Báo cáo y học: "p53 tumor suppressor gene mutations in fibroblast-like synoviocytes from erosion synovium and non-erosion synovium in rheumatoid arthritis"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: p53 tumor suppressor gene mutations in fibroblast-like synoviocytes from erosion synovium and non-erosion synovium in rheumatoid arthritis. | Available online http content 7 1 R12 Research article p53 tumor suppressor gene mutations in fibroblast-like synoviocytes from erosion synovium and non-erosion synovium in rheumatoid arthritis Yuji Yamanishi1 2 David L Boyle2 Douglas R Green3 Edward C Keystone4 Alison Connor4 Susan Zollman4 and Gary S Firestein2 Department of Rheumatology Hiroshima City Hospital Hiroshima Japan 2Division of Rheumatology Allergy and Immunology School of Medicine University of California at San Diego La Jolla California USA 3La Jolla Institute of Allergy and Immunology La Jolla California USA department of Medicine University of Toronto Canada Corresponding author Gary S Firestein gfirestein@ Received 9 May 2004 Revisions requested 8 Jun 2004 Revisions received 9 Aug 2004 Accepted 8 Sep 2004 Published 29 Oct 2004 Arthritis Res Ther 2005 7 R12-R1 8 DOI ar1448 2004 Yamanishi et al. licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is cited. Open Access Abstract Abnormalities in the p53 tumor suppressor gene have been detected in rheumatoid arthritis RA and could contribute to the pathogenesis of chronic disease. To determine whether synoviocytes from invasive synovium in RA have an increased number of mutations compared with non-erosion synoviocytes p53 cDNA subclones from fibroblast-like synoviocytes FLS derived from erosion and non-erosion sites of the same synovium were examined in patients requiring total joint replacement. Ten erosion FLS lines and nine non-erosion FLS lines were established from nine patients with RA. Exons 5-10 from 209 p53 subclones were sequenced 114 from erosion FLS 95 from non-erosion FLS . Sixty percent of RA FLS cell lines and of the p53 subclones isolated from FLS contained p53 mutations. No

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