Frataxin knockdown causes loss of cytoplasmic iron–sulfur cluster functions, redox alterations and induction of heme transcripts
- 4 October 2006
- journal article
- Published by Elsevier in Archives of Biochemistry and Biophysics
- Vol. 457 (1), 111-122
- https://doi.org/10.1016/j.abb.2006.09.010
Abstract
No abstract availableKeywords
This publication has 55 references indexed in Scilit:
- GAA repeat expansion mutation mouse models of Friedreich ataxia exhibit oxidative stress leading to progressive neuronal and cardiac pathologyGenomics, 2006
- Mitochondrial disease activates transcripts of the unfolded protein response and cell cycle and inhibits vesicular secretion and oligodendrocyte-specific transcriptsMitochondrion, 2006
- Frataxin, Iron–Sulfur Clusters, Heme, ROS, and AgingAntioxidants and Redox Signaling, 2006
- ATF3 expression precedes death of spinal motoneurons in amyotrophic lateral sclerosis‐SOD1 transgenic mice and correlates with c‐Jun phosphorylation, CHOP expression, somato‐dendritic ubiquitination and Golgi fragmentationEuropean Journal of Neuroscience, 2005
- Extra-mitochondrial localisation of frataxin and its association with IscU1 during enterocyte-like differentiation of the human colon adenocarcinoma cell line Caco-2Journal of Cell Science, 2005
- Heightened stress response in primary fibroblasts expressing mutant eIF2B genes from CACH/VWM leukodystrophy patientsHuman Genetics, 2005
- An Integrated Stress Response Regulates Amino Acid Metabolism and Resistance to Oxidative StressMolecular Cell, 2003
- Aconitase and mitochondrial iron–sulphur protein deficiency in Friedreich ataxiaNature Genetics, 1997
- Respiratory deficiency due to loss of mitochondrial DNA in yeast lacking the frataxin homologueNature Genetics, 1997
- The little imitator--porphyria: a neuropsychiatric disorder.Journal of Neurology, Neurosurgery & Psychiatry, 1997