tailieunhanh - Báo cáo y học: "SCN-AVP release of mPer1/mPer2 double-mutant mice in vitro"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: SCN-AVP release of mPer1/mPer2 double-mutant mice in vitro. | Journal of Circadian Rhythms BioMed Central Research Open Access SCN-AVP release of mPerllmPer2 double-mutant mice in vitro Daan Rvan der Veen 1 3 Ellis GA Mulder1 Henrik Oster2 Menno P Gerkema1 and Roelof A Hut1 Address Department of Chronobiology University of Groningen . Box 14 9750 AA Haren The Netherlands 2Circadian Rhythms Group Max Planck Institute of Biophysical Chemistry Am Fassberg 11 37077 Gottingen Germany and 3University of Surrey Faculty of Health and Medical Sciences Guildford Surrey GU2 7XH UK Email Daan R van der Veen - Ellis GA Mulder - Henrik Oster - Menno P Gerkema - Roelof A Hut - Corresponding author Published 20 March 2008 Received 27 December 2007 Accepted 20 March 2008 Journal of Circadian Rhythms 2008 6 5 doi 1740-3391-6-5 This article is available from http content 6 1 5 2008 van der Veen 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 Circadian organisation of behavioural and physiological rhythms in mammals is largely driven by the clock in the suprachiasmatic nuclei SCN of the hypothalamus. In this clock a molecular transcriptional repression and activation mechanism generates near 24 hour rhythms. One of the outputs of the molecular clock in specific SCN neurons is arginine-vasopressin AVP which is responsive to transcriptional activation by clock gene products. As negative regulators the protein products of the period genes are thought to repress transcriptional activity of the positive limb after heterodimerisation with CRYPTOCHROME. When both the Perl and Per2 genes are dysfunctional by targeted deletion of the PAS heterodimer .