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6. Suppression of proliferative defects associated with processing-defective lamin A mutants by hTERT or inactivation of p53. Kudlow BA; Stanfel MN; Burtner CR; Johnston ED; Kennedy BK Mol Biol Cell; 2008 Dec; 19(12):5238-48. PubMed ID: 18843043 [TBL] [Abstract][Full Text] [Related]
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9. Incomplete processing of mutant lamin A in Hutchinson-Gilford progeria leads to nuclear abnormalities, which are reversed by farnesyltransferase inhibition. Glynn MW; Glover TW Hum Mol Genet; 2005 Oct; 14(20):2959-69. PubMed ID: 16126733 [TBL] [Abstract][Full Text] [Related]
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14. Hutchinson-Gilford progeria mutant lamin A primarily targets human vascular cells as detected by an anti-Lamin A G608G antibody. McClintock D; Gordon LB; Djabali K Proc Natl Acad Sci U S A; 2006 Feb; 103(7):2154-9. PubMed ID: 16461887 [TBL] [Abstract][Full Text] [Related]
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16. Expression of progerin does not result in an increased mutation rate. Deniaud E; Lemaître C; Boyle S; Bickmore WA Chromosome Res; 2017 Oct; 25(3-4):227-239. PubMed ID: 28477268 [TBL] [Abstract][Full Text] [Related]
17. Nuclear membrane ruptures underlie the vascular pathology in a mouse model of Hutchinson-Gilford progeria syndrome. Kim PH; Chen NY; Heizer PJ; Tu Y; Weston TA; Fong JL; Gill NK; Rowat AC; Young SG; Fong LG JCI Insight; 2021 Aug; 6(16):. PubMed ID: 34423791 [TBL] [Abstract][Full Text] [Related]
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