Evidence map›Paper›PMID 18626511›Full record

ArticleCell research2008

Differential effects of p63 mutants on transactivation of p53 and/or p63 responsive genes.

Shama K Khokhar, Ramakrishna Kommagani, Madhavi P Kadakia

Open access · bronzeAbstract read
In one paragraph

Article in Cell research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.1field-weighted citation impact, top 46% 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

6 citing papers in PubMed, 8 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

3 authors at 1 institution in 1 country.

Shama K KhokharDepartment of Biochemistry and Molecular Biology, Boonshoft School of Medicine, Wright State University, Dayton, OH 45435, USA.
Ramakrishna Kommagani
Madhavi P Kadakia
Wright State University · US

Funding

Elucidate the role of p63 in prostate cancer progressionR21CA118315 · NCI · WRIGHT STATE UNIVERSITY · PI KADAKIA, MADHAVI P · 2006 to 2007
$269k
NCI NIH HHS CA118315-2NCI NIH HHS R21 CA118315
6 · The paper itself

Abstract

p63, known to play a role in development, has more recently also been implicated in cancer progression. Mutations in p63 have been shown to be responsible for several human developmental diseases. Differential splicing of the p63 gene gives rise to p63 isoforms, which can act either as tumor suppressors or as oncogene. In this report, we studied the effects of naturally occurring TAp63gamma mutants on the regulation of p53/p63 and p63 specific target genes. We observed significant differences among p63 mutants to regulate the p53/p63 and p63 specific target genes. Additionally, we observed a differential effect of p63 mutants on wildtype-p63-mediated induction of p53/p63 and p63 specific target genes. We also demonstrated that these mutants differentially regulate the binding of wildtype p63 to the promoter of target genes. Furthermore, the effects of these mutants on cell death and survival were consistent with their ability to regulate the downstream targets when compared to wildtype TAp63gamma. In summary, our data demonstrate that p63 mutants exhibit differential effects on p63 and p53/p63 specific target genes and on the induction of apoptosis, and provide further insight into the function of p63.

Indexed as

Transcriptional ActivationApoptosisHedgehog ProteinsHumansMutationProtein IsoformsProto-Oncogene Proteins c-mdm2RNA SplicingTrans-ActivatorsTranscription FactorsTumor Cells, CulturedTumor Suppressor Protein p53Tumor Suppressor ProteinsHedgehog ProteinsMDM2 protein, humanProtein IsoformsProto-Oncogene Proteins c-mdm2SHH protein, humanTP63 protein, humanTrans-ActivatorsTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID18626511
PMCPMC2760224
OpenAlexW1987207036

What OpenQuestion holds

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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.