ArticleNucleic acids research1996
In vivo degradation of RNA polymerase II largest subunit triggered by alpha-amanitin.
Article in Nucleic acids research, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 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
128 citing papers in PubMed, 262 citations in OpenAlex.
- Transcriptional activity during seed imbibition is conserved, robust and required for germination.Nature communications · 2026Article
- A tunable CTD grammar governs the spatial programming of the transcription cycle.Nature communications · 2026Article
- Maternal IntS11 primes embryonic totipotency by organizing early zygotic transcription initiation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- RNA polymerase II degradation triggered by DNA repair occurs in trans and independently of how the lesion is recognized.Nucleic acids research · 2026Article
- Pre-marking chromatin with H3K4 methylation is required for accurate zygotic genome activation and development.Nature communications · 2025Article
- Natural degradation of RNA polymerase II is essential for oocyte chromatin reorganization and maternal-to-zygotic transition.Nature communications · 2025Article
- Article
- An alternative cytoplasmic SFPQ isoform with reduced phase separation potential is up-regulated in ALS.Science advances · 2025Article
- Super RNA Pol II domains enhance minor ZGA through 3D interaction to ensure the integrity of major transcriptional waves in late-ZGA mammals.Cell genomics · 2025Article
- CTDP1 and RPB7 stabilize Pol II and permit reinitiation.Nature communications · 2025Article
- Serum metabolomics identifies novel prognostic biomarkers inFrontiers in pharmacology · 2025Article
- CRL3Molecular cell · 2024Article
- Redundant pathways for removal of defective RNA polymerase II complexes at a promoter-proximal pause checkpoint.Molecular cell · 2024Article
- Variation of C-terminal domain governs RNA polymerase II genomic locations and alternative splicing in eukaryotic transcription.Nature communications · 2024Article
- Increased transcriptional elongation and RNA stability of GPCR ligand binding genes unveiled via RNA polymerase II degradation.Nucleic acids research · 2024Article
- Dynamic chromosome association with nuclear organelles in living cells.Histochemistry and cell biology · 2024Article
- N-terminal tagging of RNA Polymerase II shapes transcriptomes more than C-terminal alterations.iScience · 2024Article
- Transforming toxins into treatments: the revolutionary role of α-amanitin in cancer therapy.Archives of toxicology · 2024Review
- Genome-wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression.Genome biology · 2024Article
68 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alpha-Amanitin is a well-known specific inhibitor of RNA polymerase II (RNAPII) in vitro and in vivo. It is a cyclic octapeptide which binds with high affinity to the largest subunit of RNAPII, RPB1. We have found that in murine fibroblasts exposure to alpha-amanitin triggered degradation of the RPB1 subunit, while other RNAPII subunits, RPB5 and RPB8, remained almost unaffected. Transcriptional inhibition in alpha-amanitin-treated cells was slow and closely followed the disappearance of RPB1. The degradation rate of RPB1 was alpha-amanitin dose dependent and was not a consequence of transcriptional arrest. Alpha-Amanitin-promoted degradation of RPB1 was prevented in cells exposed to actinomycin D, another transcriptional inhibitor. Epitope-tagged recombinant human RPB1 subunits were expressed in mouse fibroblasts. In cells exposed to alpha-amanitin the wild-type recombinant subunit was degraded like the endogenous protein, but a mutated alpha-amanitin-resistant subunit remained unaffected. Hence, alpha-amanitin did not activate a proteolytic system, but instead its binding to mRPB1 likely represented a signal for degradation. Thus, in contrast to other inhibitors, such as actinomycin D or 5,6-dichloro-1-beta-D-ribofuranosyl-benzimidazole, which reversibly act on transcription, inhibition by alpha-amanitin cannot be but an irreversible process because of the destruction of RNAPII.
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.