期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
卷 1863, 期 11, 页码 2681-2689出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2016.08.011
关键词
Caveolin-2; Homo-oligomerization; A-type lamin; Inner nuclear membrane microdomain; Epigenetic regulators
资金
- National Research Foundation of Korea (NRF) grants - Ministry of Science, ICT & Future Planning [NRF-2011-0014898]
- Ministry of Education (ME) [NRF-2015R1D1A3A01016537, NRF-2012R1A1A2041550, NRF-2015R1D1A4A01017437, NRF-2015R1A6A3A01016424]
- National R&D Program for Cancer Control, Ministry of Health and Welfare, Republic of Korea [1631090]
- Rural Development Administration of Korea (SSAC) [PJ01137901]
- Development Fund Foundation
- Gyeongsang National University
- Global Ph.D. Fellowship Program [NRF-2013H1A2A1034489]
- Graduate Research Fellowship from Gyeongsang National University
- BK21 Plus Program
- Korea Health Promotion Institute [1631090] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Association of Caveolin-2 in the inner nuclear membrane specifically with A-type lamin is crucial for the maintenance of its Tyr-19 phosphorylation to promote insulin-response epigenetic activation at the nuclear periphery. Here, we identify that pY19-Caveolin-2 in the inner nuclear membrane exists as homo-oligomeric forms and the A-type lamin is required for sustenance of its oligomeric status. Oligomerization-defective and hence pY19-dephosphorylated monomeric Caveolin-2 in the inner nuclear membrane is unable to carry out Caveolin-2-mediated epigenetic activation of Egr-1 and JunB genes and transactivation of Elk-1 and STAT3 in response to insulin. The homo-oligomeric pY19-Caveolin-2 localizes in and recruits epigenetic modifiers to the A -type lamin-enriched inner nuclear membrane microdomain for the epigenetic activation. Our data show that A -type lamin-dependent Caveolin-2 homo-oligomerization in the inner nuclear membrane microdomain is a precondition for pY19-Caveolin-2-mediated insulin-response epigenetic activation at the nuclear periphery. (C) 2016 Elsevier B.V. All rights reserved.
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