ArticleMolecular and cellular biology2005
TFIIH operates through an expanded proximal promoter to fine-tune c-myc expression.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 59 citations in OpenAlex.
- FUBP3 enhances HIV-1 transcriptional activity and regulates immune response pathways in T cells.Molecular therapy. Nucleic acids · 2025Article
- MYC: a complex problem.Trends in cell biology · 2023Review
- Identification of a key glioblastoma candidate gene, FUBP3, based on weighted gene co-expression network analysis.BMC neurology · 2022Article
- FUBP1 and FUBP2 enforce distinct epigenetic setpoints for MYC expression in primary single murine cells.Communications biology · 2020Article
- The master regulator FUBP1: its emerging role in normal cell function and malignant development.Cellular and molecular life sciences : CMLS · 2019Review
- FUBP/KH domain proteins in transcription: Back to the future.Transcription · 2017Review
- Article
- O-GlcNAcase Is an RNA Polymerase II Elongation Factor Coupled to Pausing Factors SPT5 and TIF1β.The Journal of biological chemistry · 2016Article
- Article
- Far Upstream Element Binding Protein Plays a Crucial Role in Embryonic Development, Hematopoiesis, and Stabilizing Myc Expression Levels.The American journal of pathology · 2016Article
- Defective Hfp-dependent transcriptional repression of dMYC is fundamental to tissue overgrowth in Drosophila XPB models.Nature communications · 2015Article
- Loss of the xeroderma pigmentosum group B protein binding site impairs p210 BCR/ABL1 leukemogenic activity.Blood cancer journal · 2013Article
- Eukaryotic transcriptional dynamics: from single molecules to cell populations.Nature reviews. Genetics · 2013Review
- Interactions between SAP155 and FUSE-binding protein-interacting repressor bridges c-Myc and P27Kip1 expression.Molecular cancer research : MCR · 2013Article
- Far upstream element binding protein 1: a commander of transcription, translation and beyond.Oncogene · 2013Review
- Incompatible effects of p53 and HDAC inhibition on p21 expression and cell cycle progression.Cell death & disease · 2013Article
- The role of XPD in cell apoptosis and viability and its relationship with p53 and cdk2 in hepatoma cells.Medical oncology (Northwood, London, England) · 2012Article
- Real-time imaging of cotranscriptional splicing reveals a kinetic model that reduces noise: implications for alternative splicing regulation.The Journal of cell biology · 2011Article
- JTV1 co-activates FBP to induce USP29 transcription and stabilize p53 in response to oxidative stress.The EMBO journal · 2011Article
- On the traces of XPD: cell cycle matters - untangling the genotype-phenotype relationship of XPD mutations.Cell division · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 4 countries.
Funding
Abstract
A continuous stream of activating and repressing signals is processed by the transcription complex paused at the promoter of the c-myc proto-oncogene. The general transcription factor IIH (TFIIH) is held at promoters prior to promoter escape and so is well situated to channel the input of activators and repressors to modulate c-myc expression. We have compared cells expressing only a mutated p89 (xeroderma pigmentosum complementation group B [XPB]), the largest TFIIH subunit, with the same cells functionally complemented with the wild-type protein (XPB/wt-p89). Here, we show structural, compositional, and functional differences in transcription complexes between XPB and XPB/wt-89 cells at the native c-myc promoter. Remarkably, although the mean levels of c-Myc are only modestly elevated in XPB compared to those in XPB/wt-p89 cells, the range of expression and the cell-to-cell variation of c-Myc are markedly increased. Our modeling indicates that the data can be explained if TFIIH integrates inputs from multiple signals, regulating transcription at multiple kinetically equivalent steps between initiation and promoter escape. This helps to suppress the intrinsic noise of transcription and to ensure the steady transcriptional output of c-myc necessary for cellular homeostasis.
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.