Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome. - Test2 - elhamkhani - TriplyDB

Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome.

Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome.

http://www.wikidata.org/entity/Q33847777

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Progeria: a rare genetic premature ageing disorder The FNTB promoter polymorphism rs11623866 as a potential predictive biomarker for lonafarnib treatment of ovarian cancer patients.Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype How Research on Human Progeroid and Antigeroid Syndromes Can Contribute to the Longevity Dividend Initiative Drug screening on Hutchinson Gilford progeria pluripotent stem cells reveals aminopyrimidines as new modulators of farnesylation.Tipifarnib prevents development of hypoxia-induced pulmonary hypertension.Metformin decreases progerin expression and alleviates pathological defects of Hutchinson-Gilford progeria syndrome cells.DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome.Preventing farnesylation of the dynein adaptor Spindly contributes to the mitotic defects caused by farnesyltransferase inhibitors.Nesprin-2G, a Component of the Nuclear LINC Complex, Is Subject to Myosin-Dependent Tension.Modulation of LMNA splicing as a strategy to treat prelamin A diseases.Prelamin A processing, accumulation and distribution in normal cells and laminopathy disorders.Clinical Trial of the Protein Farnesylation Inhibitors Lonafarnib, Pravastatin, and Zoledronic Acid in Children With Hutchinson-Gilford Progeria Syndrome Cardiac electrical defects in progeroid mice and Hutchinson-Gilford progeria syndrome patients with nuclear lamina alterations.Comparing lamin proteins post-translational relative stability using a 2A peptide-based system reveals elevated resistance of progerin to cellular degradation.A novel somatic mutation achieves partial rescue in a child with Hutchinson-Gilford progeria syndrome.Nuclear lamina remodelling and its implications for human disease.Hutchinson-Gilford Progeria Syndrome: A Premature Aging Disease.Speeding up the clock: The past, present and future of progeria.The nuclear lamina in health and disease.Hutchinson-Gilford Progeria Syndrome: A premature aging disease caused by LMNA gene mutations.Arterial Calcification in Diabetes Mellitus: Preclinical Models and Translational Implications.Exploring the biochemistry of the prenylome and its role in disease through proteomics: progress and potential.Progerin impairs chromosome maintenance by depleting CENP-F from metaphase kinetochores in Hutchinson-Gilford progeria fibroblasts.Vitamin D receptor signaling improves Hutchinson-Gilford progeria syndrome cellular phenotypes.MG132-induced progerin clearance is mediated by autophagy activation and splicing regulation.Vascular Aging: Implications for Cardiovascular Disease and Therapy.Intermittent treatment with farnesyltransferase inhibitor and sulforaphane improves cellular homeostasis in Hutchinson-Gilford progeria fibroblasts.Seeking a Cure for One of the Rarest Diseases: Progeria.The decision-making process and criteria in selecting candidate drugs for progeria clinical trials.An encouraging progress report on the treatment of progeria and its implications for atherogenesis.Metformin alleviates ageing cellular phenotypes in Hutchinson-Gilford progeria syndrome dermal fibroblasts.Heart rate reduction and longevity in mice.Computational Exploration for Lead Compounds That Can Reverse the Nuclear Morphology in Progeria.Protein Lipidation: Occurrence, Mechanisms, Biological Functions, and Enabling Technologies.Emerging candidate treatment strategies for Hutchinson-Gilford progeria syndrome.Shared molecular and cellular mechanisms of premature ageing and ageing-associated diseases.Farnesyltransferase inhibitors prevent HIV protease inhibitor (lopinavir/ritonavir)-induced lipodystrophy and metabolic syndrome in mice.The clinical characteristics of Asian patients with classical-type Hutchinson-Gilford progeria syndrome.Vascular Smooth Muscle-Specific Progerin Expression Accelerates Atherosclerosis and Death in a Mouse Model of Hutchinson-Gilford Progeria Syndrome.

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Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome.

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Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome.

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Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome.

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Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome.

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Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome.

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Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome.

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Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome

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Joe Massaro

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Leslie B Gordon

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Monica E Kleinman

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Progeria Clinical Trials Collaborative

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Ralph B D'Agostino

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Susan E Campbell

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W Ted Brown

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P2860

Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome

Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome

Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome

Phenotype and course of Hutchinson-Gilford progeria syndrome

Neurologic features of Hutchinson-Gilford progeria syndrome after lonafarnib treatment

A farnesyltransferase inhibitor prevents both the onset and late progression of cardiovascular disease in a progeria mouse model

Lamin A-dependent nuclear defects in human aging

Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome

Nuclear lamins: laminopathies and their role in premature ageing.

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

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