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Direct synthesis of lamin A, bypassing prelamin a processing, causes misshapen nuclei in fibroblasts but no detectable pathology in mice.

Coffinier C, Jung HJ, Li Z, Nobumori C, Yun UJ, Farber EA, Davies BS, Weinstein MM, Yang SH, Lammerding J, Farahani JN, Bentolila LA, Fong LG, Young SG.

J Biol Chem. 2010 Jul 2;285(27):20818-26. doi: 10.1074/jbc.M110.128835. Epub 2010 May 3.


Investigating the purpose of prelamin A processing.

Davies BS, Coffinier C, Yang SH, Barnes RH 2nd, Jung HJ, Young SG, Fong LG.

Nucleus. 2011 Jan-Feb;2(1):4-9. doi: 10.1093/hmg/ddq158. Review.


An accumulation of non-farnesylated prelamin A causes cardiomyopathy but not progeria.

Davies BS, Barnes RH 2nd, Tu Y, Ren S, Andres DA, Spielmann HP, Lammerding J, Wang Y, Young SG, Fong LG.

Hum Mol Genet. 2010 Jul 1;19(13):2682-94. doi: 10.1093/hmg/ddq158. Epub 2010 Apr 26.


Prelamin A and lamin A appear to be dispensable in the nuclear lamina.

Fong LG, Ng JK, Lammerding J, Vickers TA, Meta M, Coté N, Gavino B, Qiao X, Chang SY, Young SR, Yang SH, Stewart CL, Lee RT, Bennett CF, Bergo MO, Young SG.

J Clin Invest. 2006 Mar;116(3):743-52.


Eliminating the synthesis of mature lamin A reduces disease phenotypes in mice carrying a Hutchinson-Gilford progeria syndrome allele.

Yang SH, Qiao X, Farber E, Chang SY, Fong LG, Young SG.

J Biol Chem. 2008 Mar 14;283(11):7094-9. doi: 10.1074/jbc.M708138200. Epub 2008 Jan 4.


Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice.

Fong LG, Ng JK, Meta M, Coté N, Yang SH, Stewart CL, Sullivan T, Burghardt A, Majumdar S, Reue K, Bergo MO, Young SG.

Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):18111-6. Epub 2004 Dec 17.


Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation.

Yang SH, Bergo MO, Toth JI, Qiao X, Hu Y, Sandoval S, Meta M, Bendale P, Gelb MH, Young SG, Fong LG.

Proc Natl Acad Sci U S A. 2005 Jul 19;102(29):10291-6. Epub 2005 Jul 12.


New Lmna knock-in mice provide a molecular mechanism for the 'segmental aging' in Hutchinson-Gilford progeria syndrome.

Jung HJ, Tu Y, Yang SH, Tatar A, Nobumori C, Wu D, Young SG, Fong LG.

Hum Mol Genet. 2014 Mar 15;23(6):1506-15. doi: 10.1093/hmg/ddt537. Epub 2013 Nov 7.


Accumulation of distinct prelamin A variants in human diploid fibroblasts differentially affects cell homeostasis.

Candelario J, Borrego S, Reddy S, Comai L.

Exp Cell Res. 2011 Feb 1;317(3):319-29. doi: 10.1016/j.yexcr.2010.10.014. Epub 2010 Oct 23.


Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes.

Toth JI, Yang SH, Qiao X, Beigneux AP, Gelb MH, Moulson CL, Miner JH, Young SG, Fong LG.

Proc Natl Acad Sci U S A. 2005 Sep 6;102(36):12873-8. Epub 2005 Aug 29.


Inhibiting farnesylation reverses the nuclear morphology defect in a HeLa cell model for Hutchinson-Gilford progeria syndrome.

Mallampalli MP, Huyer G, Bendale P, Gelb MH, Michaelis S.

Proc Natl Acad Sci U S A. 2005 Oct 4;102(40):14416-21. Epub 2005 Sep 26.


Requirements for efficient proteolytic cleavage of prelamin A by ZMPSTE24.

Barrowman J, Hamblet C, Kane MS, Michaelis S.

PLoS One. 2012;7(2):e32120. doi: 10.1371/journal.pone.0032120. Epub 2012 Feb 15.


Prelamin A farnesylation and progeroid syndromes.

Young SG, Meta M, Yang SH, Fong LG.

J Biol Chem. 2006 Dec 29;281(52):39741-5. Epub 2006 Nov 7. Review.


Emerin-prelamin A interplay in human fibroblasts.

Capanni C, Del Coco R, Mattioli E, Camozzi D, Columbaro M, Schena E, Merlini L, Squarzoni S, Maraldi NM, Lattanzi G.

Biol Cell. 2009 Sep;101(9):541-54. doi: 10.1042/BC20080175.


Lipodystrophy-linked LMNA p.R482W mutation induces clinical early atherosclerosis and in vitro endothelial dysfunction.

Bidault G, Garcia M, Vantyghem MC, Ducluzeau PH, Morichon R, Thiyagarajah K, Moritz S, Capeau J, Vigouroux C, Béréziat V.

Arterioscler Thromb Vasc Biol. 2013 Sep;33(9):2162-71. doi: 10.1161/ATVBAHA.113.301933. Epub 2013 Jul 11.


Absence of progeria-like disease phenotypes in knock-in mice expressing a non-farnesylated version of progerin.

Yang SH, Chang SY, Ren S, Wang Y, Andres DA, Spielmann HP, Fong LG, Young SG.

Hum Mol Genet. 2011 Feb 1;20(3):436-44. doi: 10.1093/hmg/ddq490. Epub 2010 Nov 18.


Analysis of prelamin A biogenesis reveals the nucleus to be a CaaX processing compartment.

Barrowman J, Hamblet C, George CM, Michaelis S.

Mol Biol Cell. 2008 Dec;19(12):5398-408. doi: 10.1091/mbc.E08-07-0704. Epub 2008 Oct 15.


Prelamin A-mediated nuclear envelope dynamics in normal and laminopathic cells.

Lattanzi G.

Biochem Soc Trans. 2011 Dec;39(6):1698-704. doi: 10.1042/BST20110657. Review.


LMNA missense mutations causing familial partial lipodystrophy do not lead to an accumulation of prelamin A.

Tu Y, Sánchez-Iglesias S, Araújo-Vilar D, Fong LG, Young SG.

Nucleus. 2016 Sep 2;7(5):512-521.

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