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Sep 22
Prof. Zhongjun Zhou's scientific report
Auditorium, A109, Haike Rd. Campus

Time and Date:1:30 PM, Sept. 22, 2014
Location:Auditorium, A109, Haike Rd. Campus
Reporter:Prof. Zhou, Zhongjun(周中军)
                    The University of Hong Kong
Title:  Nuclear matrix in chromatin remodeling, DNA repair and aging

Host:Ming Lei, Researcher

Welcome to attend!


Nuclear Matrix (NM) is composed of nuclear lamins and their interacting proteins. It exists not only under the nuclear envelop but also throughout the nucleoplasm. NM is required for the integrity of nuclear function and mutations in lamins have significant impacts on the maintenance of nuclear homeostasis which in turn compromises various biological activities in the nucleus. The LMNA gene mutations result in several diseases affecting skeletal muscles, fat, heart and neurons. Specific mutation in LMNA gene gives rise to premature aging called Hutchinson-Gilford Progeria Syndrome (HGPS). The diverse symptoms caused by a single gene suggested that the phenotypes observed in patients with different LMNA mutation are likely caused by lamin A interacting proteins. We have been investigating how specific mutation of LMNA gene could accelerate aging processes. Using genetically modified mice and human HGPS cells, we found that progeroid mutations in LMNA gene specifically compromised the functions of several epigenetic regulators including MOF, SIRT1/6 and SUV49H1, resulting in defective chromatin remodeling and genomic maintenance, leading to accelerated aging. The progeroid phenotypes could be significantly ameliorated through modulating these epigenetic alterations, providing a therapeutic intervention to HGPS and potentially age-related diseases. 

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