Evidence map›Paper›PMID 10848610›Full record

ArticleMolecular and cellular biology2000

p53 recruitment of CREB binding protein mediated through phosphorylated CREB: a novel pathway of tumor suppressor regulation.

H A Giebler, I Lemasson, J K Nyborg

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Characterization of BoHV-4 ORF45.Frontiers in microbiology · 2023
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  16. NF-κB, an active player in human cancers.Cancer immunology research · 2014
    Review
  17. Article
  18. Article
  19. Article
  20. Alteration of Ryanodine-receptors in Cultured Rat Aortic Smooth Muscle Cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2011
    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

3 authors at 1 institution in 1 country.

H A GieblerDepartment of Biochemistry and Molecular Biology, Colorado State University, Fort Collins 80523-1870, USA.
I Lemasson
J K Nyborg
Colorado State University · US

Funding

Tax regulation of HTLV-I Gene Expression through CBPR01CA080002 · NCI · COLORADO STATE UNIVERSITY-FORT COLLINS · PI NYBORG, JENNIFER K. · 1999 to 2008
$3.2M
NCI NIH HHS CA80002NCI NIH HHS R01 CA080002
6 · The paper itself

Abstract

CREB binding protein (CBP) is a 270-kDa nuclear protein required for activated transcription of a large number of cellular genes. Although CBP was originally discovered through its interaction with phosphorylated CREB (pCREB), it is utilized by a multitude of cellular transcription factors and viral oncoproteins. Both CREB and the tumor suppressor p53 have been shown to directly interact with the KIX domain of CBP. Although coactivator competition is an emerging theme in transcriptional regulation, we have made the fortuitous observation that protein kinase A-phosphorylated CREB strongly enhances p53 association with KIX. Phosphorylated CREB also facilitates interaction of a p53 mutant, defective for KIX binding, indicating that CREB functions in a novel way to bridge p53 and the coactivator. This is accomplished through direct interaction between the bZIP domain of CREB and the amino terminus of p53; a protein-protein interaction that is also detected in vivo. Consistent with our biochemical observations, we show that stimulation of the intracellular cyclic AMP (cAMP) pathway, which leads to CREB phosphorylation, strongly enhances both the transcriptional activation and apoptotic properties of p53. We propose that phosphorylated CREB mediates recruitment of CBP to p53-responsive promoters through direct interaction with p53. These observations provide evidence for a novel pathway that integrates cAMP signaling and p53 transcriptional activity.

Indexed as

ColforsinCREB-Binding ProteinCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansJurkat CellsLeucine ZippersNuclear ProteinsPhosphorylationPromoter Regions, GeneticSignal TransductionTrans-ActivatorsTumor Suppressor Protein p53ColforsinCREB-Binding ProteinCREBBP protein, humanCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinNuclear ProteinsTrans-ActivatorsTumor Suppressor Protein p53

Identifiers

PMID10848610
PMCPMC85936
OpenAlexW2115318437

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.