Tonegawa S; Papaioannou VE. 1992. RAG-1-deficient mice have no mature B and T lymphocytes. Cell 68(5):869-77PubMed: 1547488MGI: J:1934

免疫相关疾病模型

干细胞打靶

Kitamura D; Roes J; Kuhn R; Rajewsky K. 1991. A B cell-deficient mouse by targeted disruption of the membrane exon of the immunoglobulin mu chain gene. Nature 350(6317):423-6PubMed: 1901381MGI: J:70398

免疫相关疾病模型

干细胞打靶

Dalton DK, Pitts-Meek S, Keshav S, et al. Multiple defects of immune cell function in mice with disrupted interferon-gamma genes. Science 1993, Volume: 259 Issue: 5102; Pages: 1739-42

免疫相关疾病模型

1.Tominaga, S. A putative protein of a growth specific cDNA from BALB/c-3T3 cells is highly similar to the extracellular portion of mouse interleukin 1 receptor. FEBS Lett. 1989，258: 301-304 2.Rimal B, Greenberg AK, Rom WN. Basic pathogenetic mechanisms in silicosis: current understanding. Curr Opin Pulm Med. 2005, 11(2):169-173. Tominaga S, Yokota T, Yanagisawa K, et al. Nucleotide sequence of a complementary DNA for human ST2. Biochim. Biophys. Acta 1992, 1171: 215-218.

免疫相关疾病模型

基因敲除小鼠

1. Bonecchi, R.; Bianchi, G.; Bordignon, et al, Differential expression of chemokine receptors and chemotactic responsiveness of type 1 T helper cells (Th1s) and Th2s. J. Exp. Med. 187: 129-134, 1998. 2. Booth, V.; Keizer, D. W.; Kamphuis, M. B. et al, The CXCR3 binding chemokine IP-10/CXCL10: structure and receptor interactions. Biochemistry 41: 10418-10425, 2002. 3. Campbell, J. J.; Brightling, C. E.; Symon, F. A.; Qin, S.; Murphy, K. E.; Hodge, M.; Andrew, D. P.; Wu, L.; Butcher, E. C.; Wardlaw, A. J. , Expression of chemokine receptors by lung T cells from normal and asthmatic subjects. J. Immun. 166: 2842-2848, 2001.

代谢相关

转基因小鼠

1. Huh, G. S.; Boulanger, L. M.; Du, H.; Functional requirement for class I MHC in CNS development and plasticity. Science 290: 2155-2159, 2000. 2. Wani, M. A.; Haynes, L. D.; Kim, J.; et al.Familial hypercatabolic hypoproteinemia caused by deficiency of the neonatal Fc receptor, FcRn, due to a mutant beta-2-microglobulin gene. Proc. Nat. Acad. Sci. 103: 5084-5089, 2006.