-
1
-
-
0036347096
-
Life at the edge: the nuclear envelope and human disease
-
Burke B., Stewart C.L. Life at the edge: the nuclear envelope and human disease. Nat Rev Mol Cell Biol 2002, 3:575-585.
-
(2002)
Nat Rev Mol Cell Biol
, vol.3
, pp. 575-585
-
-
Burke, B.1
Stewart, C.L.2
-
2
-
-
8144227710
-
The nuclear envelope and human disease
-
Muchir A., Worman H.J. The nuclear envelope and human disease. Physiology (Bethesda) 2004, 19:309-314.
-
(2004)
Physiology (Bethesda)
, vol.19
, pp. 309-314
-
-
Muchir, A.1
Worman, H.J.2
-
3
-
-
34249788998
-
" Laminopathies": a wide spectrum of human diseases
-
Worman H.J., Bonne G. " Laminopathies": a wide spectrum of human diseases. Exp Cell Res 2007, 313:2121-2133.
-
(2007)
Exp Cell Res
, vol.313
, pp. 2121-2133
-
-
Worman, H.J.1
Bonne, G.2
-
4
-
-
0035169030
-
The A-Type lamins: nuclear structural proteins as a focus for muscular dystrophy and cardiovascular diseases
-
Mounkes L.C., Burke B., Stewart C.L. The A-Type lamins: nuclear structural proteins as a focus for muscular dystrophy and cardiovascular diseases. Trends Cardiovasc Med 2001, 11:280-285.
-
(2001)
Trends Cardiovasc Med
, vol.11
, pp. 280-285
-
-
Mounkes, L.C.1
Burke, B.2
Stewart, C.L.3
-
5
-
-
0034176682
-
The nuclear envelope, muscular dystrophy and gene expression
-
Wilson K.L. The nuclear envelope, muscular dystrophy and gene expression. Trends Cell Biol 2000, 10:125-129.
-
(2000)
Trends Cell Biol
, vol.10
, pp. 125-129
-
-
Wilson, K.L.1
-
6
-
-
0023032014
-
CDNA sequencing of nuclear lamins A and C reveals primary and secondary structural homology to intermediate filament proteins
-
Fisher D.Z., Chaudhary N., Blobel G. cDNA sequencing of nuclear lamins A and C reveals primary and secondary structural homology to intermediate filament proteins. Proc Natl Acad Sci USA 1986, 83:6450-6454.
-
(1986)
Proc Natl Acad Sci USA
, vol.83
, pp. 6450-6454
-
-
Fisher, D.Z.1
Chaudhary, N.2
Blobel, G.3
-
7
-
-
0027257461
-
Structural organization of the human gene encoding nuclear lamin A and nuclear lamin C
-
Lin F., Worman H.J. Structural organization of the human gene encoding nuclear lamin A and nuclear lamin C. J Biol Chem 1993, 268:16321-16326.
-
(1993)
J Biol Chem
, vol.268
, pp. 16321-16326
-
-
Lin, F.1
Worman, H.J.2
-
8
-
-
0027050783
-
Biochemistry of protein prenylation
-
Casey P.J. Biochemistry of protein prenylation. J Lipid Res 1992, 33:1731-1740.
-
(1992)
J Lipid Res
, vol.33
, pp. 1731-1740
-
-
Casey, P.J.1
-
9
-
-
0029966304
-
Protein prenyltransferases
-
Casey P.J., Seabra M.C. Protein prenyltransferases. J Biol Chem 1996, 271:5289-5292.
-
(1996)
J Biol Chem
, vol.271
, pp. 5289-5292
-
-
Casey, P.J.1
Seabra, M.C.2
-
10
-
-
0029898894
-
Protein prenylation: molecular mechanisms and functional consequences
-
Zhang F.L., Casey P.J. Protein prenylation: molecular mechanisms and functional consequences. Annu Rev Biochem 1996, 65:241-269.
-
(1996)
Annu Rev Biochem
, vol.65
, pp. 241-269
-
-
Zhang, F.L.1
Casey, P.J.2
-
11
-
-
0027076554
-
Protein prenylation: genes, enzymes, targets, and functions
-
Schafer W.R., Rine J. Protein prenylation: genes, enzymes, targets, and functions. Annu Rev Genet 1992, 26:209-237.
-
(1992)
Annu Rev Genet
, vol.26
, pp. 209-237
-
-
Schafer, W.R.1
Rine, J.2
-
12
-
-
0033605596
-
Disruption of the mouse Rce1 gene results in defective Ras processing and mislocalization of Ras within cells
-
Kim E., et al. Disruption of the mouse Rce1 gene results in defective Ras processing and mislocalization of Ras within cells. J Biol Chem 1999, 274:8383-8390.
-
(1999)
J Biol Chem
, vol.274
, pp. 8383-8390
-
-
Kim, E.1
-
13
-
-
0141530040
-
A carboxyl-terminal interaction of lamin B1 is dependent on the CAAX endoprotease Rce1 and carboxymethylation
-
Maske C.P., Hollinshead M.S., Higbee N.C., Bergo M.O., Young S.G., Vaux D.J. A carboxyl-terminal interaction of lamin B1 is dependent on the CAAX endoprotease Rce1 and carboxymethylation. J Cell Biol 2003, 162:1223-1232.
-
(2003)
J Cell Biol
, vol.162
, pp. 1223-1232
-
-
Maske, C.P.1
Hollinshead, M.S.2
Higbee, N.C.3
Bergo, M.O.4
Young, S.G.5
Vaux, D.J.6
-
14
-
-
0033605743
-
Cloning and characterization of a mammalian prenyl protein-specific protease
-
Otto J.C., Kim E., Young S.G., Casey P.J. Cloning and characterization of a mammalian prenyl protein-specific protease. J Biol Chem 1999, 274:8379-8382.
-
(1999)
J Biol Chem
, vol.274
, pp. 8379-8382
-
-
Otto, J.C.1
Kim, E.2
Young, S.G.3
Casey, P.J.4
-
15
-
-
0036791026
-
Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect
-
Bergo M.O., et al. Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect. Proc Natl Acad Sci USA 2002, 99:13049-13054.
-
(2002)
Proc Natl Acad Sci USA
, vol.99
, pp. 13049-13054
-
-
Bergo, M.O.1
-
16
-
-
17144398001
-
Prelamin A endoproteolytic processing in vitro by recombinant Zmpste24
-
Corrigan D.P., et al. Prelamin A endoproteolytic processing in vitro by recombinant Zmpste24. Biochem J 2005, 387:129-138.
-
(2005)
Biochem J
, vol.387
, pp. 129-138
-
-
Corrigan, D.P.1
-
17
-
-
0000081175
-
Posttranslational modification of the Ha-ras oncogene protein: evidence for a third class of protein carboxyl methyltransferases
-
Clarke S., Vogel J.P., Deschenes R.J., Stock J. Posttranslational modification of the Ha-ras oncogene protein: evidence for a third class of protein carboxyl methyltransferases. Proc Natl Acad Sci USA 1988, 85:4643-4647.
-
(1988)
Proc Natl Acad Sci USA
, vol.85
, pp. 4643-4647
-
-
Clarke, S.1
Vogel, J.P.2
Deschenes, R.J.3
Stock, J.4
-
18
-
-
0032511057
-
Mammalian prenylcysteine carboxyl methyltransferase is in the endoplasmic reticulum
-
Dai Q., et al. Mammalian prenylcysteine carboxyl methyltransferase is in the endoplasmic reticulum. J Biol Chem 1998, 273:15030-15034.
-
(1998)
J Biol Chem
, vol.273
, pp. 15030-15034
-
-
Dai, Q.1
-
19
-
-
0035937112
-
Isoprenylcysteine carboxyl methyltransferase deficiency in mice
-
Bergo M.O., et al. Isoprenylcysteine carboxyl methyltransferase deficiency in mice. J Biol Chem 2001, 276:5841-5845.
-
(2001)
J Biol Chem
, vol.276
, pp. 5841-5845
-
-
Bergo, M.O.1
-
20
-
-
0034625181
-
Targeted inactivation of the isoprenylcysteine carboxyl methyltransferase gene causes mislocalization of K-Ras in mammalian cells
-
Bergo M.O., Leung G.K., Ambroziak P., Otto J.C., Casey P.J., Young S.G. Targeted inactivation of the isoprenylcysteine carboxyl methyltransferase gene causes mislocalization of K-Ras in mammalian cells. J Biol Chem 2000, 275:17605-17610.
-
(2000)
J Biol Chem
, vol.275
, pp. 17605-17610
-
-
Bergo, M.O.1
Leung, G.K.2
Ambroziak, P.3
Otto, J.C.4
Casey, P.J.5
Young, S.G.6
-
21
-
-
0024094640
-
Incorporation of a product of mevalonic acid metabolism into proteins of Chinese hamster ovary cell nuclei
-
Beck L.A., Hosick T.J., Sinensky M. Incorporation of a product of mevalonic acid metabolism into proteins of Chinese hamster ovary cell nuclei. J Cell Biol 1988, 107:1307-1316.
-
(1988)
J Cell Biol
, vol.107
, pp. 1307-1316
-
-
Beck, L.A.1
Hosick, T.J.2
Sinensky, M.3
-
22
-
-
0023917971
-
Evidence for modification of lamin B by a product of mevalonic acid
-
Wolda S.L., Glomset J.A. Evidence for modification of lamin B by a product of mevalonic acid. J Biol Chem 1988, 263:5997-6000.
-
(1988)
J Biol Chem
, vol.263
, pp. 5997-6000
-
-
Wolda, S.L.1
Glomset, J.A.2
-
23
-
-
0030839323
-
A- and B-type lamins are differentially expressed in normal human tissues
-
Broers J.L., et al. A- and B-type lamins are differentially expressed in normal human tissues. Histochem Cell Biol 1997, 107:505-517.
-
(1997)
Histochem Cell Biol
, vol.107
, pp. 505-517
-
-
Broers, J.L.1
-
24
-
-
0025272702
-
Cells of the cellular immune and hemopoietic system of the mouse lack lamins A/C: distinction versus other somatic cells
-
Rober R.A., Sauter H., Weber K., Osborn M. Cells of the cellular immune and hemopoietic system of the mouse lack lamins A/C: distinction versus other somatic cells. J Cell Sci 1990, 95(Pt 4):587-598.
-
(1990)
J Cell Sci
, vol.95
, Issue.PART 4
, pp. 587-598
-
-
Rober, R.A.1
Sauter, H.2
Weber, K.3
Osborn, M.4
-
25
-
-
0024561417
-
Differential timing of nuclear lamin A/C expression in the various organs of the mouse embryo and the young animal: a developmental study
-
Rober R.A., Weber K., Osborn M. Differential timing of nuclear lamin A/C expression in the various organs of the mouse embryo and the young animal: a developmental study. Development 1989, 105:365-378.
-
(1989)
Development
, vol.105
, pp. 365-378
-
-
Rober, R.A.1
Weber, K.2
Osborn, M.3
-
26
-
-
0023646768
-
Teratocarcinoma stem cells and early mouse embryos contain only a single major lamin polypeptide closely resembling lamin B
-
Stewart C., Burke B. Teratocarcinoma stem cells and early mouse embryos contain only a single major lamin polypeptide closely resembling lamin B. Cell 1987, 51:383-392.
-
(1987)
Cell
, vol.51
, pp. 383-392
-
-
Stewart, C.1
Burke, B.2
-
27
-
-
33749045115
-
Lamin B1 duplications cause autosomal dominant leukodystrophy
-
Padiath Q.S., et al. Lamin B1 duplications cause autosomal dominant leukodystrophy. Nat Genet 2006, 38:1114-1123.
-
(2006)
Nat Genet
, vol.38
, pp. 1114-1123
-
-
Padiath, Q.S.1
-
28
-
-
3142696838
-
Lamin B1 is required for mouse development and nuclear integrity
-
Vergnes L., PÇterfy M., Bergo M.O., Young S.G., Reue K. Lamin B1 is required for mouse development and nuclear integrity. Proc Natl Acad Sci USA 2004, 101:10428-10433.
-
(2004)
Proc Natl Acad Sci USA
, vol.101
, pp. 10428-10433
-
-
Vergnes, L.1
Pçterfy, M.2
Bergo, M.O.3
Young, S.G.4
Reue, K.5
-
29
-
-
0033636843
-
Head and/or CaaX domain deletions of lamin proteins disrupt preformed lamin A and C but not lamin B structure in mammalian cells
-
Izumi M., Vaughan O.A., Hutchison C.J., Gilbert D.M. Head and/or CaaX domain deletions of lamin proteins disrupt preformed lamin A and C but not lamin B structure in mammalian cells. Mol Biol Cell 2000, 11:4323-4337.
-
(2000)
Mol Biol Cell
, vol.11
, pp. 4323-4337
-
-
Izumi, M.1
Vaughan, O.A.2
Hutchison, C.J.3
Gilbert, D.M.4
-
30
-
-
0024444733
-
The conserved carboxy-terminal cysteine of nuclear lamins is essential for lamin association with the nuclear envelope
-
Krohne G., Waizenegger I., Hoger T.H. The conserved carboxy-terminal cysteine of nuclear lamins is essential for lamin association with the nuclear envelope. J Cell Biol 1989, 109:2003-2011.
-
(1989)
J Cell Biol
, vol.109
, pp. 2003-2011
-
-
Krohne, G.1
Waizenegger, I.2
Hoger, T.H.3
-
31
-
-
0029091930
-
The farnesyl protein transferase inhibitor BZA-5B blocks farnesylation of nuclear lamins and p21ras but does not affect their function or localization
-
Dalton M.B., et al. The farnesyl protein transferase inhibitor BZA-5B blocks farnesylation of nuclear lamins and p21ras but does not affect their function or localization. Cancer Res 1995, 55:3295-3304.
-
(1995)
Cancer Res
, vol.55
, pp. 3295-3304
-
-
Dalton, M.B.1
-
32
-
-
0024439979
-
A second higher vertebrate B-type lamin. cDNA sequence determination and in vitro processing of chicken lamin B2
-
Vorburger K., Lehner C.F., Kitten G.T., Eppenberger H.M., Nigg E.A. A second higher vertebrate B-type lamin. cDNA sequence determination and in vitro processing of chicken lamin B2. J Mol Biol 1989, 208:405-415.
-
(1989)
J Mol Biol
, vol.208
, pp. 405-415
-
-
Vorburger, K.1
Lehner, C.F.2
Kitten, G.T.3
Eppenberger, H.M.4
Nigg, E.A.5
-
33
-
-
0025165401
-
Characterization of a second highly conserved B-type lamin present in cells previously thought to contain only a single B-type lamin
-
Hoger T.H., Zatloukal K., Waizenegger I., Krohne G. Characterization of a second highly conserved B-type lamin present in cells previously thought to contain only a single B-type lamin. Chromosoma 1990, 99:379-390.
-
(1990)
Chromosoma
, vol.99
, pp. 379-390
-
-
Hoger, T.H.1
Zatloukal, K.2
Waizenegger, I.3
Krohne, G.4
-
34
-
-
77950394590
-
Abnormal development of the cerebral cortex and cerebellum in the setting of lamin B2 deficiency
-
Coffinier C., et al. Abnormal development of the cerebral cortex and cerebellum in the setting of lamin B2 deficiency. Proc Natl Acad Sci USA 2010, 107:5076-5081.
-
(2010)
Proc Natl Acad Sci USA
, vol.107
, pp. 5076-5081
-
-
Coffinier, C.1
-
35
-
-
33749338937
-
Neuronal polarity in CNS development
-
Solecki D.J., Govek E.E., Tomoda T., Hatten M.E. Neuronal polarity in CNS development. Genes Dev 2006, 20:2639-2647.
-
(2006)
Genes Dev
, vol.20
, pp. 2639-2647
-
-
Solecki, D.J.1
Govek, E.E.2
Tomoda, T.3
Hatten, M.E.4
-
36
-
-
33744827404
-
The cellular roles of the lissencephaly gene LIS1, and what they tell us about brain development
-
Vallee R.B., Tsai J.W. The cellular roles of the lissencephaly gene LIS1, and what they tell us about brain development. Genes Dev 2006, 20:1384-1393.
-
(2006)
Genes Dev
, vol.20
, pp. 1384-1393
-
-
Vallee, R.B.1
Tsai, J.W.2
-
37
-
-
0035868823
-
LIS1 and dynein motor function in neuronal migration and development
-
Wynshaw-Boris A., Gambello M.J. LIS1 and dynein motor function in neuronal migration and development. Genes Dev 2001, 15:639-651.
-
(2001)
Genes Dev
, vol.15
, pp. 639-651
-
-
Wynshaw-Boris, A.1
Gambello, M.J.2
-
38
-
-
33846040831
-
Trekking across the brain: the journey of neuronal migration
-
Ayala R., Shu T., Tsai L.H. Trekking across the brain: the journey of neuronal migration. Cell 2007, 128:29-43.
-
(2007)
Cell
, vol.128
, pp. 29-43
-
-
Ayala, R.1
Shu, T.2
Tsai, L.H.3
-
39
-
-
0034255316
-
Neuronal migration disorders: from genetic diseases to developmental mechanisms
-
Gleeson J.G., Walsh C.A. Neuronal migration disorders: from genetic diseases to developmental mechanisms. Trends Neurosci 2000, 23:352-359.
-
(2000)
Trends Neurosci
, vol.23
, pp. 352-359
-
-
Gleeson, J.G.1
Walsh, C.A.2
-
40
-
-
34548565750
-
Lissencephaly and LIS1: insights into the molecular mechanisms of neuronal migration and development
-
Wynshaw-Boris A. Lissencephaly and LIS1: insights into the molecular mechanisms of neuronal migration and development. Clin Genet 2007, 72:296-304.
-
(2007)
Clin Genet
, vol.72
, pp. 296-304
-
-
Wynshaw-Boris, A.1
-
41
-
-
0033007990
-
Subcellular localization and partial purification of prelamin A endoprotease: an enzyme which catalyzes the conversion of farnesylated prelamin A to mature lamin A
-
Kilic F., Johnson D.A., Sinensky M. Subcellular localization and partial purification of prelamin A endoprotease: an enzyme which catalyzes the conversion of farnesylated prelamin A to mature lamin A. FEBS Lett 1999, 450:61-65.
-
(1999)
FEBS Lett
, vol.450
, pp. 61-65
-
-
Kilic, F.1
Johnson, D.A.2
Sinensky, M.3
-
42
-
-
19944428509
-
Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice
-
Fong L.G., et al. Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice. Proc Natl Acad Sci USA 2004, 101:18111-18116.
-
(2004)
Proc Natl Acad Sci USA
, vol.101
, pp. 18111-18116
-
-
Fong, L.G.1
-
43
-
-
0036578920
-
Defective prelamin A processing and muscular and adipocyte alterations in Zmpste24 metalloproteinase-deficient mice
-
Pendas A.M., et al. Defective prelamin A processing and muscular and adipocyte alterations in Zmpste24 metalloproteinase-deficient mice. Nat Genet 2002, 31:94-99.
-
(2002)
Nat Genet
, vol.31
, pp. 94-99
-
-
Pendas, A.M.1
-
44
-
-
0028118904
-
The processing pathway of prelamin A
-
Sinensky M., Fantle K., Trujillo M., McLain T., Kupfer A., Dalton M. The processing pathway of prelamin A. J Cell Sci 1994, 107(Pt 1):61-67.
-
(1994)
J Cell Sci
, vol.107
, Issue.PART 1
, pp. 61-67
-
-
Sinensky, M.1
Fantle, K.2
Trujillo, M.3
McLain, T.4
Kupfer, A.5
Dalton, M.6
-
45
-
-
0034902488
-
Both emerin and lamin C depend on lamin A for localization at the nuclear envelope
-
Vaughan O.A., et al. Both emerin and lamin C depend on lamin A for localization at the nuclear envelope. J Cell Sci 2001, 114:2577-2590.
-
(2001)
J Cell Sci
, vol.114
, pp. 2577-2590
-
-
Vaughan, O.A.1
-
46
-
-
33644651157
-
Prelamin A and lamin A appear to be dispensable in the nuclear lamina
-
Fong L.G., et al. Prelamin A and lamin A appear to be dispensable in the nuclear lamina. J Clin Invest 2006, 116:743-752.
-
(2006)
J Clin Invest
, vol.116
, pp. 743-752
-
-
Fong, L.G.1
-
47
-
-
22544440839
-
Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation
-
Yang S.H., et al. Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation. Proc Natl Acad Sci USA 2005, 102:10291-10296.
-
(2005)
Proc Natl Acad Sci USA
, vol.102
, pp. 10291-10296
-
-
Yang, S.H.1
-
48
-
-
33746715642
-
A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation
-
Yang S.H., et al. A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation. J Clin Invest 2006, 116:2115-2121.
-
(2006)
J Clin Invest
, vol.116
, pp. 2115-2121
-
-
Yang, S.H.1
-
49
-
-
55849129996
-
Progerin elicits disease phenotypes of progeria in mice whether or not it is farnesylated
-
Yang S.H., Andres D.A., Spielmann H.P., Young S.G., Fong L.G. Progerin elicits disease phenotypes of progeria in mice whether or not it is farnesylated. J Clin Invest 2008, 118:3291-3300.
-
(2008)
J Clin Invest
, vol.118
, pp. 3291-3300
-
-
Yang, S.H.1
Andres, D.A.2
Spielmann, H.P.3
Young, S.G.4
Fong, L.G.5
-
50
-
-
78651095782
-
Absence of progeria-like disease phenotypes in knock-in mice expressing a nonfarnesylated version of progerin
-
Yang S.H., et al. Absence of progeria-like disease phenotypes in knock-in mice expressing a nonfarnesylated version of progerin. Hum Mol Genet 2011, 20:436-444.
-
(2011)
Hum Mol Genet
, vol.20
, pp. 436-444
-
-
Yang, S.H.1
-
51
-
-
77954159278
-
An accumulation of non-farnesylated prelamin A causes cardiomyopathy but not progeria
-
Davies B.S., et al. An accumulation of non-farnesylated prelamin A causes cardiomyopathy but not progeria. Hum Mol Genet 2010, 19:2682-2694.
-
(2010)
Hum Mol Genet
, vol.19
, pp. 2682-2694
-
-
Davies, B.S.1
-
52
-
-
77954234017
-
Direct synthesis of lamin A, bypassing prelamin a processing, causes misshapen nuclei in fibroblasts but no detectable pathology in mice
-
Coffinier C., et al. Direct synthesis of lamin A, bypassing prelamin a processing, causes misshapen nuclei in fibroblasts but no detectable pathology in mice. J Biol Chem 2010, 285:20818-20826.
-
(2010)
J Biol Chem
, vol.285
, pp. 20818-20826
-
-
Coffinier, C.1
-
53
-
-
79952691505
-
Investigating the purpose of prelamin A processing
-
Davies B.S., et al. Investigating the purpose of prelamin A processing. Nucleus 2011, 2:4-9.
-
(2011)
Nucleus
, vol.2
, pp. 4-9
-
-
Davies, B.S.1
-
54
-
-
0033615969
-
Loss of A-type lamin expression compromises nuclear envelope integrity leading to muscular dystrophy
-
Sullivan T., et al. Loss of A-type lamin expression compromises nuclear envelope integrity leading to muscular dystrophy. J Cell Biol 1999, 147:913-920.
-
(1999)
J Cell Biol
, vol.147
, pp. 913-920
-
-
Sullivan, T.1
-
55
-
-
1542317663
-
Lamin A/C deficiency causes defective nuclear mechanics and mechanotransduction
-
Lammerding J., et al. Lamin A/C deficiency causes defective nuclear mechanics and mechanotransduction. J Clin Invest 2004, 113:370-378.
-
(2004)
J Clin Invest
, vol.113
, pp. 370-378
-
-
Lammerding, J.1
-
56
-
-
39149083716
-
Lamin A/C haploinsufficiency causes dilated cardiomyopathy and apoptosis-triggered cardiac conduction system disease
-
Wolf C.M., et al. Lamin A/C haploinsufficiency causes dilated cardiomyopathy and apoptosis-triggered cardiac conduction system disease. J Mol Cell Cardiol 2008, 44:293-303.
-
(2008)
J Mol Cell Cardiol
, vol.44
, pp. 293-303
-
-
Wolf, C.M.1
-
57
-
-
0032977685
-
Mutations in the gene encoding lamin A/C cause autosomal dominant Emery-Dreifuss muscular dystrophy
-
Bonne G., et al. Mutations in the gene encoding lamin A/C cause autosomal dominant Emery-Dreifuss muscular dystrophy. Nat Genet 1999, 21:285-288.
-
(1999)
Nat Genet
, vol.21
, pp. 285-288
-
-
Bonne, G.1
-
58
-
-
0042327845
-
Expanding the phenotype of LMNA mutations in dilated cardiomyopathy and functional consequences of these mutations
-
Sebillon P., et al. Expanding the phenotype of LMNA mutations in dilated cardiomyopathy and functional consequences of these mutations. J Med Genet 2003, 40:560-567.
-
(2003)
J Med Genet
, vol.40
, pp. 560-567
-
-
Sebillon, P.1
-
59
-
-
12544256294
-
The lethal phenotype of a homozygous nonsense mutation in the lamin A/C gene
-
van Engelen B.G., Muchir A., Hutchison C.J., van der Kooi A.J., Bonne G., Lammens M. The lethal phenotype of a homozygous nonsense mutation in the lamin A/C gene. Neurology 2005, 64:374-376.
-
(2005)
Neurology
, vol.64
, pp. 374-376
-
-
van Engelen, B.G.1
Muchir, A.2
Hutchison, C.J.3
van der Kooi, A.J.4
Bonne, G.5
Lammens, M.6
-
60
-
-
0035800833
-
Biochemical studies of Zmpste24-deficient mice
-
Leung G.K., et al. Biochemical studies of Zmpste24-deficient mice. J Biol Chem 2001, 276:29051-29058.
-
(2001)
J Biol Chem
, vol.276
, pp. 29051-29058
-
-
Leung, G.K.1
-
61
-
-
24644459728
-
Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes
-
Toth J.I., et al. Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes. Proc Natl Acad Sci USA 2005, 102:12873-12878.
-
(2005)
Proc Natl Acad Sci USA
, vol.102
, pp. 12873-12878
-
-
Toth, J.I.1
-
62
-
-
44349132197
-
A potent HIV protease inhibitor, Darunavir, does not inhibit ZMPSTE24 or lead to an accumulation of farnesyl-prelamin A in cells
-
Coffinier C., et al. A potent HIV protease inhibitor, Darunavir, does not inhibit ZMPSTE24 or lead to an accumulation of farnesyl-prelamin A in cells. J Biol Chem 2008, 283:9797-9804.
-
(2008)
J Biol Chem
, vol.283
, pp. 9797-9804
-
-
Coffinier, C.1
-
63
-
-
30844451421
-
Homozygous and compound heterozygous mutations in ZMPSTE24 cause the laminopathy restrictive dermopathy
-
Moulson C.L., Go G., van der Wal A.C., Smitt J.H., van Hagen J.M., Miner J.H. Homozygous and compound heterozygous mutations in ZMPSTE24 cause the laminopathy restrictive dermopathy. J Invest Dermatol 2005, 125:913-919.
-
(2005)
J Invest Dermatol
, vol.125
, pp. 913-919
-
-
Moulson, C.L.1
Go, G.2
van der Wal, A.C.3
Smitt, J.H.4
van Hagen, J.M.5
Miner, J.H.6
-
64
-
-
20444506041
-
Loss of ZMPSTE24 (FACE-1) causes autosomal recessive restrictive dermopathy and accumulation of Lamin A precursors
-
Navarro C.L., et al. Loss of ZMPSTE24 (FACE-1) causes autosomal recessive restrictive dermopathy and accumulation of Lamin A precursors. Hum Mol Genet 2005, 14:1503-1513.
-
(2005)
Hum Mol Genet
, vol.14
, pp. 1503-1513
-
-
Navarro, C.L.1
-
65
-
-
0036833825
-
Oral and maxillofacial surgical considerations for a case of Hutchinson-Gilford progeria
-
Batstone M.D., Macleod A.W.G. Oral and maxillofacial surgical considerations for a case of Hutchinson-Gilford progeria. Int J Paediatr Dent 2002, 12:429-432.
-
(2002)
Int J Paediatr Dent
, vol.12
, pp. 429-432
-
-
Batstone, M.D.1
Macleod, A.W.G.2
-
66
-
-
0015319601
-
The Hutchinson-Gilford progeria syndrome. Report of 4 cases and review of the literature
-
DeBusk F.L. The Hutchinson-Gilford progeria syndrome. Report of 4 cases and review of the literature. J Pediatr 1972, 80:697-724.
-
(1972)
J Pediatr
, vol.80
, pp. 697-724
-
-
DeBusk, F.L.1
-
67
-
-
0037673950
-
Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome
-
Eriksson M., et al. Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome. Nature 2003, 423:293-298.
-
(2003)
Nature
, vol.423
, pp. 293-298
-
-
Eriksson, M.1
-
68
-
-
0033462185
-
Can Hutchinson-Gilford progeria syndrome be a neonatal condition?
-
Faivre L., Kien P.K.V., Madinier-Chappat N., Nivelon-Chevallier A., Beer F., LeMerrer M. Can Hutchinson-Gilford progeria syndrome be a neonatal condition?. Am J Hum Genet 1999, 87:450-452.
-
(1999)
Am J Hum Genet
, vol.87
, pp. 450-452
-
-
Faivre, L.1
Kien, P.K.V.2
Madinier-Chappat, N.3
Nivelon-Chevallier, A.4
Beer, F.5
LeMerrer, M.6
-
69
-
-
0027104845
-
Report on a case of Hutchinson-Gilford progeria, with special reference to orthopedic problems
-
Fernandez-Palazzi F., McLaren A.T., Slowie D.F. Report on a case of Hutchinson-Gilford progeria, with special reference to orthopedic problems. Eur J Pediatr Surg 1992, 2:378-382.
-
(1992)
Eur J Pediatr Surg
, vol.2
, pp. 378-382
-
-
Fernandez-Palazzi, F.1
McLaren, A.T.2
Slowie, D.F.3
-
70
-
-
0024600833
-
Hutchinson-Gilford progeria syndrome: report of a Libyan family and evidence of autosomal recessive inheritance
-
Khalifa M.M. Hutchinson-Gilford progeria syndrome: report of a Libyan family and evidence of autosomal recessive inheritance. Clin Genet 1989, 35:125-132.
-
(1989)
Clin Genet
, vol.35
, pp. 125-132
-
-
Khalifa, M.M.1
-
71
-
-
0345355134
-
Lethal neonatal Hutchinson-Gilford progeria syndrome
-
Rodríguez J.I., Perez-Alonso P., Funes R., Perez-Rodríguez J. Lethal neonatal Hutchinson-Gilford progeria syndrome. Am J Med Genet 1999, 82:242-248.
-
(1999)
Am J Med Genet
, vol.82
, pp. 242-248
-
-
Rodríguez, J.I.1
Perez-Alonso, P.2
Funes, R.3
Perez-Rodríguez, J.4
-
72
-
-
34247383902
-
Alterations in mitosis and cell cycle progression caused by a mutant lamin A known to accelerate human aging
-
Dechat T., et al. Alterations in mitosis and cell cycle progression caused by a mutant lamin A known to accelerate human aging. Proc Natl Acad Sci USA 2007, 104:4955-4960.
-
(2007)
Proc Natl Acad Sci USA
, vol.104
, pp. 4955-4960
-
-
Dechat, T.1
-
73
-
-
2942643923
-
Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome
-
Goldman R.D., et al. Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome. Proc Natl Acad Sci USA 2004, 101:8963-8968.
-
(2004)
Proc Natl Acad Sci USA
, vol.101
, pp. 8963-8968
-
-
Goldman, R.D.1
-
74
-
-
43749111384
-
Eliminating the synthesis of mature lamin A reduces disease phenotypes in mice carrying a Hutchinson-Gilford Progeria Syndrome allele
-
Yang S.H., Qiao X., Farber E., Chang S.Y., Fong L.G., Young S.G. Eliminating the synthesis of mature lamin A reduces disease phenotypes in mice carrying a Hutchinson-Gilford Progeria Syndrome allele. J Biol Chem 2008, 283:7094-7099.
-
(2008)
J Biol Chem
, vol.283
, pp. 7094-7099
-
-
Yang, S.H.1
Qiao, X.2
Farber, E.3
Chang, S.Y.4
Fong, L.G.5
Young, S.G.6
-
75
-
-
24644520772
-
Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome
-
Capell B.C., et al. Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome. Proc Natl Acad Sci USA 2005, 102:12879-12884.
-
(2005)
Proc Natl Acad Sci USA
, vol.102
, pp. 12879-12884
-
-
Capell, B.C.1
-
76
-
-
27544498316
-
Incomplete processing of mutant lamin A in Hutchinson-Gilford progeria leads to nuclear abnormalities, which are reversed by farnesyltransferase inhibition
-
Glynn M.W., Glover T.W. Incomplete processing of mutant lamin A in Hutchinson-Gilford progeria leads to nuclear abnormalities, which are reversed by farnesyltransferase inhibition. Hum Mol Genet 2005, 14:2959-2969.
-
(2005)
Hum Mol Genet
, vol.14
, pp. 2959-2969
-
-
Glynn, M.W.1
Glover, T.W.2
-
77
-
-
26444463068
-
Inhibiting farnesylation reverses the nuclear morphology defect in a HeLa cell model for Hutchinson-Gilford progeria syndrome
-
Mallampalli M.P., Huyer G., Bendale P., Gelb M.H., Michaelis S. Inhibiting farnesylation reverses the nuclear morphology defect in a HeLa cell model for Hutchinson-Gilford progeria syndrome. Proc Natl Acad Sci USA 2005, 102:14416-14421.
-
(2005)
Proc Natl Acad Sci USA
, vol.102
, pp. 14416-14421
-
-
Mallampalli, M.P.1
Huyer, G.2
Bendale, P.3
Gelb, M.H.4
Michaelis, S.5
-
78
-
-
33645060977
-
A protein farnesyltransferase inhibitor ameliorates disease in a mouse model of progeria
-
Fong L.G., et al. A protein farnesyltransferase inhibitor ameliorates disease in a mouse model of progeria. Science 2006, 311:1621-1623.
-
(2006)
Science
, vol.311
, pp. 1621-1623
-
-
Fong, L.G.1
-
79
-
-
77949527805
-
Assessing the efficacy of protein farnesyltransferase inhibitors in mouse models of progeria
-
Yang S.H., Chang S.Y., Andres D.A., Spielmann H.P., Young S.G., Fong L.G. Assessing the efficacy of protein farnesyltransferase inhibitors in mouse models of progeria. J Lipid Res 2010, 51:400-405.
-
(2010)
J Lipid Res
, vol.51
, pp. 400-405
-
-
Yang, S.H.1
Chang, S.Y.2
Andres, D.A.3
Spielmann, H.P.4
Young, S.G.5
Fong, L.G.6
-
80
-
-
39049111972
-
Treatment with a farnesyltransferase inhibitor improves survival in mice with a Hutchinson-Gilford progeria syndrome mutation
-
Yang S.H., Qiao X., Fong L.G., Young S.G. Treatment with a farnesyltransferase inhibitor improves survival in mice with a Hutchinson-Gilford progeria syndrome mutation. Biochim Biophys Acta 2008, 1781:36-39.
-
(2008)
Biochim Biophys Acta
, vol.1781
, pp. 36-39
-
-
Yang, S.H.1
Qiao, X.2
Fong, L.G.3
Young, S.G.4
-
81
-
-
0034702027
-
Identification of mutations in the gene encoding lamins A/C in autosomal dominant limb girdle muscular dystrophy with atrioventricular conduction disturbances (LGMD1B)
-
Muchir A., et al. Identification of mutations in the gene encoding lamins A/C in autosomal dominant limb girdle muscular dystrophy with atrioventricular conduction disturbances (LGMD1B). Hum Mol Genet 2000, 9:1453-1459.
-
(2000)
Hum Mol Genet
, vol.9
, pp. 1453-1459
-
-
Muchir, A.1
-
82
-
-
1542437955
-
Mutation analysis of the lamin A/C gene (LMNA) among patients with different cardiomuscular phenotypes
-
Vytopil M., et al. Mutation analysis of the lamin A/C gene (LMNA) among patients with different cardiomuscular phenotypes. J Med Genet 2003, 40:e132.
-
(2003)
J Med Genet
, vol.40
-
-
Vytopil, M.1
-
83
-
-
19944426537
-
Mouse model carrying H222P-Lmna mutation develops muscular dystrophy and dilated cardiomyopathy similar to human striated muscle laminopathies
-
Arimura T., et al. Mouse model carrying H222P-Lmna mutation develops muscular dystrophy and dilated cardiomyopathy similar to human striated muscle laminopathies. Hum Mol Genet 2005, 14:155-169.
-
(2005)
Hum Mol Genet
, vol.14
, pp. 155-169
-
-
Arimura, T.1
-
84
-
-
26444595257
-
Expression of an LMNA-N195K variant of A-type lamins results in cardiac conduction defects and death in mice
-
Mounkes L.C., Kozlov S.V., Rottman J.N., Stewart C.L. Expression of an LMNA-N195K variant of A-type lamins results in cardiac conduction defects and death in mice. Hum Mol Genet 2005, 14:2167-2180.
-
(2005)
Hum Mol Genet
, vol.14
, pp. 2167-2180
-
-
Mounkes, L.C.1
Kozlov, S.V.2
Rottman, J.N.3
Stewart, C.L.4
-
85
-
-
0030923192
-
K- and N-Ras are geranylgeranylated in cells treated with farnesyl protein transferase inhibitors
-
Whyte D.B., et al. K- and N-Ras are geranylgeranylated in cells treated with farnesyl protein transferase inhibitors. J Biol Chem 1997, 272:14459-14464.
-
(1997)
J Biol Chem
, vol.272
, pp. 14459-14464
-
-
Whyte, D.B.1
-
86
-
-
33748760066
-
Farnesylated lamins, progeroid syndromes and farnesyl transferase inhibitors
-
Rusinol A.E., Sinensky M.S. Farnesylated lamins, progeroid syndromes and farnesyl transferase inhibitors. J Cell Sci 2006, 119:3265-3272.
-
(2006)
J Cell Sci
, vol.119
, pp. 3265-3272
-
-
Rusinol, A.E.1
Sinensky, M.S.2
-
87
-
-
77952306898
-
Genetic studies on the functional relevance of the protein prenyltransferases in skin keratinocytes
-
Lee R., et al. Genetic studies on the functional relevance of the protein prenyltransferases in skin keratinocytes. Hum Mol Genet 2010, 19:1603-1617.
-
(2010)
Hum Mol Genet
, vol.19
, pp. 1603-1617
-
-
Lee, R.1
-
88
-
-
46849106102
-
Combined treatment with statins and aminobisphosphonates extends longevity in a mouse model of human premature aging
-
Varela I., et al. Combined treatment with statins and aminobisphosphonates extends longevity in a mouse model of human premature aging. Nat Med 2008, 14:767-772.
-
(2008)
Nat Med
, vol.14
, pp. 767-772
-
-
Varela, I.1
-
89
-
-
63449124344
-
Increasing the length of progerin's isoprenyl anchor does not worsen bone disease or survival in mice with Hutchinson-Gilford progeria syndrome
-
Davies B.S., et al. Increasing the length of progerin's isoprenyl anchor does not worsen bone disease or survival in mice with Hutchinson-Gilford progeria syndrome. J Lipid Res 2009, 50:126-134.
-
(2009)
J Lipid Res
, vol.50
, pp. 126-134
-
-
Davies, B.S.1
-
90
-
-
77950904083
-
Targeting the protein prenyltransferases efficiently reduces tumor development in mice with K-RAS-induced lung cancer
-
Liu M., et al. Targeting the protein prenyltransferases efficiently reduces tumor development in mice with K-RAS-induced lung cancer. Proc Natl Acad Sci USA 2010, 107:6471-6476.
-
(2010)
Proc Natl Acad Sci USA
, vol.107
, pp. 6471-6476
-
-
Liu, M.1
-
91
-
-
0025362748
-
Isoprenylation is required for the processing of the lamin A precursor
-
Beck L.A., Hosick T.J., Sinensky M. Isoprenylation is required for the processing of the lamin A precursor. J Cell Biol 1990, 110:1489-1499.
-
(1990)
J Cell Biol
, vol.110
, pp. 1489-1499
-
-
Beck, L.A.1
Hosick, T.J.2
Sinensky, M.3
-
92
-
-
0026559677
-
Nucleoplasmic localization of prelamin A: implications for prenylation-dependent lamin A assembly into the nuclear lamina
-
Lutz R.J., Trujillo M.A., Denham K.S., Wenger L., Sinensky M. Nucleoplasmic localization of prelamin A: implications for prenylation-dependent lamin A assembly into the nuclear lamina. Proc Natl Acad Sci USA 1992, 89:3000-3004.
-
(1992)
Proc Natl Acad Sci USA
, vol.89
, pp. 3000-3004
-
-
Lutz, R.J.1
Trujillo, M.A.2
Denham, K.S.3
Wenger, L.4
Sinensky, M.5
-
93
-
-
0024839672
-
Modification of nuclear lamin proteins by a mevalonic acid derivative occurs in reticulocyte lysates and requires the cysteine residue of the C-terminal CXXM motif
-
Vorburger K., Kitten G.T., Nigg E.A. Modification of nuclear lamin proteins by a mevalonic acid derivative occurs in reticulocyte lysates and requires the cysteine residue of the C-terminal CXXM motif. EMBO J 1989, 8:4007-4013.
-
(1989)
EMBO J
, vol.8
, pp. 4007-4013
-
-
Vorburger, K.1
Kitten, G.T.2
Nigg, E.A.3
-
94
-
-
0024828257
-
Maturation of nuclear lamin A involves a specific carboxy-terminal trimming, which removes the polyisoprenylation site from the precursor; implications for the structure of the nuclear lamina
-
Weber K., Plessmann U., Traub P. Maturation of nuclear lamin A involves a specific carboxy-terminal trimming, which removes the polyisoprenylation site from the precursor; implications for the structure of the nuclear lamina. FEBS Lett 1989, 257:411-414.
-
(1989)
FEBS Lett
, vol.257
, pp. 411-414
-
-
Weber, K.1
Plessmann, U.2
Traub, P.3
-
95
-
-
0028274845
-
The role of isoprenylation in membrane attachment of nuclear lamins. A single point mutation prevents proteolytic cleavage of the lamin A precursor and confers membrane binding properties
-
Hennekes H., Nigg E.A. The role of isoprenylation in membrane attachment of nuclear lamins. A single point mutation prevents proteolytic cleavage of the lamin A precursor and confers membrane binding properties. J Cell Sci 1994, 107(Pt 4):1019-1029.
-
(1994)
J Cell Sci
, vol.107
, Issue.PART 4
, pp. 1019-1029
-
-
Hennekes, H.1
Nigg, E.A.2
|