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Ilia Zhidkov
Researcher at Ben-Gurion University of the Negev
Publications - 7
Citations - 240
Ilia Zhidkov is an academic researcher from Ben-Gurion University of the Negev. The author has contributed to research in topics: Mitochondrial DNA & Human mitochondrial genetics. The author has an hindex of 6, co-authored 7 publications receiving 204 citations. Previous affiliations of Ilia Zhidkov include National Institute of Biotechnology.
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Mitochondrial DNA heteroplasmy in diabetes and normal adults: role of acquired and inherited mutational patterns in twins
Gal Avital,Mor Buchshtav,Ilia Zhidkov,Jeanette Tuval,Sarah Dadon,Eitan Rubin,Eitan Rubin,Daniel Glass,Tim D. Spector,Dan Mishmar +9 more
TL;DR: The twin study found clear evidence of a heritable influence on the accumulation of HMs as well as the signatures of selection in heteroplasmic mutations.
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Functional Recurrent Mutations in the Human Mitochondrial Phylogeny: Dual Roles in Evolution and Disease
TL;DR: This is the most comprehensive analysis of selective signatures in the mtDNA not only within proteins but also within RNA genes and some functional RNMs occurred in unrelated mtDNA lineages that independently altered susceptibility to the same diseases, thus suggesting common functionality.
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mtDNA mutation pattern in tumors and human evolution are shaped by similar selective constraints
TL;DR: By analyzing similarities rather than differences in patterns of mtDNA mutations in tumor and human evolution, it is discovered evidence for similar selective constraints, suggesting a functional potential for these mutations.
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MitoBamAnnotator: A web-based tool for detecting and annotating heteroplasmy in human mitochondrial DNA sequences.
TL;DR: MitoBamAnnotator provides the user with a comprehensively annotated overview of mitochondrial genetic variation, allowing for an in-depth analysis with no prior knowledge in programming.
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Evolution and disease converge in the mitochondrion.
Dan Mishmar,Ilia Zhidkov +1 more
TL;DR: Evidence is provided showing that the two types of mutations obey the rules of evolution, including random genetic drift and natural selection, and that the very same mutations could either mark ancient evolutionary changes or cause disease.