S
Steven R. Ellis
Researcher at University of Louisville
Publications - 81
Citations - 3345
Steven R. Ellis is an academic researcher from University of Louisville. The author has contributed to research in topics: Diamond–Blackfan anemia & Ribosomal protein. The author has an hindex of 29, co-authored 78 publications receiving 2963 citations. Previous affiliations of Steven R. Ellis include Eaton Corporation.
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Journal ArticleDOI
A new system for naming ribosomal proteins
Nenad Ban,Roland Beckmann,Jamie H. D. Cate,Jonathan D. Dinman,François Dragon,Steven R. Ellis,Denis L. J. Lafontaine,Lasse Lindahl,Anders Liljas,Jeffrey M. Lipton,Michael A. McAlear,Peter B. Moore,Harry F. Noller,Joaquin Ortega,Vikram Govind Panse,Venki Ramakrishnan,Christian M. T. Spahn,Thomas A. Steitz,Marek Tchórzewski,David Tollervey,Alan J. Warren,James R. Williamson,Daniel N. Wilson,Ada Yonath,Marat Yusupov +24 more
TL;DR: A system for naming ribosomal proteins is described, designed so that new names are similar enough to old names to be easily recognized, but are written in a format that unambiguously identifies them as 'new system' names.
Journal ArticleDOI
The ribosomal basis of Diamond-Blackfan Anemia: mutation and database update.
Ilenia Boria,Emanuela Garelli,Hanna T. Gazda,Hanna T. Gazda,Anna Aspesi,Paola Quarello,Elisa Pavesi,Daniela Ferrante,Joerg J Meerpohl,Mutlu Kartal,Lydie Da Costa,Lydie Da Costa,Alexis Proust,Thierry Leblanc,Maud Simansour,Niklas Dahl,Anne-Sophie Fröjmark,Dagmar Pospisilova,Radek Cmejla,Alan H. Beggs,Alan H. Beggs,Mee Rie Sheen,Michael Landowski,Christopher Buros,Catherine Clinton,Lori J. Dobson,Adrianna Vlachos,Adrianna Vlachos,Eva Atsidaftos,Eva Atsidaftos,Jeffrey M. Lipton,Jeffrey M. Lipton,Steven R. Ellis,Ugo Ramenghi,Irma Dianzani +34 more
TL;DR: Experimental evidence supports the hypothesis that DBA is primarily the result of defective ribosome synthesis, and bioinformatic tools show that gene conversion mechanism is not common in RP genes mutagenesis, notwithstanding the abundance of RP pseudogenes.
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Ribosomal protein SA haploinsufficiency in humans with isolated congenital asplenia.
Alexandre Bolze,Alexandre Bolze,Nizar Mahlaoui,Minji Byun,Bridget Turner,Nikolaus S. Trede,Steven R. Ellis,Avinash Abhyankar,Yuval Itan,Etienne Patin,Samuel Brebner,Paul Sackstein,Anne Puel,Anne Puel,Capucine Picard,Capucine Picard,Capucine Picard,Laurent Abel,Laurent Abel,Laurent Abel,Lluis Quintana-Murci,Saul N. Faust,Saul N. Faust,Anthony P. Williams,Anthony P. Williams,Richard Baretto,Michael Duddridge,Usha Kini,Andrew J. Pollard,Catherine Gaud,Pierre Frange,Pierre Frange,Daniel Orbach,Jean-François Emile,Jean-Louis Stephan,Ricardo U. Sorensen,Alessandro Plebani,Lennart Hammarström,Mary Ellen Conley,Licia Selleri,Jean-Laurent Casanova +40 more
TL;DR: An essential role for RPSA in human spleen development is established after sequence analysis of familial and sporadic cases found that ICA patients carry mutations in the gene encoding ribosomal protein SA and as a result express about half the normal amount of this protein.
Journal ArticleDOI
Maf1p, a negative effector of RNA polymerase III in Saccharomyces cerevisiae.
Krzysztof Dariusz Pluta,Olivier Lefebvre,Nancy C. Martin,Wieslaw J. Smagowicz,David R. Stanford,Steven R. Ellis,Anita K. Hopper,André Sentenac,Magdalena Boguta +8 more
TL;DR: It is shown that tRNA levels are elevated in maf1 mutant cells and Maf1p acts as a negative effector of Pol III synthesis, indicating that this potential regulator ofPol III transcription is likely conserved since orthologs of MAF1p are present in other eukaryotes, including humans.
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Mice with ribosomal protein S19 deficiency develop bone marrow failure and symptoms like patients with Diamond-Blackfan anemia.
Pekka Jaako,Johan Flygare,Johan Flygare,Karin Olsson,Ronan Quere,Mats Ehinger,Adrianna Henson,Steven R. Ellis,Axel Schambach,Christopher Baum,Johan Richter,Jonas Larsson,David Bryder,Stefan Karlsson +13 more
TL;DR: Both RPS19 gene transfer and the loss of p53 rescue the DBA phenotype implying the potential of the models for testing novel therapies, and the feasibility of transgenic RNA interference to generate mouse models for human diseases caused by haploinsufficient expression of a gene.