Evidence map›Paper›PMID 17873903›Full record

ArticleOncogene2008

Coiled-coil domain containing 85B suppresses the beta-catenin activity in a p53-dependent manner.

A Iwai, M Hijikata, T Hishiki, O Isono, T Chiba, K Shimotohno

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.1field-weighted citation impact, top 47% 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

18 citing papers in PubMed, 23 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

6 authors at 1 institution in 1 country.

A IwaiDivision of Gastroenterology and Hepatology, Department of Medicine, Kyoto University, Kyoto, Japan.
M Hijikata
T Hishiki
O Isono
T Chiba
K Shimotohno
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant accumulation of beta-catenin is closely related to carcinogenesis. Mutations in the p53 gene are reported to induce the aberrant accumulation of beta-catenin in the absence of dysfunction in the glycogen synthase kinase 3beta (GSK3beta)-mediated degradation pathway, but the mechanism remains incompletely understood. Here, we show that human coiled-coil domain containing 85B (CCDC85B) is induced by p53 and regulates beta-catenin activity via interaction with the T-cell factor 4 in the nucleus. Moreover, CCDC85B enhances the degradation of beta-catenin and suppresses tumor cell growth. In conclusion, we revealed that CCDC85B-induced degradation of beta-catenin is independent of GSK3beta and other p53-inducible products, Siah-1L, suggesting that CCDC85B constitutes the one of the frameworks of p53-induced multiple regulatory pathways for beta-catenin activity.

Indexed as

Adaptor Proteins, Signal Transducingbeta CateninCarrier ProteinsCell NucleusCells, CulturedCysteine Proteinase InhibitorsFluorescent Antibody TechniqueGene Expression ProfilingGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHepatocyte Nuclear Factor 1-alphaHumansImmunoblottingImmunoprecipitationLeupeptinsOligonucleotide Array Sequence AnalysisAdaptor Proteins, Signal Transducingbenzyloxycarbonylleucyl-leucyl-leucine aldehydebeta CateninCarrier ProteinsCCDC85B protein, humanCysteine Proteinase InhibitorsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanHepatocyte Nuclear Factor 1-alphaHNF1A protein, humanLeupeptinsRepressor ProteinsTCF7L2 protein, humanTCF Transcription FactorsTP53 protein, humanTranscription Factor 7-Like 2 ProteinTumor Suppressor Protein p53Ubiquitin

Identifiers

PMID17873903
OpenAlexW2021832401

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.