ArticleThe Journal of biological chemistry2010
The C-terminal repeat domain of Spt5 plays an important role in suppression of Rad26-independent transcription coupled repair.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 65 citations in OpenAlex.
- Spt5's central KOW domains and the Pol II stalk collaborate to regulate chromatin and 3'-end processing in Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2026Article
- Dysregulated nuclear Lamin B1 in DYT1 dystonia thickens nuclear lamina and disrupts 14-3-3 proteins.Cell death discovery · 2026Article
- The CDK9-SPT5 Axis in Control of Transcription Elongation by RNAPII.Journal of molecular biology · 2025Review
- NusG-Spt5 Transcription Factors: Universal, Dynamic Modulators of Gene Expression.Journal of molecular biology · 2025Review
- Spt5 orchestrates cryptic transcript suppression and transcriptional directionality.Communications biology · 2024Article
- RANBP17 Overexpression Restores Nucleocytoplasmic Transport and Ameliorates Neurodevelopment in Induced DYT1 Dystonia Motor Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Elf1 promotes Rad26's interaction with lesion-arrested Pol II for transcription-coupled repair.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Paf1 complex is required for RNA polymerase II removal in response to DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Spt4 facilitates the movement of RNA polymerase II through the +2 nucleosomal barrier.Cell reports · 2021Article
- Transcription-coupled nucleotide excision repair: New insights revealed by genomic approaches.DNA repair · 2021Review
- Causes and consequences of RNA polymerase II stalling during transcript elongation.Nature reviews. Molecular cell biology · 2021Review
- Genome-wide role of Rad26 in promoting transcription-coupled nucleotide excision repair in yeast chromatin.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- DAF-16/FOXO requires Protein Phosphatase 4 to initiate transcription of stress resistance and longevity promoting genes.Nature communications · 2020Article
- The Cellular Response to Transcription-Blocking DNA Damage.Trends in biochemical sciences · 2018Review
- Architecture of the RNA polymerase II elongation complex: new insights into Spt4/5 and Elf1.Transcription · 2018Review
- Sen1, the yeast homolog of human senataxin, plays a more direct role than Rad26 in transcription coupled DNA repair.Nucleic acids research · 2016Article
- Biochemical Analysis of Yeast Suppressor of Ty 4/5 (Spt4/5) Reveals the Importance of Nucleic Acid Interactions in the Prevention of RNA Polymerase II Arrest.The Journal of biological chemistry · 2016Article
- Suppressor of Ty homolog-5, a novel tumor-specific human telomerase reverse transcriptase promoter-binding protein and activator in colon cancer cells.Oncotarget · 2015Article
- Structures and Functions of the Multiple KOW Domains of Transcription Elongation Factor Spt5.Molecular and cellular biology · 2015Article
- Ubiquitous transcription factors display structural plasticity and diverse functions: NusG proteins - Shifting shapes and paradigms.BioEssays : news and reviews in molecular, cellular and developmental biology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In eukaryotic cells, transcription coupled nucleotide excision repair (TCR) is believed to be initiated by RNA polymerase II (Pol II) stalled at a lesion in the transcribed strand of a gene. Rad26, the yeast homolog of the human Cockayne syndrome group B (CSB) protein, plays an important role in TCR. Spt4, a transcription elongation factor that forms a complex with Spt5, has been shown to suppress TCR in rad26Delta cells. Here we present evidence that Spt4 indirectly suppresses Rad26-independent TCR by protecting Spt5 from degradation and stabilizing the interaction of Spt5 with Pol II. We further found that the C-terminal repeat (CTR) domain of Spt5, which is dispensable for cell viability and is not involved in interactions with Spt4 and Pol II, plays an important role in the suppression. The Spt5 CTR is phosphorylated by the Bur kinase. Inactivation of the Bur kinase partially alleviates TCR in rad26Delta cells. We propose that the Spt5 CTR suppresses Rad26-independent TCR by serving as a platform for assembly of a multiple protein suppressor complex that is associated with Pol II. Phosphorylation of the Spt5 CTR by the Bur kinase may facilitate the assembly of the suppressor complex.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.