Evidence map›Paper›PMID 27864306›Full record

ReviewCold Spring Harbor perspectives in medicine2017

The Transactivation Domains of the p53 Protein.

Nitin Raj, Laura D Attardi

Abstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

98 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Targeting p53 pathways: mechanisms, structures, and advances in therapy.Signal transduction and targeted therapy · 2023
    Pooled it
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  19. The multifunctional proline-rich domain of p53 tumor suppressor.Biochimica et biophysica acta. Reviews on cancer · 2025
    Review
  20. Review

38 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

2 authors.

Nitin RajDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305.
Laura D AttardiDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California 94305.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p53 tumor suppressor is a transcriptional activator, with discrete domains that participate in sequence-specific DNA binding, tetramerization, and transcriptional activation. Mutagenesis and reporter studies have delineated two distinct activation domains (TADs) and specific hydrophobic residues within these TADs that are critical for their function. Knockin mice expressing p53 mutants with alterations in either or both of the two TADs have revealed that TAD1 is critical for responses to acute DNA damage, whereas both TAD1 and TAD2 participate in tumor suppression. Biochemical and structural studies have identified factors that bind either or both TADs, including general transcription factors (GTFs), chromatin modifiers, and negative regulators, helping to elaborate a model through which p53 activates transcription. Posttranslational modifications (PTMs) of the p53 TADs through phosphorylation also regulate TAD activity. Together, these studies on p53 TADs provide great insight into how p53 serves as a tumor suppressor.

Indexed as

Protein Processing, Post-TranslationalTranscriptional ActivationAnimalsDNA DamageGene Expression Regulation, NeoplasticHumansMiceTranscription FactorsTumor Suppressor Protein p53Transcription FactorsTumor Suppressor Protein p53

Identifiers

PMID27864306
PMCPMC5204331

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.