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Ethan Bier
Researcher at University of California, San Diego
Publications - 123
Citations - 11554
Ethan Bier is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Gene drive & Gene. The author has an hindex of 50, co-authored 115 publications receiving 10163 citations. Previous affiliations of Ethan Bier include University of California, San Francisco & University of California, Los Angeles.
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A Systematic Analysis of Human Disease-Associated Gene Sequences In Drosophila melanogaster
TL;DR: A systematic analysis of 929 human disease gene entries associated with at least one mutant allele in the Online Mendelian Inheritance in Man (OMIM) database against the recently completed genome sequence of Drosophila melanogaster identified 714 distinct human disease genes matching 548 unique Dosophila sequences.
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Highly efficient Cas9-mediated gene drive for population modification of the malaria vector mosquito Anopheles stephensi
Valentino M. Gantz,Nijole Jasinskiene,Olga Tatarenkova,Aniko Fazekas,Vanessa M. Macias,Ethan Bier,Anthony A. James +6 more
TL;DR: A highly effective autonomous Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-associated protein 9 (Cas9)-mediated gene-drive system in the Asian malaria vector Anopheles stephensi, adapted from the mutagenic chain reaction (MCR).
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Drosophila, the golden bug, emerges as a tool for human genetics.
TL;DR: Drosophila melanogaster is emerging as one of the most effective tools for analyzing the function of human disease genes, including those responsible for developmental and neurological disorders, cancer, cardiovascular disease, metabolic and storage diseases, and genes required for the function the visual, auditory and immune systems.
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The mutagenic chain reaction: A method for converting heterozygous to homozygous mutations
Valentino M. Gantz,Ethan Bier +1 more
TL;DR: In Drosophila, it is found that MCR mutations efficiently spread from their chromosome of origin to the homologous chromosome, thereby converting heterozygous mutations to homozygosity in the vast majority of somatic and germline cells.
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Sestrin as a feedback inhibitor of TOR that prevents age-related pathologies
Jun Hee Lee,Andrei V. Budanov,Eek Joong Park,Ryan T. Birse,Teddy E. Kim,Guy Perkins,Karen Ocorr,Mark H. Ellisman,Rolf Bodmer,Ethan Bier,Michael Karin +10 more
TL;DR: Drosophila sestrin dSesn appears to be a negative feedback regulator of TOR that integrates metabolic and stress inputs and prevents pathologies caused by chronic TOR activation that may result from diminished autophagic clearance of damaged mitochondria, protein aggregates, or lipids.