Ultima Vez Modificado: 20 de marzo del 2008
Conference Dates: Thursday, May 29, 2008
Conference Location: Boston, Massachusetts
Sponsoring Group: Abcam, Inc.
Conference Web Page URL: http://www.abcam.com/dnadamage08
Topics Covered: - Higher order chromatin structures and double strand break repair. - Chromatin remodeling complexes implicated in the repair of DNA breaks. - Chromatin structure adjacent to DNA double strand breaks. - The role of histones and histone modifications in DNA damage signaling, including key modifications such as H2AX phosphorylation, histone methylation and histone ubiquitination. - Formation of DNA repair complexes at DNA double strand breaks.
Conference Objectives: The 2008 "Cellular Responses to DNA Damage" Symposium will explore the links between chromatin dynamics, histone modification and the repair of DNA double strand breaks. The compact nature of chromatin presents a significant barrier to DNA-dependent transactions, including gene transcription and DNA replication. Access to specific regions of chromatin is regulated at multiple levels, including remodeling of chromatin structure, local deposition of specific histone variants, post-translational modification of histones and the recruitment of specific proteins to these modified histones. The ability of cells to detect and repair DNA double strand breaks appears to be dependent on many of these same regulatory processes. By bringing together a diverse array of experts from the fields of chromatin structure, histone modification, chromatin remodeling and DNA double-strand break repair, this symposium aims to highlight the critical role of histones and chromatin structure in the detection and repair of DNA double strand breaks.
Who Should Attend: Those looking to learn, present, and improve their research ideas within the scientific community
Conference Fees: $115 ($35 student and postdocs) Includes lunch, wine reception, and coffee breaks.
Continuing Education: No
Nov 6, 2012 - The mitogen-activated protein kinase p90 ribosomal S6 kinase appears to play a role in the poor response of melanoma cells to DNA-damaging agents, according to research published online Oct. 29 in Oncogene.
Nov 6, 2012
Dec 22, 2014
Dec 22, 2014