Evidence map›Paper›PMID 24826056›Full record

ArticleChinese journal of cancer research = Chung-kuo yen cheng yen chiu2014

Does not hUTP14a promoter form a regulation feedback loop with P53?

Jingyi Zhang, Yafei Guo, Xiaojuan Du, Baocai Xing

Open access · greenAbstract read
In one paragraph

Article in Chinese journal of cancer research = Chung-kuo yen cheng yen chiu, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 49% 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

3 citing papers in PubMed, 3 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.

Jingyi Zhang1 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Hepatic, Biliary & Pancreatic Surgery I, Peking University Cancer Hospital & Institute, Beijing 100142, China ; 2 Department of Cell Biology, Peking University Health Science Center, Beijing 100191, China.
Yafei Guo1 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Hepatic, Biliary & Pancreatic Surgery I, Peking University Cancer Hospital & Institute, Beijing 100142, China ; 2 Department of Cell Biology, Peking University Health Science Center, Beijing 100191, China.
Xiaojuan Du1 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Hepatic, Biliary & Pancreatic Surgery I, Peking University Cancer Hospital & Institute, Beijing 100142, China ; 2 Department of Cell Biology, Peking University Health Science Center, Beijing 100191, China.
Baocai Xing1 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Hepatic, Biliary & Pancreatic Surgery I, Peking University Cancer Hospital & Institute, Beijing 100142, China ; 2 Department of Cell Biology, Peking University Health Science Center, Beijing 100191, China.
Ministry of Education · ET

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveWe previously found that hUTP14a binds P53 and promotes P53 degradation. However, if hUTP14a is a downstream gene of P53 remains to be determined. This study aimed to identify the promoter of hUTP14a and investigate if hUTP14a is regulated by P53.

methodsThe hUTP14a promoter region was cloned into pGL3-Basic-luciferase reporter plasmid to get pGL3-hUTP14a-luc. The reporter plasmid was transfected into 293T cells and luciferase activity was evaluated by the Dual-Luciferase Reporter Assay System. Putative transcription factors were identified through searching MatInspector Professional and Algorismica i Genetica databases. Either pGL3-hUTP14a-luc or p21 promoter reporter plasmid was co-transfected with increasing dose of p53 plasmid, and luciferase activity was evaluated. A series of deletion constructs of pGL3-hUTP14a-luc were constructed and minimal promoter region of hUTP14a was determined. Differences of the luciferase activities between different groups were assessed by statistical analysis.

resultsThe hUTP14a gene promoter reporter construct was correctly cloned and was demonstrated to possess promoter activity. The transcription of hUTP14a was not regulated by P53. The minimal promoter region of hUTP14a gene is located between -203 to -100 of the transcription initiation site.

conclusionUnlike other P53-interacting proteins such as MDM2, Pirh2 and Cop I which promote P53 degradation and whose transcriptions are regulated by P53, does not hUTP14a transcription form a regulation feedback loop with P53.

Indexed as

hUTP14aluciferase activityP53promotertranscription factor

Identifiers

PMID24826056
PMCPMC4000906
OpenAlexW142794801

What OpenQuestion holds

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Registered trials

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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.