Evidence map›Paper›PMID 23370271›Full record

ArticleCell death and differentiation2013

Grail as a molecular determinant for the functions of the tumor suppressor p53 in tumorigenesis.

Y-C Chen, J Y-H Chan, Y-L Chiu, S-T Liu, G Lozano, S-L Wang, C-L Ho, S-M Huang

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

34 citing papers in PubMed, 43 citations in OpenAlex.

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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

8 authors at 3 institutions in 2 countries.

Y-C ChenGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan, Republic of China.
J Y-H Chan
Y-L Chiu
S-T Liu
G Lozano
S-L Wang
C-L Ho
S-M Huang
National Defense Medical Center · TWThe University of Texas MD Anderson Cancer Center · USTri-Service General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor p53 is a multifunctional tumor suppressor that arrests the cell cycle in response to stress and modulates the DNA repair process or induces apoptosis. The cellular level and activity of p53 are tightly controlled to maintain proper functioning. This study identified a novel p53-binding glycoprotein, gene related to anergy in lymphocytes (Grail), which formed a negative feedback loop (similar to that of Mdm2). Grail physically and functionally interacted with the N-terminus of p53 to target its degradation and modulate its transactivation activity. Grail also senses and regulates cellular p53 levels, modulates a panel of p53-targeted promoters, and has a role in p53-induced apoptosis in cultured cells. Overexpression of Grail inhibited p53-induced apoptosis by increasing p53 degradation. However, cells not expressing Grail failed to undergo p53-dependent apoptosis, resulting in p21-dependent G1 arrest. Thus, Grail may provide a novel regulatory route for controlling p53 activity under stress conditions.

Indexed as

G1 Phase Cell Cycle CheckpointsAnimalsApoptosisCell Line, TumorCell Transformation, NeoplasticCyclin-Dependent Kinase Inhibitor p21HeLa CellsHumansMicePromoter Regions, GeneticProtein Interaction Domains and MotifsRatsRNA InterferenceRNA, Small InterferingSignal TransductionTranscriptional ActivationCyclin-Dependent Kinase Inhibitor p21RNA, Small InterferingRNF128 protein, humanTP53 protein, humanTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID23370271
PMCPMC3619241
OpenAlexW2095850456

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.