نتایج جستجو برای: fxn gene

تعداد نتایج: 1141411  

Journal: :Parkinsonism & related disorders 2014
Emil Ygland Franco Taroni Cinzia Gellera Serena Caldarazzo Morten Duno Maria Soller Andreas Puschmann

BACKGROUND Compound heterozygosity for a trinucleotide repeat expansion and a point mutation in the FXN gene is a rare cause of Friedreich ataxia (FRDA). METHODS We identified three Swedish FRDA patients with an FXN p.R165P missense mutation and compared their clinical features with six homozygote trinucleotide repeat expansion carriers. Patients were assessed clinically. Trinucleotide expans...

Journal: :The Lancet 2014
David R Lynch Kenneth H Fischbeck

Friedreich’s ataxia is an autosomal recessive neurodegenerative disorder caused by mutations in the frataxin gene (FXN), leading to progressive ataxia, cardiomyopathy, scoliosis, and various other clinical features. Most patients have GAA repeat expansions in intron 1 of FXN, leading to decreased concentrations of frataxin protein and downstream mitochondrial dysfunction. The GAA repeats lead t...

2016
Abd-Elgawad Radi Nadia Abd El-Ghany Tarek Wahdan

A novel electrochemical sensing approach, based on electropolymerization of a molecularly imprinted polypyrrole (MIPpy) film onto a glassy carbon electrode (GCE) surface, was developed for the detection of flunixin (FXN). The sensing conditions and the performance of the constructed sensor were assessed by cyclic, differential pulse and (DPV) square wave voltammetry (SWV). The sensor exhibited ...

2013
Cláudio M. Gomes Renata Santos

Friedreich's ataxia is the most common inherited autosomal recessive ataxia and is characterized by progressive degeneration of the peripheral and central nervous systems and cardiomyopathy. This disease is caused by the silencing of the FXN gene and reduced levels of the encoded protein, frataxin. Frataxin is a mitochondrial protein that functions primarily in iron-sulfur cluster synthesis. Th...

2014
Wei-Shih Du

and Applied Analysis 3 (w3) for any ε > 0, there exists δ > 0 such that p(z, x) ≤ δ and p(z, y) ≤ δ imply d(x, y) ≤ ε. A function p : X×X → [0,∞) is said to be a τ-function [5, 10, 14, 15, 27–29], first introduced and studied by Lin and Du, if the following conditions hold: (τ1) p(x, z) ≤ p(x, y) + p(y, z) for all x, y, z ∈ X; (τ2) if x ∈ X and {yn} in X with limn→∞yn = y such that p(x, yn) ≤ M...

Journal: :American journal of physiology. Heart and circulatory physiology 2015
Shravanthi Mouli Gayani Nanayakkara Abdullah AlAlasmari Haitham Eldoumani Xiaoyu Fu Avery Berlin Madhukar Lohani Ben Nie Robert D Arnold Andreas Kavazis Forrest Smith Ronald Beyers Thomas Denney Muralikrishnan Dhanasekaran Juming Zhong John Quindry Rajesh Amin

Doxorubicin (DOX) is a highly effective anti-neoplastic agent; however, its cumulative dosing schedules are clinically limited by the development of cardiotoxicity. Previous studies have attributed the cause of DOX-mediated cardiotoxicity to mitochondrial iron accumulation and the ensuing reactive oxygen species (ROS) formation. The present study investigates the role of frataxin (FXN), a mitoc...

2018
Elena Britti Fabien Delaspre Anat Feldman Melissa Osborne Hagar Greif Jordi Tamarit Joaquim Ros

Friedreich ataxia (FA) is a rare disease caused by deficiency of frataxin, a mitochondrial protein. As there is no cure available for this disease, many strategies have been developed to reduce the deleterious effects of such deficiency. One of these approaches is based on delivering frataxin to the tissues by coupling the protein to trans-activator of transcription (TAT) peptides, which enable...

Journal: :The Lancet 2014
Vincenzo Libri Cihangir Yandim Stavros Athanasopoulos Naomi Loyse Theona Natisvili Pui Pik Law Ping Kei Chan Tariq Mohammad Marta Mauri Kin Tung Tam James Leiper Sophie Piper Aravind Ramesh Michael H Parkinson Les Huson Paola Giunti Richard Festenstein

BACKGROUND Friedreich's ataxia is a progressive degenerative disorder caused by deficiency of the frataxin protein. Expanded GAA repeats within intron 1 of the frataxin (FXN) gene lead to its heterochromatinisation and transcriptional silencing. Preclinical studies have shown that the histone deacetylase inhibitor nicotinamide (vitamin B3) can remodel the pathological heterochromatin and upregu...

2015
Jill Sergesketter Butler Marek Napierala

Reduced expression of the mitochondrial protein Frataxin (FXN) is the underlying cause of Friedreich's ataxia. We propose a model of premature termination of FXN transcription induced by pathogenic expanded GAA repeats that links R-loop structures, antisense transcription, and heterochromatin formation as a novel mechanism of transcriptional repression in Friedreich's ataxia.

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