Báo cáo y học: "The tandem CCCH zinc finger protein tristetraprolin and its relevance to cytokine mRNA turnover and 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: The tandem CCCH zinc finger protein tristetraprolin and its relevance to cytokine mRNA turnover and arthritis. | Arthritis Research Therapy Vol 6 No 6 Carrick et al. Review The tandem CCCH zinc finger protein tristetraprolin and its relevance to cytokine mRNA turnover and arthritis Danielle M Carrick1 Wi S Lai2 and Perry J Blackshear1 2 3 Office of Clinical Research National Institute of Environmental Health Sciences Research Triangle Park North Carolina USA 2Laboratory of Neurobiology National Institute of Environmental Health Sciences Research Triangle Park North Carolina USA 3Departments of Medicine and Biochemistry Duke University Medical Center Durham North Carolina USA Corresponding author Perry J Blackshear black009@ Published 8 October 2004 Arthritis Res Ther 2004 6 248-264 DOI ar1441 2004 BioMed Central Ltd Abstract Tristetraprolin TTP is the best-studied member of a small family of three proteins in humans that is characterized by a tandem CCCH zinc finger TZF domain with highly conserved sequences and spacing. Although initially discovered as a gene that could be induced rapidly and transiently by the stimulation of fibroblasts with growth factors and mitogens it is now known that TTP can bind to AUrich elements in mRNA leading to the removal of the poly A tail from that mRNA and increased rates of mRNA turnover. This activity was discovered after TTP-deficient mice were created and found to have a systemic inflammatory syndrome with severe polyarticular arthritis and autoimmunity as well as medullary and extramedullary myeloid hyperplasia. The syndrome seemed to be due predominantly to excess circulating tumor necrosis factor-a TNF-a resulting from the increased stability of the TNF-a mRNA and subsequent higher rates of secretion of the cytokine. The myeloid hyperplasia might be due in part to increased stability of granulocyte-macrophage colony-stimulating factor GM-CSF . This review highlights briefly the characteristics of the TTP-deficiency syndrome in mice and its possible genetic modifiers as well as recent data on the characteristics of

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