ArticleEukaryotic cell2012
Editosome accessory factors KREPB9 and KREPB10 in Trypanosoma brucei.
Article in Eukaryotic cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Blastocrithidia nonstop mitochondrial genome and its expression are remarkably insulated from nuclear codon reassignment.Nucleic acids research · 2024Article
- Deep mutational scanning of the RNase III-like domain inFrontiers in cellular and infection microbiology · 2024Article
- RNA editing catalytic complexes edit multiple mRNA sites non-processively in Trypanosoma brucei.Molecular and biochemical parasitology · 2023Article
- Editosome RNase III domain interactions are essential for editing and differ between life cycle stages inRNA (New York, N.Y.) · 2019Article
- Dynamic RNA holo-editosomes with subcomplex variants: Insights into the control of trypanosome editing.Wiley interdisciplinary reviews. RNA · 2018Review
- The essential functions of KREPB4 are developmentally distinct and required for endonuclease association with editosomes.RNA (New York, N.Y.) · 2017Article
- The eIF3 complex ofRNA (New York, N.Y.) · 2017Article
- The Architecture of Trypanosoma brucei editosomes.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- U-Insertion/Deletion mRNA-Editing Holoenzyme: Definition in Sight.Trends in parasitology · 2016Review
- Identification by Random Mutagenesis of Functional Domains in KREPB5 That Differentially Affect RNA Editing between Life Cycle Stages of Trypanosoma brucei.Molecular and cellular biology · 2015Article
- Differential Editosome Protein Function between Life Cycle Stages of Trypanosoma brucei.The Journal of biological chemistry · 2015Article
- Leishmania major telomerase TERT protein has a nuclear/mitochondrial eclipsed distribution that is affected by oxidative stress.Infection and immunity · 2015Article
- Mutational analysis of Trypanosoma brucei editosome proteins KREPB4 and KREPB5 reveals domains critical for function.RNA (New York, N.Y.) · 2012Article
- Selection of binding targets in parasites using phage-display and aptamer libraries in vivo and in vitro.Frontiers in immunology · 2012Article
- Article
- Stunning Intricacies of RNA Editing Complexes RECC, RESC, and REH2C: Functional Organization, Developmental Regulation, and Evolutionary History in Kinetoplastid Protists.Wiley interdisciplinary reviews. RNAReview
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6 authors.
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Abstract
Multiprotein complexes, called editosomes, catalyze the uridine insertion and deletion RNA editing that forms translatable mitochondrial mRNAs in kinetoplastid parasites. We have identified here two new U1-like zinc finger proteins that associate with editosomes and have shown that they are related to KREPB6, KREPB7, and KREPB8, and thus we have named them Kinetoplastid RNA Editing Proteins, KREPB9 and KREPB10. They are conserved and syntenic in trypanosomatids although KREPB10 is absent in Trypanosoma vivax and both are absent in Leishmania. Tandem affinity purification (TAP)-tagged KREPB9 and KREPB10 incorporate into ~20S editosomes and/or subcomplexes thereof and preferentially associate with deletion subcomplexes, as do KREPB6, KREPB7, and KREPB8. KREPB10 also associates with editosomes that are isolated via a chimeric endonuclease, KREN1 in KREPB8 RNA interference (RNAi) cells, or MEAT1. The purified complexes have precleaved editing activities and endonuclease cleavage activity that appears to leave a 5' OH on the 3' product. RNAi knockdowns did not affect growth but resulted in relative reductions of both edited and unedited mitochondrial mRNAs. The similarity of KREPB9 and KREPB10 to KREPB6, KREPB7, and KREPB8 suggests they may be accessory factors that affect editing endonuclease activity and as a consequence may affect mitochondrial mRNA stability. KREPB9 and KREPB10, along with KREPB6, KREPB7, and KREPB8, may enable the endonucleases to discriminate among and accurately cleave hundreds of different editing sites and may be involved in the control of differential editing during the life cycle of T. brucei.
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