Regulation of mitochondrial iron accumulation by Yfh1p, a putative homolog of frataxin.

by: M Babcock, D de Silva, R Oaks, S Davis-Kaplan, S Jiralerspong, L Montermini, M Pandolfo, J Kaplan

Science (New York, N.Y.), Vol. 276, No. 5319. (13 June 1997), pp. 1709-1712.

View FullText article

Pubmed, Hubmed, WormBase

Reviews [Write a review of this article]

There are no reviews of this article

Find related articles from these CiteULike users

C. elegans / WormBase (group), tharris, giovanni

Find related articles with these CiteULike tags

article, caenorhabditis_elegans, celegans, c_elegans, elegans, frda, nematode, wormbase

Abstract

The gene responsible for Friedreich's ataxia, a disease characterized by neurodegeneration and cardiomyopathy, has recently been cloned and its product designated frataxin. A gene in Saccharomyces cerevisiae was characterized whose predicted protein product has high sequence similarity to the human frataxin protein. The yeast gene (yeast frataxin homolog, YFH1) encodes a mitochondrial protein involved in iron homeostasis and respiratory function. Human frataxin also was shown to be a mitochondrial protein. Characterizing the mechanism by which YFH1 regulates iron homeostasis in yeast may help to define the pathologic process leading to cell damage in Friedreich's ataxia.

@article{citeulike:2959130, abstract = {The gene responsible for Friedreich's ataxia, a disease characterized by neurodegeneration and cardiomyopathy, has recently been cloned and its product designated frataxin. A gene in Saccharomyces cerevisiae was characterized whose predicted protein product has high sequence similarity to the human frataxin protein. The yeast gene (yeast frataxin homolog, YFH1) encodes a mitochondrial protein involved in iron homeostasis and respiratory function. Human frataxin also was shown to be a mitochondrial protein. Characterizing the mechanism by which YFH1 regulates iron homeostasis in yeast may help to define the pathologic process leading to cell damage in Friedreich's ataxia.}, address = {Department of Pathology, School of Medicine, University of Utah, Salt Lake City, UT 84132, USA.}, author = {Babcock, M. and de Silva, D. and Oaks, R. and Davis-Kaplan, S. and Jiralerspong, S. and Montermini, L. and Pandolfo, M. and Kaplan, J. }, citeulike-article-id = {2959130}, issn = {0036-8075}, journal = {Science (New York, N.Y.)}, keywords = {frda}, month = {June}, number = {5319}, pages = {1709--1712}, posted-at = {2008-07-03 13:32:33}, priority = {2}, title = {Regulation of mitochondrial iron accumulation by Yfh1p, a putative homolog of frataxin.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/9180083}, volume = {276}, year = {1997} }

RIS record

TY - JOUR ID - citeulike:2959130 L3 - citeulike-article-id:2959130 TI - Regulation of mitochondrial iron accumulation by Yfh1p, a putative homolog of frataxin. JF - Science (New York, N.Y.) VL - 276 IS - 5319 SP - 1709 EP - 1712 AD - Department of Pathology, School of Medicine, University of Utah, Salt Lake City, UT 84132, USA. SN - 0036-8075 N2 - The gene responsible for Friedreich's ataxia, a disease characterized by neurodegeneration and cardiomyopathy, has recently been cloned and its product designated frataxin. A gene in Saccharomyces cerevisiae was characterized whose predicted protein product has high sequence similarity to the human frataxin protein. The yeast gene (yeast frataxin homolog, YFH1) encodes a mitochondrial protein involved in iron homeostasis and respiratory function. Human frataxin also was shown to be a mitochondrial protein. Characterizing the mechanism by which YFH1 regulates iron homeostasis in yeast may help to define the pathologic process leading to cell damage in Friedreich's ataxia. KW - frda AU - Babcock, M AU - de Silva, D AU - Oaks, R AU - Davis-Kaplan, S AU - Jiralerspong, S AU - Montermini, L AU - Pandolfo, M AU - Kaplan, J PY - 1997/06/13/ UR - http://view.ncbi.nlm.nih.gov/pubmed/9180083 ER -

RIS BibTeX