ArticleProceedings of the National Academy of Sciences of the United States of America2008
Hierarchical mechanisms build the DNA-binding specificity of FUSE binding protein.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 39 citations in OpenAlex.
- FUBP1 in human cancer: Characteristics, functions, and potential applications.Translational oncology · 2024Review
- PRMT5-mediated FUBP1 methylation accelerates prostate cancer progression.The Journal of clinical investigation · 2024Article
- Article
- FUSE binding protein FUBP3 is a potent regulator in Japanese encephalitis virus infection.Virology journal · 2021Article
- FUBP1 and FUBP2 enforce distinct epigenetic setpoints for MYC expression in primary single murine cells.Communications biology · 2020Article
- Comparative structural analyses and nucleotide-binding characterization of the four KH domains of FUBP1.Scientific reports · 2020Article
- Article
- Identification of FUBP1 as a Long Tail Cancer Driver and Widespread Regulator of Tumor Suppressor and Oncogene Alternative Splicing.Cell reports · 2019Article
- The master regulator FUBP1: its emerging role in normal cell function and malignant development.Cellular and molecular life sciences : CMLS · 2019Review
- Interplay between transcription regulators RUNX1 and FUBP1 activates an enhancer of the oncogene c-KIT and amplifies cell proliferation.Nucleic acids research · 2018Article
- FUBP/KH domain proteins in transcription: Back to the future.Transcription · 2017Review
- Nucleic acid clamp-mediated recognition and stabilization of the physiologically relevant MYC promoter G-quadruplex.Nucleic acids research · 2016Article
- Controlling gene expression by DNA mechanics: emerging insights and challenges.Biophysical reviews · 2016Review
- Defining the essential function of FBP/KSRP proteins: Drosophila Psi interacts with the mediator complex to modulate MYC transcription and tissue growth.Nucleic acids research · 2016Article
- Controlling gene expression by DNA mechanics: emerging insights and challenges.Biophysical reviews · 2016Review
- Far Upstream Element Binding Protein Plays a Crucial Role in Embryonic Development, Hematopoiesis, and Stabilizing Myc Expression Levels.The American journal of pathology · 2016Article
- FUBP1: a new protagonist in splicing regulation of the DMD gene.Nucleic acids research · 2015Article
- The splicing factor FUBP1 is required for the efficient splicing of oncogene MDM2 pre-mRNA.The Journal of biological chemistry · 2014Article
- Cellular MYCro economics: Balancing MYC function with MYC expression.Cold Spring Harbor perspectives in medicine · 2013Review
- Far upstream element-binding protein 1 and RNA secondary structure both mediate second-step splicing repression.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The far upstream element (FUSE) binding protein (FBP), a single-stranded nucleic acid binding protein, is recruited to the c-myc promoter after melting of FUSE by transcriptionally generated dynamic supercoils. Via interactions with TFIIH and FBP-interacting repressor (FIR), FBP modulates c-myc transcription. Here, we investigate the contributions of FBP's 4 K Homology (KH) domains to sequence selectivity. EMSA and missing contact point analysis revealed that FBP contacts 4 separate patches spanning a large segment of FUSE. A SELEX procedure using paired KH-domains defined the preferred subsequences for each KH domain. Unexpectedly, there was also a strong selection for the noncontacted residues between these subsequences, showing that the contact points must be optimally presented in a backbone that minimizes secondary structure. Strategic mutation of contact points defined in this study disabled FUSE activity in vivo. Because the biological specificity of FBP is tuned at several layers: (i) accessibility of the site; (ii) supercoil-driven melting; (iii) presentation of unhindered bases for recognition; and (iv) modular interaction of KH-domains with cognate bases, the FBP-FIR system and sequence-specific, single-strand DNA binding proteins in general are likely to prove versatile tools for adjusting gene expression.
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.