Evidence map›Paper›PMID 10594026›Full record

ArticleMolecular and cellular biology2000

ei24, a p53 response gene involved in growth suppression and apoptosis.

Z Gu, C Flemington, T Chittenden, G P Zambetti

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 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 115 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

4 authors at 1 institution in 1 country.

Z GuDepartment of Biochemistry, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
C Flemington
T Chittenden
G P Zambetti
St. Jude Children's Research Hospital · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
MUTANT P53 GAIN OF FUNCTION IN TURMORIGENISISR01CA063230 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI ZAMBETTI, GERARD PAUL · 1995 to 2007
$2.3M
NCI NIH HHS 5 P30 CA21765NCI NIH HHS CA63230NCI NIH HHS P30 CA021765NCI NIH HHS R01 CA063230
6 · The paper itself

Abstract

DNA damage and/or hyperproliferative signals activate the wild-type p53 tumor suppressor protein, which induces a G(1) cell cycle arrest or apoptosis. Although the mechanism of p53-mediated cell cycle arrest is fairly well defined, the p53-dependent pathway regulating apoptosis is poorly understood. Here we report the functional characterization of murine ei24 (also known as PIG8), a gene directly regulated by p53, whose overexpression negatively controls cell growth and induces apoptotic cell death. Ectopic ei24 expression markedly inhibits cell colony formation, induces the morphological features of apoptosis, and reduces the number of beta-galactosidase-marked cells, which is efficiently blocked by coexpression of Bcl-X(L). The ei24/PIG8 gene is localized on human chromosome 11q23, a region frequently altered in human cancers. These results suggest that ei24 may play an important role in negative cell growth control by functioning as an apoptotic effector of p53 tumor suppressor activities.

Indexed as

Gene Expression RegulationGenes, p53Amino Acid SequenceAnimalsApoptosisApoptosis Regulatory ProteinsCell DivisionCell LineHumansMiceMolecular Sequence DataMutationNuclear ProteinsPhosphoproteinsApoptosis Regulatory ProteinsEI24 protein, humanNuclear ProteinsPhosphoproteins

Identifiers

PMID10594026
PMCPMC85079
OpenAlexW1978311772

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.