Evidence map›Paper›PMID 24508259›Full record

ArticleBiochemical and biophysical research communications2014

Yin Yang 1 regulates the transcriptional repression of Survivin.

Nicholas R Galloway, Carlos J Diaz Osterman, Karl Reiber, Jessica M S Jutzy, Fengzhi Li, Guangchao Sui, Ubaldo Soto, Nathan R Wall

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Yin Yang 1 Promotes Thymocyte Survival by Downregulating p53.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Article
  7. Article
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 1 country.

Nicholas R GallowayCenter for Health Disparities Research and Molecular Medicine, Division of Biochemistry and Microbiology, Loma Linda University, Loma Linda, CA 92350, United States; Department of Basic Sciences, Division of Biochemistry and Microbiology, Loma Linda University, Loma Linda, CA 92350, United States. Electronic address: ngalloway@llu.edu.
Carlos J Diaz OstermanCenter for Health Disparities Research and Molecular Medicine, Division of Biochemistry and Microbiology, Loma Linda University, Loma Linda, CA 92350, United States; Department of Basic Sciences, Division of Biochemistry and Microbiology, Loma Linda University, Loma Linda, CA 92350, United States. Electronic address: cdiazosterman@llu.edu.
Karl ReiberCenter for Health Disparities Research and Molecular Medicine, Division of Biochemistry and Microbiology, Loma Linda University, Loma Linda, CA 92350, United States; Department of Basic Sciences, Division of Biochemistry and Microbiology, Loma Linda University, Loma Linda, CA 92350, United States. Electronic address: kreiber@llu.edu.
Jessica M S JutzyCenter for Health Disparities Research and Molecular Medicine, Division of Biochemistry and Microbiology, Loma Linda University, Loma Linda, CA 92350, United States; Department of Basic Sciences, Division of Biochemistry and Microbiology, Loma Linda University, Loma Linda, CA 92350, United States. Electronic address: jjutzy@llu.edu.
Fengzhi LiDepartment of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, NY 14263, United States. Electronic address: Fengzhi.Li@RoswellPark.org.
Guangchao SuiDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, United States. Electronic address: gsui@wfubmc.edu.
Ubaldo SotoDepartment of Basic Sciences, Division of Biochemistry and Microbiology, Loma Linda University, Loma Linda, CA 92350, United States. Electronic address: usoto@llu.edu.
Nathan R WallCenter for Health Disparities Research and Molecular Medicine, Division of Biochemistry and Microbiology, Loma Linda University, Loma Linda, CA 92350, United States; Department of Basic Sciences, Division of Biochemistry and Microbiology, Loma Linda University, Loma Linda, CA 92350, United States. Electronic address: nwall@llu.edu.
Loma Linda University · USRoswell Park Comprehensive Cancer Center · USWake Forest University · US

Funding

NIH-LLU Initiative for Maximizing Student DiversityR25GM060507 · NIGMS · LOMA LINDA UNIVERSITY · PI DE LEON, MARINO · 2001 to 2022
$11.3M
The role of imidazoline receptor in type-2 diabetesP20MD001632 · NIMHD · LOMA LINDA UNIVERSITY · PI DE LEON, DAISY D. · 2005 to 2009
$8.0M
Research Training/Education CoreP20MD006988 · NIMHD · LOMA LINDA UNIVERSITY · PI CASIANO, CARLOS A. · 2012 to 2016
$6.2M
NIGMS NIH HHS 2 R25 GM060507NIGMS NIH HHS R25 GM060507NIMHD NIH HHS 5P20MD001632NIMHD NIH HHS P20 MD001632NIMHD NIH HHS P20 MD006988NIMHD NIH HHS P20MD006988
6 · The paper itself

Abstract

The mechanisms for regulation of the Inhibitor of Apoptosis (IAP) Survivin in cells undergoing stress associated with tumor development and the tumor microenvironment are not well understood. The stress response transcription factors HIF-1α and Yin Yang 1 (YY1) were hypothesized to contribute to the upregulation of Survivin in tumor cells. As expected, U2OS cells overexpressing HIF-1α showed a 2- to 3-fold transactivation when transfected. Surprisingly, when YY1 was overexpressed in this survivin promoter reporter system, luciferase expression was repressed 30- to 40-fold. YY1 involvement in survivin promoter repression was confirmed using siRNA directed against YY1. These studies showed that knockdown of YY1 releases the survivin promoter from the observed repression and leads to a 3- to 5-fold increase in promoter activity above basal levels. A U2OS cell line containing a stable YY1 Tet-off system was used to determine whether a temporal increase in YY1 expression affects Survivin protein levels. A low to moderate decrease in Survivin protein was observed 24h and 48h after Tet removal. Studies also confirmed that YY1 is capable of directly binding to the survivin promoter. Collectively, these findings identify novel basal transcriptional requirements of survivin gene expression which are likely to play important roles in the development of cancer and resistance to its treatment.

Indexed as

Gene Expression Regulation, NeoplasticTranscription, GeneticBase SequenceBinding SitesBlotting, WesternCell Line, TumorHumansHypoxia-Inducible Factor 1, alpha SubunitInhibitor of Apoptosis ProteinsLuciferasesMolecular Sequence DataPromoter Regions, GeneticProtein BindingReverse Transcriptase Polymerase Chain ReactionRNA InterferenceSurvivinBIRC5 protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitInhibitor of Apoptosis ProteinsLuciferasesSurvivinYY1 protein, humanYY1 Transcription FactorHIF-1IAPSurvivinTranscriptional repressorYY1

Identifiers

PMID24508259
PMCPMC4071961
OpenAlexW1969771659

What OpenQuestion holds

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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.