2018
DOI: 10.1111/acel.12824
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Abstract: Defects in stress response are main determinants of cellular senescence and organism aging. In fibroblasts from patients affected by Hutchinson–Gilford progeria, a severe LMNA‐linked syndrome associated with bone resorption, cardiovascular disorders, and premature aging, we found altered modulation of CDKN1A, encoding p21, upon oxidative stress induction, and accumulation of senescence markers during stress recovery. In this context, we unraveled a dynamic interaction of lamin A/C with HDAC2, an histone deacet… Show more

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Cited by 37 publications
(70 citation statements)
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“…BAG3 encodes a Z-discassociated protein that mediates selective macroautophagy and promotes cell survival through interaction with apoptosis regulator BCL2 35 . CDKN1A encodes p21, a potent cell cycle inhibitor that mediates post-natal cardiomyocyte cell cycle arrest 36 and is implicated in LMNA-mediated cellular stress responses 37 . KLHL3 is a negative regulator of the thiazidesensitive Na + Cl − cotransporter (SLC12A3) in the distal nephron; loss of function variants cause familial hyperkalaemic hypertension (FHHt) by increasing constitutive sodium and chloride resorption 38 .…”
Section: Prioritisation Of Putative Effector Genes By Expression Analmentioning
confidence: 99%
“…BAG3 encodes a Z-discassociated protein that mediates selective macroautophagy and promotes cell survival through interaction with apoptosis regulator BCL2 35 . CDKN1A encodes p21, a potent cell cycle inhibitor that mediates post-natal cardiomyocyte cell cycle arrest 36 and is implicated in LMNA-mediated cellular stress responses 37 . KLHL3 is a negative regulator of the thiazidesensitive Na + Cl − cotransporter (SLC12A3) in the distal nephron; loss of function variants cause familial hyperkalaemic hypertension (FHHt) by increasing constitutive sodium and chloride resorption 38 .…”
Section: Prioritisation Of Putative Effector Genes By Expression Analmentioning
confidence: 99%
“…In addition, the organization of the nuclear lamina affects the stability of the genome. A decrease in the amount of lamin B1, the accumulation of toxic levels of prelamin A and the expression of progerin (the pathogenic form of lamin A) lead to defects in the structure of the nucleus and are associated with cellular senescence and an organism aging [ 2 , 88 , 89 ]. Mutations in genes of a nuclear lamina cause premature aging syndromes called laminopathies (including Hutchinson–Gilford syndrome) [ 90 , 91 ].…”
Section: Impairment Of the Mechanisms For Maintaining Genome Stabimentioning
confidence: 99%
“…HA tagged PCAF in pCI expression vector was a gift from Dr. Melanie Ott, Gladstone Institute, UCSF, San Francisco, CA (USA). Flag tagged HDAC2 in pCMV10–3xFlag vector has been previously described [ 24 , 30 ]. Flag-HDAC2 construct was used as a template for QuickChange site-directed mutagenesis (Agilent Technologies, Milan, Italy) with primers carrying the indicated mutations.…”
Section: Methodsmentioning
confidence: 99%
“…We have previously demonstrated that lamin A/C binds HDAC2 in human fibroblasts [ 24 ]. While lamin A/C-HDAC2 interaction is not affected by the HDAC2 phosphorylation state, HDAC2 acetylation might regulate its binding to A type lamins, as suggested by the observation that HDAC inhibitors known to favor HDAC2 acetylation [ 4 ] were able to increase lamin A/C-HDAC2 binding [ 25 ].…”
Section: Introductionmentioning
confidence: 99%