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10.1038/cdd.2015.12 http://scihub22266oqcxt.onion/10.1038/cdd.2015.12 C4532777!4532777 !25744025     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25744025 &cmd=llinks): Failed to open stream: HTTP request failed! 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Nesprin-2-dependent ERK1/2 compartmentalisation regulates the DNA damage response in vascular smooth muscle cell ageing |pdf=|usr=}}{{25744025 }} gab.com Text Nesprin-2-dependent ERK1/2 compartmentalisation regulates the DNA damage response in vascular smooth muscle cell ageing JO: Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=25744025 #FOAvip Prelamin A accumulation and persistent DNA damage response (DDR) are hallmarks of vascular smooth muscle cell (VSMC) ageing and dysfunction. Although prelamin A is proposed to interfere with DNA repair, our understanding of the crosstalk between prelamin A and the repair process remains limited. The extracellular signal-regulated kinases 1 and 2 (ERK1/2) have emerged as key players in the DDR and are known to enhance ataxia telangiectasia-mutated protein (ATM) activity at DNA lesions, and in this study, we identified a novel relationship between prelamin A accumulation and ERK1/2 nuclear compartmentalisation during VSMC ageing. We show both prelamin A accumulation and increased DNA damage occur concomitantly, before VSMC replicative senescence, and induce the localisation of ERK1/2 to promyelocytic leukaemia protein nuclear bodies (PML NBs) at the sites of DNA damage via nesprin-2 and lamin A interactions. Importantly, VSMCs treated with DNA damaging agents also displayed prelamin A accumulation and ERK compartmentalisation at PML NBs, suggesting that prelamin A and nesprin-2 are novel components of the DDR. In support of this, disruption of ERK compartmentalisation at PML NBs, by either depletion of nesprin-2 or lamins A/C, resulted in the loss of ATM from DNA lesions. However, ATM signalling and DNA repair remained intact after lamins A/C depletion, whereas nesprin-2 disruption ablated downstream Chk2 activation and induced genomic instability. We conclude that lamins A/C and PML act as scaffolds to organise DNA-repair foci and compartmentalise nesprin-2/ERK signalling. However, nesprin-2/ERK signalling fidelity, but not their compartmentalisation at PML NBs, is essential for efficient DDR in VSMCs. Twit Text FOAVip Nesprin-2-dependent ERK1/2 compartmentalisation regulates the DNA damage response in vascular smooth muscle cell ageing ????Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=25744025 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25744025 #FOAvip English Wikipedia <ref>{{Cite pmid|25744025 }}</ref> Nesprin-2-dependent ERK1/2 compartmentalisation regulates the DNA damage response in vascular smooth muscle cell ageing #MMPMID25744025 Warren DT ; Tajsic T ; Porter LJ ; Minaisah RM ; Cobb A ; Jacob A ; Rajgor D ; Zhang QP ; Shanahan CM Cell Death Differ 2015[Sep]; 22 (9 ): 1540-50 PMID25744025 show ga Prelamin A accumulation and persistent DNA damage response (DDR) are hallmarks of vascular smooth muscle cell (VSMC) ageing and dysfunction. Although prelamin A is proposed to interfere with DNA repair, our understanding of the crosstalk between prelamin A and the repair process remains limited. The extracellular signal-regulated kinases 1 and 2 (ERK1/2) have emerged as key players in the DDR and are known to enhance ataxia telangiectasia-mutated protein (ATM) activity at DNA lesions, and in this study, we identified a novel relationship between prelamin A accumulation and ERK1/2 nuclear compartmentalisation during VSMC ageing. We show both prelamin A accumulation and increased DNA damage occur concomitantly, before VSMC replicative senescence, and induce the localisation of ERK1/2 to promyelocytic leukaemia protein nuclear bodies (PML NBs) at the sites of DNA damage via nesprin-2 and lamin A interactions. Importantly, VSMCs treated with DNA damaging agents also displayed prelamin A accumulation and ERK compartmentalisation at PML NBs, suggesting that prelamin A and nesprin-2 are novel components of the DDR. In support of this, disruption of ERK compartmentalisation at PML NBs, by either depletion of nesprin-2 or lamins A/C, resulted in the loss of ATM from DNA lesions. However, ATM signalling and DNA repair remained intact after lamins A/C depletion, whereas nesprin-2 disruption ablated downstream Chk2 activation and induced genomic instability. We conclude that lamins A/C and PML act as scaffolds to organise DNA-repair foci and compartmentalise nesprin-2/ERK signalling. However, nesprin-2/ERK signalling fidelity, but not their compartmentalisation at PML NBs, is essential for efficient DDR in VSMCs. |*DNA Damage [MESH] |Adult [MESH] |Cell Cycle/physiology [MESH] |Cellular Senescence/physiology [MESH] |DNA Repair [MESH] |Female [MESH] |Humans [MESH] |Intranuclear Inclusion Bodies/genetics/metabolism [MESH] |Lamin Type A/metabolism [MESH] |Male [MESH] |Microfilament Proteins/genetics/*metabolism [MESH] |Middle Aged [MESH] |Mitogen-Activated Protein Kinase 1/genetics/*metabolism [MESH] |Mitogen-Activated Protein Kinase 3/genetics/*metabolism [MESH] |Muscle, Smooth, Vascular/*cytology/enzymology/*metabolism [MESH] |Nerve Tissue Proteins/genetics/*metabolism [MESH] |Nuclear Proteins/genetics/*metabolism [MESH] |Transfection [MESH]Nesprin-2-dependent ERK1/2 compartmentalisation regulates the DNA dama(epmc).pdf DeepDyve Pubget Overpricing