Clinical trial of a farnesyltransferase inhibitor in children with Hutchinson-Gilford progeria syndrome. - Test2 - elhamkhani - TriplyDB

Clinical trial of a farnesyltransferase inhibitor in children with Hutchinson-Gilford progeria syndrome.

Clinical trial of a farnesyltransferase inhibitor in children with Hutchinson-Gilford progeria syndrome.

http://www.wikidata.org/entity/Q34033699

about

Progeria: a rare genetic premature ageing disorder Targeting protein prenylation in progeria Neurologic features of Hutchinson-Gilford progeria syndrome after lonafarnib treatment The epidemiology of premature aging and associated comorbidities Hallmarks of progeroid syndromes: lessons from mice and reprogrammed cells Molecular insights into the premature aging disease progeria When lamins go bad: nuclear structure and disease Post-translational modifications of intermediate filament proteins: mechanisms and functions The nuclear envelope: an intriguing focal point for neurogenetic disease Recent advances in understanding the role of lamins in health and disease Interruption of progerin-lamin A/C binding ameliorates Hutchinson-Gilford progeria syndrome phenotype Farnesylation of lamin B1 is important for retention of nuclear chromatin during neuronal migration.Drug screening on Hutchinson Gilford progeria pluripotent stem cells reveals aminopyrimidines as new modulators of farnesylation.DNA damage and lamins Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome.Metformin decreases progerin expression and alleviates pathological defects of Hutchinson-Gilford progeria syndrome cells.Initial cutaneous manifestations of Hutchinson-Gilford progeria syndrome Origin of product selectivity in a prenyl transfer reaction from the same intermediate: exploration of multiple FtmPT1-catalyzed prenyl transfer pathways.Computed tomography-based rigidity analysis: a review of the approach in preclinical and clinical studies.DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome.A mutation abolishing the ZMPSTE24 cleavage site in prelamin A causes a progeroid disorder Rapamycin treatment of Mandibuloacral dysplasia cells rescues localization of chromatin-associated proteins and cell cycle dynamics Protein prenylation: enzymes, therapeutics, and biotechnology applications.Transformation by Hras(G12V) is consistently associated with mutant allele copy gains and is reversed by farnesyl transferase inhibition.Gene-rich chromosomal regions are preferentially localized in the lamin B deficient nuclear blebs of atypical progeria cells.Oral prenylation inhibition with lonafarnib in chronic hepatitis D infection: a proof-of-concept randomised, double-blind, placebo-controlled phase 2A trial.All-trans retinoic acid and rapamycin normalize Hutchinson Gilford progeria fibroblast phenotype.Correlated alterations in genome organization, histone methylation, and DNA-lamin A/C interactions in Hutchinson-Gilford progeria syndrome.mTORC1 and p53: clash of the gods?Modulation of LMNA splicing as a strategy to treat prelamin A diseases.Cell Mechanosensitivity is Enabled by the LINC Nuclear Complex.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 How to Target Activated Ras Proteins: Direct Inhibition vs. Induced Mislocalization.Reflections on a life in biomedicine: leading change Progeroid syndrome patients with ZMPSTE24 deficiency could benefit when treated with rapamycin and dimethylsulfoxide Comparing lamin proteins post-translational relative stability using a 2A peptide-based system reveals elevated resistance of progerin to cellular degradation.Broken nuclei--lamins, nuclear mechanics, and disease.Induced pluripotent stem cells reveal functional differences between drugs currently investigated in patients with hutchinson-gilford progeria syndrome.Mechanisms of Chromosome Congression during Mitosis.

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Clinical trial of a farnesyltransferase inhibitor in children with Hutchinson-Gilford progeria syndrome.

http://www.wikidata.org/entity/Q34033699

description

2012 nî lūn-bûn

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2012 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

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2012 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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Clinical trial of a farnesyltr ...... son-Gilford progeria syndrome.

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Clinical trial of a farnesyltr ...... son-Gilford progeria syndrome.

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PNAS.1202529109

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Proceedings of the National Academy of Sciences of the United States of America

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Clinical trial of a farnesyltr ...... son-Gilford progeria syndrome.

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Amy Regen

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Anita Giobbie-Hurder

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Annette Correia

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Ara Nazarian

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Brian D Snyder

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Brian Fligor

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Catherine M Gordon

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Christine Ploski

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David T Miller

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Donna S Neuberg

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P2860

The cell nucleus and aging: tantalizing clues and hopeful promises

The mutant form of lamin A that causes Hutchinson-Gilford progeria is a biomarker of cellular aging in human skin

Hutchinson-Gilford progeria mutant lamin A primarily targets human vascular cells as detected by an anti-Lamin A G608G antibody.

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

Phenotype and course of Hutchinson-Gilford progeria syndrome

Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts

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

Predicting basal metabolic rate, new standards and review of previous work

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109

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Armin Schwartzman

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