Associated Papers
Pathological variants in nuclear genes causing mitochondrial complex III deficiency: An update.
Čunátová K et al.
Journal of Inherited Metabolic Disease, 2024
Are transient protein-protein interactions more dispensable?
Ghadie MA et al.
Plos Computational Biology, 2022
35404956 (PubMed )
Supplement: pcbi.1010013.s002.xlsx › _D__Lit-SI_disMut_edgotypes
Mitochondrial protein dysfunction in pathogenesis of neurological diseases.
Wang L et al.
Frontiers in Molecular Neuroscience, 2022
An Overview of Mitochondrial Protein Defects in Neuromuscular Diseases.
Marra F et al.
Biomolecules, 2021
Mutation Edgotype Drives Fitness Effect in Human.
Ghadie M et al.
Frontiers in Bioinformatics, 2021
36303776 (PubMed )
Supplement: Table2.XLSX › _D__Lit-SI_pathMt_edgotype
Molecular mechanism of mitochondrial respiratory chain assembly and its relation to mitochondrial diseases.
Mukherjee S et al.
Mitochondrion, 2020
The Israeli national population program of genetic carrier screening for reproductive purposes. How should it be continued?
Zlotogora J
Israel Journal of Health Policy Research, 2019
31839005 (PubMed )
Supplement: 13584_2019_345_MOESM1_ESM.xlsx › Negev_Bedouins
Estimating dispensable content in the human interactome.
Ghadie M et al.
Nature Communications, 2019
31324802 (PubMed )
Supplement: 41467_2019_11180_MOESM6_ESM.xlsx › _D__IntAct-SI_disease_mut
Nuclear gene mutations as the cause of mitochondrial complex III deficiency.
Fernández-Vizarra E et al.
Frontiers in Genetics, 2015
Infantile mitochondrial encephalopathy.
Uziel G et al.
Seminars in Fetal & Neonatal Medicine, 2011
Pathogenic mutations of nuclear genes associated with mitochondrial disorders.
Zhu X et al.
Acta Biochimica Et Biophysica Sinica, 2009
Mitochondrial complex III deficiency associated with a homozygous mutation in UQCRQ.
Barel O et al.
American Journal of Human Genetics, 2008
[Complex III deficiency due to mutations in the cytochrome b gene].
Ishii A et al.
Nihon Rinsho. Japanese Journal of Clinical Medicine, 2002
Respiratory complex III dysfunction in humans and the use of yeast as a model organism to study mitochondrial myopathy and associated diseases.
Meunier B et al.
Biochimica Et Biophysica Acta, 0
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