tailieunhanh - Báo cáo y học: " Early The glucocorticoid RU24858 does not distinguish between transrepression and transactivation in primary human eosinophils"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Early The glucocorticoid RU24858 does not distinguish between transrepression and transactivation in primary human eosinophils. | BioMed Central Journal of Inflammation Open Access The glucocorticoid RU24858 does not distinguish between transrepression and transactivation in primary human eosinophils Mirkka Janka-Junttila1 Eeva Moilanen1 Hannele Hasala1 Xianzhi Zhang1 3 Ian Adcock2 and Hannu Kankaanranta 1 4 Address rhe Immunopharmacology Research Group Medical School FIN-33014 University of Tampere and Research Unit Tampere University Hospital Tampere Finland 2Department of Thoracic Medicine National Heart and Lung Institute Imperial College London UK 3The Center for Infection and Immunity Institute of Biophysics Chinese Academy of Sciences Beijing China and 4Department of Pulmonary Medicine Tampere University Hospital Tampere Finland Email Mirkka Janka-Junttila - Eeva Moilanen - Hannele Hasala - Xianzhi Zhang - Ian Adcock - Hannu Kankaanranta - Corresponding author Published 12 July 2006 Received 04 January 2006 Journal of Inflammation 2006 3 10 doi 1476-9255-3-10 Accepted 12 July 2006 This article is available from http content 3 1 10 2006 Janka-Junttila 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 properly cited. Abstract Background Glucocorticoids are used to treat chronic inflammatory diseases such as asthma. Induction of eosinophil apoptosis is considered to be one of the main mechanisms behind the anti-asthmatic effect of glucocorticoids. Glucocorticoid binding to its receptor GR can have a dual effect on gene transcription. Activated GR can activate transcription transactivation or by interacting with other transcription factors such as NF-kB suppress transcription .