scholarly article | Q13442814 |
P356 | DOI | 10.1089/REJ.2010.1088 |
P953 | full work available online at | https://www.liebertpub.com/doi/full-xml/10.1089/rej.2010.1088 |
https://www.liebertpub.com/doi/pdf/10.1089/rej.2010.1088 | ||
P698 | PubMed publication ID | 21208065 |
P5875 | ResearchGate publication ID | 49730567 |
P2093 | author name string | Ryan N. Serio | |
P2860 | cites work | Nuclear lamins: building blocks of nuclear architecture | Q22065781 |
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Regulation and mechanisms of mammalian double-strand break repair | Q22121978 | ||
Feedback between p21 and reactive oxygen production is necessary for cell senescence | Q24299631 | ||
Chk2 activates E2F-1 in response to DNA damage | Q24300634 | ||
Nucleosome assembly by a complex of CAF-1 and acetylated histones H3/H4 | Q24313176 | ||
Regulation of E2F1 function by the nuclear corepressor KAP1 | Q24337687 | ||
Lamin A/C binding protein LAP2alpha is required for nuclear anchorage of retinoblastoma protein | Q24541561 | ||
Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome | Q24562621 | ||
Lamin A-dependent misregulation of adult stem cells associated with accelerated ageing | Q24649634 | ||
Barrier-to-autointegration factor: major roles in chromatin decondensation and nuclear assembly | Q24671798 | ||
The Polycomb group proteins bind throughout the INK4A-ARF locus and are disassociated in senescent cells | Q24680814 | ||
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A pathway of double-strand break rejoining dependent upon ATM, Artemis, and proteins locating to gamma-H2AX foci. | Q27919669 | ||
Mechanisms of alternative pre-messenger RNA splicing | Q28131822 | ||
Recurrent de novo point mutations in lamin A cause Hutchinson–Gilford progeria syndrome | Q28201199 | ||
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Comparative analysis identifies exonic splicing regulatory sequences--The complex definition of enhancers and silencers | Q28247879 | ||
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Human laminopathies: nuclei gone genetically awry | Q28276671 | ||
Ageing-related chromatin defects through loss of the NURD complex | Q28750018 | ||
Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors | Q29614306 | ||
Obesity, cigarette smoking, and telomere length in women | Q29615467 | ||
Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence | Q29620428 | ||
Alterations in mitosis and cell cycle progression caused by a mutant lamin A known to accelerate human aging | Q30479111 | ||
Phosphorylation of nucleotide excision repair factor xeroderma pigmentosum group A by ataxia telangiectasia mutated and Rad3-related-dependent checkpoint pathway promotes cell survival in response to UV irradiation | Q33236676 | ||
Involvement of xeroderma pigmentosum group A (XPA) in progeria arising from defective maturation of prelamin A. | Q33298574 | ||
Genomic instability and DNA damage responses in progeria arising from defective maturation of prelamin A. | Q33511965 | ||
Chromatin modifications: the driving force of senescence and aging? | Q33588661 | ||
Aging and nuclear organization: lamins and progeria | Q33978333 | ||
Inhibiting farnesylation reverses the nuclear morphology defect in a HeLa cell model for Hutchinson-Gilford progeria syndrome | Q34063471 | ||
Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence | Q34124543 | ||
Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect. | Q34191451 | ||
Lamin a truncation in Hutchinson-Gilford progeria. | Q34191501 | ||
The spliceosome: the most complex macromolecular machine in the cell? | Q34278742 | ||
Progeria: a human-disease model of accelerated aging | Q34419908 | ||
Protein composition of human prespliceosomes isolated by a tobramycin affinity-selection method | Q34429680 | ||
Nuclear and chromatin reorganization during cell senescence and aging - a mini-review | Q34540621 | ||
Molecular bases of progeroid syndromes. | Q34567458 | ||
Combinatorial control of exon recognition. | Q34585102 | ||
Mutant nuclear lamin A leads to progressive alterations of epigenetic control in premature aging | Q34652089 | ||
Nucleoplasmic lamins and their interaction partners, LAP2alpha, Rb, and BAF, in transcriptional regulation. | Q34654052 | ||
Telomere length, stem cells and aging | Q34689235 | ||
Hutchinson-Gilford progeria syndrome, aging, and the nuclear lamina | Q34747138 | ||
ATM signaling facilitates repair of DNA double-strand breaks associated with heterochromatin | Q34801409 | ||
A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation. | Q34803249 | ||
The functions of E(Z)/EZH2-mediated methylation of lysine 27 in histone H3. | Q35804605 | ||
The highly conserved nuclear lamin Ig-fold binds to PCNA: its role in DNA replication | Q36562914 | ||
Retinoblastoma tumor suppressor protein-dependent methylation of histone H3 lysine 27 is associated with irreversible cell cycle exit | Q36639090 | ||
Replication fork stalling at natural impediments | Q36755308 | ||
Progerin elicits disease phenotypes of progeria in mice whether or not it is farnesylated. | Q36852109 | ||
Nucleoplasmic localization of prelamin A: implications for prenylation-dependent lamin A assembly into the nuclear lamina | Q36932679 | ||
Suppression of proliferative defects associated with processing-defective lamin A mutants by hTERT or inactivation of p53. | Q36992979 | ||
The A- and B-type nuclear lamin networks: microdomains involved in chromatin organization and transcription | Q37023583 | ||
Alternative splicing and tumor progression | Q37222930 | ||
Activating the synthesis of progerin, the mutant prelamin A in Hutchinson-Gilford progeria syndrome, with antisense oligonucleotides | Q37223285 | ||
Epigenetic factors in aging and longevity | Q37600686 | ||
Nucleoplasmic LAP2alpha-lamin A complexes are required to maintain a proliferative state in human fibroblasts | Q39731192 | ||
The impact of heterochromatin on DSB repair | Q39851599 | ||
Telomere length in Hutchinson-Gilford progeria syndrome | Q39854171 | ||
The Hutchinson-Gilford progeria syndrome. Report of 4 cases and review of the literature | Q39914175 | ||
Chromatin relaxation in response to DNA double-strand breaks is modulated by a novel ATM- and KAP-1 dependent pathway | Q40252252 | ||
Nuclear organization of DNA replication in primary mammalian cells. | Q40445454 | ||
Senescing human cells and ageing mice accumulate DNA lesions with unrepairable double-strand breaks | Q40593721 | ||
Hypersensitivity of ataxia telangiectasia fibroblasts to ionizing radiation is associated with a repair deficiency of DNA double-strand breaks | Q41090992 | ||
Kinetics of DNA Double-strand Break Repair Throughout the Cell Cycle as Assayed by Pulsed Field Gel Electrophoresis in CHO Cells | Q41682717 | ||
Rescue of heterochromatin organization in Hutchinson-Gilford progeria by drug treatment | Q42013273 | ||
DNA damage responses in progeroid syndromes arise from defective maturation of prelamin A. | Q42101728 | ||
Novel lamin A/C gene (LMNA) mutations in atypical progeroid syndromes | Q43073760 | ||
Chromatin changes induced by lamin A/C deficiency and the histone deacetylase inhibitor trichostatin A. | Q46658161 | ||
Specific and conserved sequences in D. melanogaster and C. elegans lamins and histone H2A mediate the attachment of lamins to chromosomes | Q47068968 | ||
Defective prelamin A processing and muscular and adipocyte alterations in Zmpste24 metalloproteinase-deficient mice | Q52545724 | ||
Increased progerin expression associated with unusual LMNA mutations causes severe progeroid syndromes. | Q53556427 | ||
Telomere positional effects and the regulation of cellular senescence | Q68007322 | ||
practitioner | Q111608397 | ||
P433 | issue | 2 | |
P407 | language of work or name | English | Q1860 |
P921 | main subject | progeria | Q213098 |
P304 | page(s) | 133-141 | |
P577 | publication date | 2011-01-05 | |
P13046 | publication type of scholarly work | review article | Q7318358 |
P1433 | published in | Rejuvenation Research | Q7310582 |
P1476 | title | Unraveling the mysteries of aging through a Hutchinson-Gilford progeria syndrome model | |
Unraveling the Mysteries of Aging Through a Hutchinson–Gilford Progeria Syndrome Model | |||
P478 | volume | 14 |
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