Evidence map›Paper›PMID 9891084›Full record

ArticleMolecular and cellular biology1999

Cell-type-dependent activity of the ubiquitous transcription factor USF in cellular proliferation and transcriptional activation.

Y Qyang, X Luo, T Lu, P M Ismail, D Krylov, C Vinson, M Sawadogo

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.9field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 166 citations in OpenAlex.

  1. Review
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  7. CREB Family Transcription Factors Are Major Mediators of BDNF Transcriptional Autoregulation in Cortical Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
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1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Y QyangDepartment of Molecular Genetics, University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
X Luo
T Lu
P M Ismail
D Krylov
C Vinson
M Sawadogo
The University of Texas MD Anderson Cancer Center · USCancer Institute (WIA) · IN

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TRAINING PROGRAM IN MOLECULAR GENETICS OF CANCERT32CA009299 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOZANO, GUILLERMINA · 1985 to 2014
$4.7M
MOUSE MODELS FOR USF FUNCTIONR01CA079578 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI SAWADOGO, MICHELE · 1998 to 2002
$454k
NCI NIH HHS CA09299NCI NIH HHS CA16672NCI NIH HHS CA79578NCI NIH HHS P30 CA016672NCI NIH HHS T32 CA009299
6 · The paper itself

Abstract

USF1 and USF2 are basic helix-loop-helix transcription factors implicated in the control of cellular proliferation. In HeLa cells, the USF proteins are transcriptionally active and their overexpression causes marked growth inhibition. In contrast, USF overexpression had essentially no effect on the proliferation of the Saos-2 osteosarcoma cell line. USF1 and USF2 also lacked transcriptional activity in Saos-2 cells when assayed by transient cotransfection with USF-dependent reporter genes. Yet, there was no difference in the expression, subcellular localization, or DNA-binding activity of the USF proteins in HeLa and Saos-2 cells. Furthermore, Gal4-USF1 and Gal4-USF2 fusion proteins activated transcription similarly in both cell lines. Mutational analysis and domain swapping experiments revealed that the small, highly conserved USF-specific region (USR) was responsible for the inactivity of USF in Saos-2 cells. In HeLa, the USR serves a dual function. It acts as an autonomous transcriptional activation domain at promoters containing an initiator element and also induces a conformational change that is required for USF activity at promoters lacking an initiator. Taken together, these results suggest a model in which the transcriptional activity of the USF proteins, and consequently their antiproliferative activity, is tightly controlled by interaction with a specialized coactivator that recognizes the conserved USR domain and, in contrast to USF, is not ubiquitous. The activity of USF is therefore context dependent, and evidence for USF DNA-binding activity in particular cells is insufficient to indicate USF function in transcriptional activation and growth control.

Indexed as

DNA-Binding ProteinsTranscriptional ActivationAmino Acid SequenceCell DivisionCell LineDNAGene ExpressionGenes, ReporterHeLa CellsHumansImmediate-Early ProteinsModels, BiologicalMolecular Sequence DataRecombinant Fusion ProteinsSubcellular FractionsTrans-ActivatorsDNADNA-Binding ProteinsIE62 protein, Human herpesvirus 3Immediate-Early ProteinsRecombinant Fusion ProteinsTrans-ActivatorsTranscription FactorsUpstream Stimulatory FactorsUSF1 protein, humanUSF2 protein, humanViral Envelope Proteins

Identifiers

PMID9891084
PMCPMC116079
OpenAlexW2139102988

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.