Evidence map›Paper›PMID 8754830›Full record

ArticleMolecular and cellular biology1996

Functional interaction between p53, the TATA-binding protein (TBP), andTBP-associated factors in vivo.

G Farmer, J Colgan, Y Nakatani, J L Manley, C Prives

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 110 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. p53 regulates Ki-67 promoter activity through p53- and Sp1-dependent manner in HeLa cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011
    Article
  9. Article
  10. Review
  11. Transcriptional regulation by p53.Cold Spring Harbor perspectives in biology · 2010
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

5 authors at 1 institution in 1 country.

G FarmerDepartment of Biological Sciences, Columbia University, New York, New York 10027, USA.
J Colgan
Y Nakatani
J L Manley
C Prives
Columbia University · US

Funding

Regulation of the p53 tumor suppressor proteinR01CA058316 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI PRIVES, CAROL · 1993 to 2017
$5.3M
REGULATION OF THE P53 TUMOR SUPPRESSOR PROTEINR37CA058316 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI PRIVES, CAROL · 1998 to 2007
$3.8M
TRANSCRIPTIONAL CONTROL OF HOMEO BOX GENE EXPRESSIONR01GM037971 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI MANLEY, JAMES L. · 1987 to 2006
$1.8M
NCI NIH HHS CA58316NIGMS NIH HHS GM 37971
6 · The paper itself

Abstract

The transcriptional activator p53 is known to interact with components of the general transcription factor TFIID in vitro. To examine the relevance of these associations to transcriptional activation in vivo, plasmids expressing a p53-GAL4 chimera and Drosophila TATA-binding protein (dTBP) were transfected into Drosophila Schneider cells. p53-GAL4 and dTBP displayed a markedly synergistic effect on activated transcription from a GAL4 site-containing reporter that was at least 10-fold greater than observed with other activators tested. A mutant p53 previously shown to be defective in both transcriptional activation in vivo and in binding to TBP-associated factors (TAFs) in vitro, although still capable of binding dTBP, did not cooperate with dTBP, suggesting that TAFs may contribute to this synergy. Providing further support for this possibility, transfected dTBP assembled into rapidly sedimenting complexes and could be immunoprecipitated with anti-TAF antibodies. While overexpression of any of several TAFs did not affect basal transcription, in either the presence or the absence of cotransfected dTBP, overexpression of TAFII230 inhibited transcriptional activation mediated by p53-GAL4 as well as by GAL4-VP16 and Sp1. Overexpression of TAFII40 and TAFII60 also inhibited activation by p53-GAL4 but had negligible effects on activation by GAL4-VP16 and Sp1, while TAFII110 did not affect any of the activators. TAF-mediated inhibition of activated transcription could be rescued by high levels of exogenous dTBP, which also restored full synergy. These data demonstrate for the first time that functional interactions can occur in vivo between TBP, TAFs, and p53.

Indexed as

Drosophila ProteinsTATA-Binding Protein Associated FactorsTranscription Factor TFIIDTranscription, GeneticAnimalsBase SequenceCell LineDNA-Binding ProteinsDNA PrimersDrosophila melanogasterMacromolecular SubstancesMolecular Sequence DataTATA-Box Binding ProteinTrans-ActivatorsTranscriptional ActivationTranscription FactorsDNA-Binding ProteinsDNA PrimersDrosophila Proteinse(y)1 protein, DrosophilaMacromolecular SubstancesTaf6 protein, DrosophilaTATA-Binding Protein Associated FactorsTATA-Box Binding ProteinTrans-ActivatorsTranscription FactorsTranscription Factor TFIIDTumor Suppressor Protein p53

Identifiers

PMID8754830
PMCPMC231428
OpenAlexW2103247252

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.