ReviewTranscription
The pleiotropic roles of SPT5 in transcription.
Review in Transcription. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Mechanisms of transcription termination across the coding and noncoding loci of the genome.Nature reviews. Molecular cell biology · 2026Review
- 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
- Kinetic control of mammalian transcription elongation.Nature structural & molecular biology · 2026Article
- Conserved protein Seb1 that interacts with RNA polymerase II and RNA is an antipausing transcription elongation factor.RNA (New York, N.Y.) · 2025Article
- DSS1 is required for proper Integrator-PP2A function.Nature communications · 2025Article
- Tripartite phosphorylation of SPT5 by CDK9 times pause release and tunes elongation rate of RNA polymerase II.Molecular cell · 2025Article
- CTDP1 and RPB7 stabilize Pol II and permit reinitiation.Nature communications · 2025Article
- Nuclear ANLN regulates transcription initiation related Pol II clustering and target gene expression.Nature communications · 2025Article
- LEDGF/p75 promotes transcriptional pausing through preventing SPT5 phosphorylation.Science advances · 2025Article
- DSIF factor Spt5 coordinates transcription, maturation and exoribonucleolysis of RNA polymerase II transcripts.Nature communications · 2025Article
- The CDK9-SPT5 Axis in Control of Transcription Elongation by RNAPII.Journal of molecular biology · 2025Review
- Toward structural understanding of eukaryotic transcription elongation.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2025Review
- Article
- Spt5 orchestrates cryptic transcript suppression and transcriptional directionality.Communications biology · 2024Article
- The transcription elongation factors Spt4 and Spt5 control neural progenitor proliferation and are implicated in neuronal remodeling duringFrontiers in cell and developmental biology · 2024Article
- Different elongation factors distinctly modulate RNA polymerase II transcription in Arabidopsis.Nucleic acids research · 2023Article
- Spt5 C-terminal repeat domain phosphorylation and length negatively regulate heterochromatin through distinct mechanisms.PLoS genetics · 2023Article
- Article
- Review
- New roles for elongation factors in RNA polymerase II ubiquitylation and degradation.Biochimica et biophysica acta. Gene regulatory mechanisms · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Initially discovered by genetic screens in budding yeast, SPT5 and its partner SPT4 form a stable complex known as DSIF in metazoa, which plays pleiotropic roles in multiple steps of transcription. SPT5 is the most conserved transcription elongation factor, being found in all three domains of life; however, its structure has evolved to include new domains and associated posttranslational modifications. These gained features have expanded transcriptional functions of SPT5, likely to meet the demand for increasingly complex regulation of transcription in higher organisms. This review discusses the pleiotropic roles of SPT5 in transcription, including RNA polymerase II (Pol II) stabilization, enhancer activation, Pol II pausing and its release, elongation, and termination, with a focus on the most recent progress of SPT5 functions in regulating metazoan transcription.
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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.