A mutation in Orai1 causes immune deficiency by abrogating CRAC channel function

著录项

• 来源
  《Nature》 |2006年第7090期|p. 179-185|共7页
• 作者

  Feske S; Gwack Y; Prakriya M; Srikanth S; Puppel SH; Tanasa B; Hogan PG; Lewis RS; Daly M; Rao A;

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• 作者单位

  Harvard Univ, Sch Med, Ctr Blood Res, Inst Biomed Res, Boston, MA 02115 USA;

  Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA;

  Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA;

  Northwestern Univ, Feinberg Sch Med, Dept Biol Chem & Mol Pharmacol, Chicago, IL 60611 USA;

  Stanford Univ, Sch Med, Dept Cellular & Mol Physiol, Stanford, CA 94305 USA;

  Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA;

  Harvard Univ, Broad Inst, Cambridge, MA 02139 USA;

  MIT, Broad Inst, Cambridge, MA 02139 USA;

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• 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
• 原文格式 PDF
• 正文语种 eng
• 中图分类 自然科学总论;
• 关键词

  T-CELL-RECEPTOR; SEVERE COMBINED IMMUNODEFICIENCY; ANHIDROTIC ECTODERMAL DYSPLASIA; ACTIVATED CALCIUM-CHANNEL; KAPPA-B; LINKAGE ANALYSIS; PORE PROPERTIES; NUCLEAR FACTOR; CA2+ CHANNELS; I-CRAC;

  机译：T细胞受体;重度联合免疫缺陷;无性皮细胞增生异常;活化钙离子通道;Kappa-B;连锁分析;孔性能;核因子;CA2 +通道;I-CRAC;