Mechanisms of Cardiovascular Disease in Accelerated Aging Syndromes
暂无分享,去创建一个
[1] T. Shimi,et al. Alterations in mitosis and cell cycle progression caused by a mutant lamin A known to accelerate human aging , 2007, Proceedings of the National Academy of Sciences.
[2] Francis S. Collins,et al. A lamin A protein isoform overexpressed in Hutchinson–Gilford progeria syndrome interferes with mitosis in progeria and normal cells , 2007, Proceedings of the National Academy of Sciences.
[3] A. Jauch,et al. Telomere dysfunction as a cause of genomic instability in Werner syndrome , 2007, Proceedings of the National Academy of Sciences.
[4] V. Bohr,et al. The role of WRN in DNA repair is affected by post-translational modifications , 2007, Mechanisms of Ageing and Development.
[5] J. Hoeijmakers,et al. A new progeroid syndrome reveals that genotoxic stress suppresses the somatotroph axis , 2006, Nature.
[6] Francis S. Collins,et al. Human laminopathies: nuclei gone genetically awry , 2006, Nature Reviews Genetics.
[7] R. Hennekam. Hutchinson–Gilford progeria syndrome: Review of the phenotype , 2006, American journal of medical genetics. Part A.
[8] V. Andrés,et al. Telomere Biology and Cardiovascular Disease , 2006, Circulation research.
[9] Y. Zou,et al. DNA damage responses in progeroid syndromes arise from defective maturation of prelamin A , 2006, Journal of Cell Science.
[10] John F. Robinson,et al. Ankyrin G overexpression in Hutchinson-Gilford progeria syndrome fibroblasts identified through biological filtering of expression profiles , 2006, Journal of Human Genetics.
[11] S. Ellard,et al. The laminopathies: a clinical review , 2006, Clinical genetics.
[12] J. Campisi,et al. Ageing: Balancing regeneration and cancer , 2006, Nature.
[13] Richard T. Lee,et al. Lamins A and C but Not Lamin B1 Regulate Nuclear Mechanics* , 2006, Journal of Biological Chemistry.
[14] F. Collins,et al. Progressive vascular smooth muscle cell defects in a mouse model of Hutchinson-Gilford progeria syndrome. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[15] D. Levy,et al. Insulin resistance, oxidative stress, hypertension, and leukocyte telomere length in men from the Framingham Heart Study , 2006, Aging cell.
[16] A. Weiss,et al. Aggrecan expression is substantially and abnormally upregulated in Hutchinson–Gilford Progeria Syndrome dermal fibroblasts , 2006, Mechanisms of Ageing and Development.
[17] M. Bergo,et al. A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation. , 2006, The Journal of clinical investigation.
[18] M. Blasco,et al. Mice Deficient in Telomerase Activity Develop Hypertension Because of an Excess of Endothelin Production , 2006, Circulation.
[19] P. Kirkpatrick,et al. Vascular Smooth Muscle Cells Undergo Telomere-Based Senescence in Human Atherosclerosis: Effects of Telomerase and Oxidative Stress , 2006, Circulation research.
[20] Paul Tempst,et al. The transcriptional repressor JHDM3A demethylates trimethyl histone H3 lysine 9 and lysine 36 , 2006, Nature.
[21] T. Misteli,et al. Distinct structural and mechanical properties of the nuclear lamina in Hutchinson–Gilford progeria syndrome , 2006, Proceedings of the National Academy of Sciences.
[22] J. Broers,et al. Nuclear lamins: laminopathies and their role in premature ageing. , 2006, Physiological reviews.
[23] V. Parnaik,et al. Expression of disease-causing lamin A mutants impairs the formation of DNA repair foci , 2006, Journal of Cell Science.
[24] B. Kennedy,et al. Stabilization of the Retinoblastoma Protein by A-Type Nuclear Lamins Is Required for INK4A-Mediated Cell Cycle Arrest , 2006, Molecular and Cellular Biology.
[25] A. Al Haj Zen,et al. Decorin overexpression reduces atherosclerosis development in apolipoprotein E-deficient mice. , 2006, Atherosclerosis.
[26] M. Fraga,et al. Epigenetic inactivation of the premature aging Werner syndrome gene in human cancer. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[27] F. Collins,et al. Mutant nuclear lamin A leads to progressive alterations of epigenetic control in premature aging. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[28] Markus Schuelke,et al. The spectrum of WRN mutations in Werner syndrome patients , 2006, Human mutation.
[29] J. Denecke,et al. A homozygous ZMPSTE24 null mutation in combination with a heterozygous mutation in the LMNA gene causes Hutchinson‐Gilford progeria syndrome (HGPS): insights into the pathophysiology of HGPS , 2006, Human mutation.
[30] T. Misteli,et al. Lamin A-Dependent Nuclear Defects in Human Aging , 2006, Science.
[31] F. Tesson,et al. Lamin A/C and cardiac diseases , 2006, Current opinion in cardiology.
[32] E. Delbarre,et al. The truncated prelamin A in Hutchinson-Gilford progeria syndrome alters segregation of A-type and B-type lamin homopolymers. , 2006, Human molecular genetics.
[33] Stephen G Young,et al. A Protein Farnesyltransferase Inhibitor Ameliorates Disease in a Mouse Model of Progeria , 2006, Science.
[34] J. Sedivy,et al. Cellular Senescence in Aging Primates , 2006, Science.
[35] P. Slagboom,et al. Impact of genetic variations in the WRN gene on age related pathologies and mortality , 2006, Mechanisms of Ageing and Development.
[36] Richard T. Lee,et al. Prelamin A and lamin A appear to be dispensable in the nuclear lamina. , 2006, The Journal of clinical investigation.
[37] É. Thorin,et al. Increased insulin, triglycerides, reactive oxygen species, and cardiac fibrosis in mice with a mutation in the helicase domain of the Werner syndrome gene homologue , 2006, Experimental Gerontology.
[38] M. Brignole,et al. Case 26-2005: loss of consciousness while jogging. , 2006, The New England journal of medicine.
[39] Y. Pinto,et al. Primary prevention of sudden death in patients with lamin A/C gene mutations. , 2006, The New England journal of medicine.
[40] H. Scherthan,et al. Nuclear deformation characterizes Werner syndrome cells , 2005, Cell biology international.
[41] Christopher J. Jones,et al. Prevention of accelerated cell aging in Werner syndrome using a p38 mitogen-activated protein kinase inhibitor. , 2005, The journals of gerontology. Series A, Biological sciences and medical sciences.
[42] Jennifer M. Gardner,et al. Homozygous and compound heterozygous mutations in ZMPSTE24 cause the laminopathy restrictive dermopathy. , 2005, The Journal of investigative dermatology.
[43] G. Novelli,et al. Rescue of heterochromatin organization in Hutchinson-Gilford progeria by drug treatment , 2005, Cellular and Molecular Life Sciences.
[44] M. W. Glynn,et al. Incomplete processing of mutant lamin A in Hutchinson-Gilford progeria leads to nuclear abnormalities, which are reversed by farnesyltransferase inhibition. , 2005, Human molecular genetics.
[45] Joel H. Janes,et al. Correction of cellular phenotypes of Hutchinson-Gilford Progeria cells by RNA interference , 2005, Human Genetics.
[46] M. Gelb,et al. Inhibiting farnesylation reverses the nuclear morphology defect in a HeLa cell model for Hutchinson-Gilford progeria syndrome. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[47] Ignacio Varela,et al. Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation , 2005, Nature.
[48] Karen N Conneely,et al. Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[49] M. Gelb,et al. Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[50] R. Hegele,et al. Genetic and physiological insights into the metabolic syndrome. , 2005, American journal of physiology. Regulatory, integrative and comparative physiology.
[51] J. Rottman,et al. Expression of an LMNA-N195K variant of A-type lamins results in cardiac conduction defects and death in mice. , 2005, Human molecular genetics.
[52] M. Gelb,et al. Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[53] Howard J Worman,et al. Dermal fibroblasts in Hutchinson-Gilford progeria syndrome with the lamin A G608G mutation have dysmorphic nuclei and are hypersensitive to heat stress , 2005, BMC Cell Biology.
[54] David J. Chen,et al. Genomic instability in laminopathy-based premature aging , 2005, Nature Medicine.
[55] C. López-Otín,et al. Loss of ZMPSTE24 (FACE-1) causes autosomal recessive restrictive dermopathy and accumulation of Lamin A precursors. , 2005, Human molecular genetics.
[56] A. Aviv,et al. Rise in Insulin Resistance Is Associated With Escalated Telomere Attrition , 2005, Circulation.
[57] N. Maraldi,et al. Laminopathies: Involvement of structural nuclear proteins in the pathogenesis of an increasing number of human diseases , 2005, Journal of cellular physiology.
[58] Y. Yamaguchi,et al. Overexpression of Hyaluronan in the Tunica Media Promotes the Development of Atherosclerosis , 2005, Circulation research.
[59] M. Patti,et al. Reduced adiponectin and HDL cholesterol without elevated C-reactive protein: clues to the biology of premature atherosclerosis in Hutchinson-Gilford Progeria Syndrome. , 2005, The Journal of pediatrics.
[60] C. Harris,et al. p53 modulates RPA-dependent and RPA-independent WRN helicase activity. , 2005, Cancer research.
[61] F. Tezuka,et al. Electrophysiological and Histopathological Characteristics of Progressive Atrioventricular Block Accompanied by Familial Dilated Cardiomyopathy Caused by a Novel Mutation of Lamin A/C Gene , 2005, Journal of cardiovascular electrophysiology.
[62] M. Bergo,et al. Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[63] R. Verdun,et al. Defective Telomere Lagging Strand Synthesis in Cells Lacking WRN Helicase Activity , 2004, Science.
[64] R. Hennekam,et al. Lamin A and ZMPSTE24 (FACE-1) defects cause nuclear disorganization and identify restrictive dermopathy as a lethal neonatal laminopathy. , 2004, Human molecular genetics.
[65] S. Benedetti,et al. Laminopathies: from the heart of the cell to the clinics , 2004, Current opinion in neurology.
[66] E. Furth,et al. Telomere Shortening Exposes Functions for the Mouse Werner and Bloom Syndrome Genes , 2004, Molecular and Cellular Biology.
[67] K. M. Krishnamoorthy,et al. Hutchinson-Gilford progeria syndrome with severe calcific aortic valve stenosis and calcific mitral valve. , 2004, The Journal of heart valve disease.
[68] C. Reddel,et al. Lamin A expression levels are unperturbed at the normal and mutant alleles but display partial splice site selection in Hutchinson-Gilford progeria syndrome , 2004, Journal of Medical Genetics.
[69] R. Hegele,et al. Laminopathies and Atherosclerosis , 2004, Arteriosclerosis, thrombosis, and vascular biology.
[70] Atul J Butte,et al. Genome‐scale expression profiling of Hutchinson–Gilford progeria syndrome reveals widespread transcriptional misregulation leading to mesodermal/mesenchymal defects and accelerated atherosclerosis , 2004, Aging cell.
[71] R. DePinho,et al. Essential role of limiting telomeres in the pathogenesis of Werner syndrome , 2004, Nature Genetics.
[72] E. Metter,et al. Werner syndrome protein 1367 variants and disposition towards coronary artery disease in Caucasian patients , 2004, Mechanisms of Ageing and Development.
[73] Richard L. Frock,et al. A-type lamins regulate retinoblastoma protein function by promoting subnuclear localization and preventing proteasomal degradation. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[74] Yosef Gruenbaum,et al. Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson–Gilford progeria syndrome , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[75] Y. Pinto,et al. Often seen but rarely recognised: cardiac complications of lamin A/C mutations. , 2004, European heart journal.
[76] V. Bohr,et al. Junction of RecQ Helicase Biochemistry and Human Disease* , 2004, Journal of Biological Chemistry.
[77] T. Ogihara,et al. LMNA mutation in a 45 year old Japanese subject with Hutchinson-Gilford progeria syndrome , 2004, Journal of Medical Genetics.
[78] K. Wilson,et al. Proteins that bind A-type lamins: integrating isolated clues , 2004, Journal of Cell Science.
[79] J. Barrett,et al. Senescing human cells and ageing mice accumulate DNA lesions with unrepairable double-strand breaks , 2004, Nature Cell Biology.
[80] Richard T. Lee,et al. Lamin A/C deficiency causes defective nuclear mechanics and mechanotransduction. , 2004, The Journal of clinical investigation.
[81] D. Orren,et al. TRF2 recruits the Werner syndrome (WRN) exonuclease for processing of telomeric DNA , 2004, Oncogene.
[82] C. Vigouroux,et al. LMNA mutations in atypical Werner's syndrome , 2003, The Lancet.
[83] C. Müller,et al. A synonymous codon change in the LMNA gene alters mRNA splicing and causes limb girdle muscular dystrophy type 1B , 2003, Journal of medical genetics.
[84] A. K. Agarwal,et al. Zinc metalloproteinase, ZMPSTE24, is mutated in mandibuloacral dysplasia. , 2003, Human molecular genetics.
[85] M. Komajda,et al. Expanding the phenotype of LMNA mutations in dilated cardiomyopathy and functional consequences of these mutations , 2003, Journal of medical genetics.
[86] Pierre Cau,et al. Lamin A Truncation in Hutchinson-Gilford Progeria , 2003, Science.
[87] Laura Scott,et al. Recurrent de novo point mutations in lamin A cause Hutchinson–Gilford progeria syndrome , 2003, Nature.
[88] N. Samani,et al. White Cell Telomere Length and Risk of Premature Myocardial Infarction , 2003, Arteriosclerosis, thrombosis, and vascular biology.
[89] Robert M. Bachoo,et al. Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageing , 2003, Nature.
[90] M. Blasco,et al. Ablation of telomerase and telomere loss leads to cardiac dilatation and heart failure associated with p53 upregulation , 2003, The EMBO journal.
[91] N. van Bruggen,et al. Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[92] G. Scarano,et al. Mandibuloacral dysplasia is caused by a mutation in LMNA-encoding lamin A/C. , 2002, American journal of human genetics.
[93] I. Komuro,et al. Endothelial Cell Senescence in Human Atherosclerosis: Role of Telomere in Endothelial Dysfunction , 2002, Circulation.
[94] C. López-Otín,et al. Defective prelamin A processing and muscular and adipocyte alterations in Zmpste24 metalloproteinase–deficient mice , 2002, Nature Genetics.
[95] J. Hoeijmakers,et al. Premature Aging in Mice Deficient in DNA Repair and Transcription , 2002, Science.
[96] Sui Huang,et al. Alteration of nuclear lamin organization inhibits RNA polymerase II–dependent transcription , 2002, The Journal of cell biology.
[97] L. Bonetta. Edible vaccines: not quite ready for prime time , 2002, Nature Medicine.
[98] D. Rader,et al. The adhesion receptor CD44 promotes atherosclerosis by mediating inflammatory cell recruitment and vascular cell activation. , 2001, The Journal of clinical investigation.
[99] C. Stewart,et al. The A-type lamins: nuclear structural proteins as a focus for muscular dystrophy and cardiovascular diseases. , 2001, Trends in cardiovascular medicine.
[100] C. Stewart,et al. The Nuclear Envelope in Muscular Dystrophy and Cardiovascular Diseases , 2001, Traffic.
[101] J. Mendell,et al. Novel and recurrent mutations in lamin A/C in patients with Emery-Dreifuss muscular dystrophy. , 2001, American journal of medical genetics.
[102] N. Samani,et al. Telomere shortening in atherosclerosis , 2001, The Lancet.
[103] B. Delahunt,et al. Smooth muscle cell depletion and collagen types in progeric arteries. , 2001, Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.
[104] A. Shimamoto,et al. Werner helicase relocates into nuclear foci in response to DNA damaging agents and co‐localizes with RPA and Rad51 , 2001, Genes to cells : devoted to molecular & cellular mechanisms.
[105] J. Skurnick,et al. Telomere Length as an Indicator of Biological Aging: The Gender Effect and Relation With Pulse Pressure and Pulse Wave Velocity , 2001, Hypertension.
[106] J. Skurnick,et al. Telomere length inversely correlates with pulse pressure and is highly familial. , 2000, Hypertension.
[107] F. Baas,et al. Identification of mutations in the gene encoding lamins A/C in autosomal dominant limb girdle muscular dystrophy with atrioventricular conduction disturbances (LGMD1B). , 2000, Human molecular genetics.
[108] D. Lockhart,et al. Mitotic misregulation and human aging. , 2000, Science.
[109] L. Mestroni,et al. Lamin A/C gene mutation associated with dilated cardiomyopathy with variable skeletal muscle involvement. , 2000, Circulation.
[110] J. Seidman,et al. Missense mutations in the rod domain of the lamin A/C gene as causes of dilated cardiomyopathy and conduction-system disease. , 1999, The New England journal of medicine.
[111] H. Youssoufian,et al. Werner helicase expression in human fetal and adult aortas , 1999, Experimental Gerontology.
[112] T. Wight,et al. Formation of hyaluronan- and versican-rich pericellular matrix is required for proliferation and migration of vascular smooth muscle cells. , 1999, Arteriosclerosis, thrombosis, and vascular biology.
[113] Sandy Chang,et al. Longevity, Stress Response, and Cancer in Aging Telomerase-Deficient Mice , 1999, Cell.
[114] F. Muntoni,et al. Mutations in the gene encoding lamin A/C cause autosomal dominant Emery-Dreifuss muscular dystrophy , 1999, Nature Genetics.
[115] P. Leder,et al. A deletion within the murine Werner syndrome helicase induces sensitivity to inhibitors of topoisomerase and loss of cellular proliferative capacity. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[116] R. DePinho,et al. Essential role of mouse telomerase in highly proliferative organs , 1998, Nature.
[117] J. Skurnick,et al. Shortened telomere length in white blood cells of patients with IDDM. , 1998, Diabetes.
[118] María A Blasco,et al. Telomere Shortening and Tumor Formation by Mouse Cells Lacking Telomerase RNA , 1997, Cell.
[119] R. Goldman,et al. Disruption of Nuclear Lamin Organization Alters the Distribution of Replication Factors and Inhibits DNA Synthesis , 1997, The Journal of cell biology.
[120] G. Schellenberg,et al. Homozygous and compound heterozygous mutations at the Werner syndrome locus. , 1996, Human molecular genetics.
[121] S Bloom,et al. Intermediate filament-mediated stretch-induced changes in chromatin: a hypothesis for growth initiation in cardiac myocytes. , 1996, Journal of molecular and cellular cardiology.
[122] G. Schellenberg,et al. Positional Cloning of the Werner's Syndrome Gene , 1996, Science.
[123] L. Gerace,et al. A chromatin binding site in the tail domain of nuclear lamins that interacts with core histones , 1995, The Journal of cell biology.
[124] M. Goto,et al. Hypercoagulable State Indicates an Additional Risk Factor for Atherosclerosis in Werner’s Syndrome , 1995, Thrombosis and Haemostasis.
[125] M. I. Melaragno,et al. Cytogenetic aspects of Werner's syndrome lymphocyte cultures , 1995, Mechanisms of Ageing and Development.
[126] M. Pasic,et al. Aortic homograft and mitral valve repair in a patient with Werner's syndrome. , 1994, The Annals of thoracic surgery.
[127] R. Faragher,et al. The expression of proliferation-dependent antigens during the lifespan of normal and progeroid human fibroblasts in culture. , 1994, Journal of cell science.
[128] W. Shim,et al. Cardiovascular findings of Hutchinson-Gilford syndrome--a Doppler and two-dimensional echocardiographic study. , 1993, Yonsei medical journal.
[129] K. Hasel,et al. The alpha‐helical rod domain of human lamins A and C contains a chromatin binding site. , 1993, The EMBO journal.
[130] E. Schönherr,et al. Deficient expression of decorin in infantile progeroid patients. , 1993, The Journal of biological chemistry.
[131] M. Clark,et al. Elevated levels of glycoprotein gp200 in progeria fibroblasts , 1993, Molecular and Cellular Biochemistry.
[132] J. Roujeau,et al. Abnormal gene expression in skin fibroblasts from a Hutchinson-Gilford patient. , 1991, Laboratory investigation; a journal of technical methods and pathology.
[133] B. Labeille,et al. Increased secretion of fibronectin and collagen by progeria (Hutchinson-Gilford) fibroblasts , 1988, European Journal of Pediatrics.
[134] J. Davidson,et al. Increased elastin production by progeria skin fibroblasts is controlled by the steady-state levels of elastin mRNA. , 1988, The Journal of investigative dermatology.
[135] P. Baker,et al. Cardiovascular abnormalities in progeria. Case report and review of the literature. , 1981, Archives of pathology & laboratory medicine.
[136] F L DeBusk,et al. The Hutchinson-Gilford progeria syndrome. Report of 4 cases and review of the literature. , 1972, The Journal of pediatrics.
[137] W. Reichel,et al. Pathologic findings in progeria: myocardial fibrosis and lipofuscin pigment. , 1970, American journal of clinical pathology.
[138] W. Yakovac,et al. Cardiovascular manifestations in progeria. Report of clinical and pathologic findings in a patient with severe arteriosclerotic heart disease and aortic stenosis. , 1962, American heart journal.
[139] M. Hashem,et al. Progeria, a pathologic study. , 1960, The Journal of pediatrics.
[140] R. Agrelo,et al. A new molecular model of cellular aging based on Werner syndrome. , 2007, Medical hypotheses.
[141] D. Pennell,et al. Primary myocardial dysfunction in autosomal dominant EDMD. A tissue doppler and cardiovascular magnetic resonance study. , 2006, Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance.
[142] N. Maraldi,et al. Nuclear envelope proteins and chromatin arrangement: a pathogenic mechanism for laminopathies. , 2006, European journal of histochemistry : EJH.
[143] S. Varnous,et al. Mouse model carrying H222P-Lmna mutation develops muscular dystrophy and dilated cardiomyopathy similar to human striated muscle laminopathies. , 2005, Human molecular genetics.
[144] N. Maraldi,et al. Implications for nuclear organization and gene transcription of lamin A/C specific mutations. , 2005, Advances in enzyme regulation.
[145] F. Pallardó,et al. Multiple Involvement of Oxidative Stress in Werner Syndrome Phenotype , 2005, Biogerontology.
[146] L. Eckel,et al. Severe heart valve calcification in a young patient with Werner syndrome. , 2000, Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.
[147] R. Schekman,et al. Mitotic Misregulation and Human Aging , 2000 .
[148] E. Gilbert-Barness,et al. Histological and ultrastructural features of atherosclerosis in progeria. , 1999, Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.
[149] A. Kupfer,et al. The processing pathway of prelamin A. , 1994, Journal of cell science.
[150] H. Hoehn,et al. Cytogenetics of Werner's syndrome cultured skin fibroblasts: variegated translocation mosaicism. , 1981, Cytogenetics and cell genetics.