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Diseases of the nuclear envelope

Cold Spring Harbor perspectives in biology, 2010-02, Vol.2 (2), p.a000760-a000760

2010

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Dynamics and molecular interactions of linker of nucleoskeleton and cytoskeleton (LINC) complex proteins

Journal of cell science, 2009-11, Vol.122 (22), p.4099-4108

2009

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Imbalanced nucleocytoskeletal connections create common polarity defects in progeria and physiological aging

Proceedings of the National Academy of Sciences - PNAS, 2019-02, Vol.116 (9), p.3578-3583

2019

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Lamin A variants that cause striated muscle disease are defective in anchoring transmembrane actin-associated nuclear lines for nuclear movement

Proceedings of the National Academy of Sciences - PNAS, 2011-01, Vol.108 (1), p.131-136

2011

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Hepatocytes Deficient in Nuclear Envelope Protein Lamina-associated Polypeptide 1 are an Ideal Mammalian System to Study Intranuclear Lipid Droplets

Journal of lipid research, 2022-10, Vol.63 (10), p.100277-100277, Article 100277

2022

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Pathogenic mutations in genes encoding nuclear envelope proteins and defective nucleocytoplasmic connections

Experimental Biology and Medicine, 2019-11, Vol.244 (15), p.1333-1344

2019

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Nuclear envelope-localized torsinA-LAP1 complex regulates hepatic VLDL secretion and steatosis

The Journal of clinical investigation, 2019-11, Vol.129 (11), p.4885-4900

2019

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The Nuclear Envelope in Lipid Metabolism and Pathogenesis of NAFLD

Biology (Basel, Switzerland), 2020-10, Vol.9 (10), p.338

2020

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A mutation abolishing the ZMPSTE24 cleavage site in prelamin A causes a progeroid disorder

Journal of cell science, 2016-05, Vol.129 (10), p.1975-1980

2016

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Linker of nucleoskeleton and cytoskeleton (LINC) complex-mediated actin-dependent nuclear positioning orients centrosomes in migrating myoblasts

Nucleus (Austin, Tex.), 2015-01, Vol.6 (1), p.77-88

2015

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Properties of lamin A mutants found in Emery-Dreifuss muscular dystrophy, cardiomyopathy and Dunnigan-type partial lipodystrophy

Journal of cell science, 2001-12, Vol.114 (Pt 24), p.4435-4445

2001

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Inhibition of TGF-β signaling at the nuclear envelope: characterization of interactions between MAN1, Smad2 and Smad3, and PPM1A

Science signaling, 2013-06, Vol.6 (280), p.ra49

2013

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Loss of a DNA binding site within the tail of prelamin A contributes to altered heterochromatin anchorage by progerin

FEBS letters, 2010-07, Vol.584 (14), p.2999-3004

2010

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The Ig-like Structure of the C-Terminal Domain of Lamin A/C, Mutated in Muscular Dystrophies, Cardiomyopathy, and Partial Lipodystrophy

Structure (London), 2002-06, Vol.10 (6), p.811-823

2002

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Dependence of Diffusional Mobility of Integral Inner Nuclear Membrane Proteins on A-Type Lamins

Biochemistry (Easton), 2006-02, Vol.45 (5), p.1374-1382

2006

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The Carboxyl-Terminal Region Common to Lamins A and C Contains a DNA Binding Domain

Biochemistry (Easton), 2003-05, Vol.42 (17), p.4819-4828

2003

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Subcellular localization of SREBP1 depends on its interaction with the C-terminal region of wild-type and disease related A-type lamins

Experimental cell research, 2011-12, Vol.317 (20), p.2800-2813

2011

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Nuclear envelope proteins and neuromuscular diseases

Muscle & nerve, 2003-04, Vol.27 (4), p.393-406

2003

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Muscular Dystrophy Mutations Impair the Nuclear Envelope Emerin Self-assembly Properties

ACS chemical biology, 2015-12, Vol.10 (12), p.2733-2742

2015

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Blocking protein farnesylation improves nuclear shape abnormalities in keratinocytes of mice expressing the prelamin A variant in Hutchinson-Gilford progeria syndrome

Nucleus (Austin, Tex.), 2010-09, Vol.1 (5), p.432-439

2010

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Effect of pathogenic mis-sense mutations in lamin A on its interaction with emerin in vivo

Journal of cell science, 2003-07, Vol.116 (Pt 14), p.3027-3035

2003

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Expression of Lamin A Mutated in the Carboxyl-Terminal Tail Generates an Aberrant Nuclear Phenotype Similar to That Observed in Cells from Patients with Dunnigan-Type Partial Lipodystrophy and Emery-Dreifuss Muscular Dystrophy

Experimental cell research, 2003, Vol.282 (1), p.14-23

2003

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Blocking farnesylation of the prelamin A variant in Hutchinson-Gilford progeria syndrome alters the distribution of A-type lamins

Nucleus (Austin, Tex.), 2012-09, Vol.3 (5), p.452-462

2012

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Intracellular trafficking of emerin, the Emery-Dreifuss muscular dystrophy protein

Journal of cell science, 1999-06, Vol.112 ( Pt 11) (11), p.1709-1719

1999

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The R439C mutation in LMNA causes lamin oligomerization and susceptibility to oxidative stress

Journal of cellular and molecular medicine, 2009-05, Vol.13 (5), p.959-971

2009

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Diseases of the nuclear envelope

Dynamics and molecular interactions of linker of nucleoskeleton and cytoskeleton (LINC) complex proteins

Imbalanced nucleocytoskeletal connections create common polarity defects in progeria and physiological aging

Lamin A variants that cause striated muscle disease are defective in anchoring transmembrane actin-associated nuclear lines for nuclear movement

Hepatocytes Deficient in Nuclear Envelope Protein Lamina-associated Polypeptide 1 are an Ideal Mammalian System to Study Intranuclear Lipid Droplets

Pathogenic mutations in genes encoding nuclear envelope proteins and defective nucleocytoplasmic connections

Nuclear envelope-localized torsinA-LAP1 complex regulates hepatic VLDL secretion and steatosis

The Nuclear Envelope in Lipid Metabolism and Pathogenesis of NAFLD

A mutation abolishing the ZMPSTE24 cleavage site in prelamin A causes a progeroid disorder

Linker of nucleoskeleton and cytoskeleton (LINC) complex-mediated actin-dependent nuclear positioning orients centrosomes in migrating myoblasts

Properties of lamin A mutants found in Emery-Dreifuss muscular dystrophy, cardiomyopathy and Dunnigan-type partial lipodystrophy

Inhibition of TGF-β signaling at the nuclear envelope: characterization of interactions between MAN1, Smad2 and Smad3, and PPM1A

Loss of a DNA binding site within the tail of prelamin A contributes to altered heterochromatin anchorage by progerin

The Ig-like Structure of the C-Terminal Domain of Lamin A/C, Mutated in Muscular Dystrophies, Cardiomyopathy, and Partial Lipodystrophy

Dependence of Diffusional Mobility of Integral Inner Nuclear Membrane Proteins on A-Type Lamins

The Carboxyl-Terminal Region Common to Lamins A and C Contains a DNA Binding Domain

Subcellular localization of SREBP1 depends on its interaction with the C-terminal region of wild-type and disease related A-type lamins

Nuclear envelope proteins and neuromuscular diseases

Muscular Dystrophy Mutations Impair the Nuclear Envelope Emerin Self-assembly Properties

Blocking protein farnesylation improves nuclear shape abnormalities in keratinocytes of mice expressing the prelamin A variant in Hutchinson-Gilford progeria syndrome

Effect of pathogenic mis-sense mutations in lamin A on its interaction with emerin in vivo

Expression of Lamin A Mutated in the Carboxyl-Terminal Tail Generates an Aberrant Nuclear Phenotype Similar to That Observed in Cells from Patients with Dunnigan-Type Partial Lipodystrophy and Emery-Dreifuss Muscular Dystrophy

Blocking farnesylation of the prelamin A variant in Hutchinson-Gilford progeria syndrome alters the distribution of A-type lamins

Intracellular trafficking of emerin, the Emery-Dreifuss muscular dystrophy protein

The R439C mutation in LMNA causes lamin oligomerization and susceptibility to oxidative stress

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