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The Reference Genetic Linkage Map for the Multinational Brassica rapa Genome Sequencing Project
Yong Pyo Lim,Su Ryun Choi,Graham R. Teakle,Prikshit Plaha,Jeong Hee Kim,Charlotte J. Allender,Elena Beynon,Zhong Yun. Piao,Tae Ho Han,Graham J. King,Guy C. Barker,Paul Hand Hand,Derek J. Lydiate,Jacqu 한국원예학회 2006 한국원예학회 기타간행물 Vol.- No.-
Association of a functional variant downstream of TNFAIP3 with systemic lupus erythematosus
Adrianto, Indra,Wen, Feng,Templeton, Amanda,Wiley, Graham,King, Jarrod B,Lessard, Christopher J,Bates, Jared S,Hu, Yanqing,Kelly, Jennifer A,Kaufman, Kenneth M,Guthridge, Joel M,Alarc처n-Riquelme, Mart Nature Publishing Group, a division of Macmillan P 2011 Nature genetics Vol.43 No.3
Systemic lupus erythematosus (SLE, MIM152700) is an autoimmune disease characterized by self-reactive antibodies resulting in systemic inflammation and organ failure. TNFAIP3, encoding the ubiquitin-modifying enzyme A20, is an established susceptibility locus for SLE. By fine mapping and genomic re-sequencing in ethnically diverse populations, we fully characterized the TNFAIP3 risk haplotype and identified a TT>A polymorphic dinucleotide (deletion T followed by a T to A transversion) associated with SLE in subjects of European (P = 1.58 ? 10<SUP>??8</SUP>, odds ratio = 1.70) and Korean (P = 8.33 ? 10<SUP>??10</SUP>, odds ratio = 2.54) ancestry. This variant, located in a region of high conservation and regulatory potential, bound a nuclear protein complex composed of NF-觀B subunits with reduced avidity. Further, compared with the non-risk haplotype, the haplotype carrying this variant resulted in reduced TNFAIP3 mRNA and A20 protein expression. These results establish this TT>A variant as the most likely functional polymorphism responsible for the association between TNFAIP3 and SLE.
Affinity for self antigen selects T<sub>reg</sub> cells with distinct functional properties
Wyss, Lena,Stadinski, Brian D,King, Carolyn G,Schallenberg, Sonja,McCarthy, Nicholas I,Lee, Jun Young,Kretschmer, Karsten,Terracciano, Luigi M,Anderson, Graham,Surh, Charles D,Huseby, Eric S,Palmer, E Nature Publishing Group, a division of Macmillan P 2016 NATURE IMMUNOLOGY Vol.17 No.9
<P>The manner in which regulatory T cells (T-reg cells) control lymphocyte homeostasis is not fully understood. We identified two T-reg cell populations with differing degrees of self-reactivity and distinct regulatory functions. We found that GITR(hi)PD-1(hi)CD25(hi) (Triple(hi)) T-reg cells were highly self-reactive and controlled lympho-proliferation in peripheral lymph nodes. GITR(lo)PD-1(lo)CD25(lo) (Triple(lo)) T-reg cells were less self-reactive and limited the development of colitis by promoting the conversion of CD4(+) T-conv cells into induced T-reg cells (iT(reg) cells). Although Foxp3-deficient (Scurfy) mice lacked T-reg cells, they contained Triple(hi)-like and Triple(lo)-like CD4(+) T cells with distinct pathological properties. Scurfy Triple(hi)CD4(+) T cells infiltrated the skin, whereas Scurfy. Triple(lo)CD4(+) T cells induced colitis and wasting disease. These findings indicate that the affinity of the T cell antigen receptor for self antigen drives the differentiation of T-reg cells into distinct subsets with non-overlapping regulatory activities.</P>