Evidence map›Paper›PMID 24384092›Full record

ArticleCancer letters2014

An N-terminal splice variant of human Stat5a that interacts with different transcription factors is the dominant form expressed in invasive ductal carcinoma.

Dunyong Tan, KuanHui E Chen, Changhui Deng, Peizhi Tang, Jianjun Huang, Trina Mansour, Richard A Luben, Ameae M Walker

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

4 citing papers in PubMed, 7 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

8 authors at 2 institutions in 2 countries.

Dunyong TanDivision of Biomedical Sciences, University of California, Riverside, Riverside, CA 92521-0121, United States; College of Medicine/Institute of Medical Sciences, Jishou University, Jishou 416000, Hunan, PR China.
KuanHui E ChenDivision of Biomedical Sciences, University of California, Riverside, Riverside, CA 92521-0121, United States.
Changhui DengDivision of Biomedical Sciences, University of California, Riverside, Riverside, CA 92521-0121, United States; Department of Biochemistry, University of California, Riverside, Riverside, CA 92521-0121, United States.
Peizhi TangPeople's Hospital of Xiangxi Autonomous Region, Jishou University, Jishou 416000, Hunan, PR China.
Jianjun HuangPeople's Hospital of Xiangxi Autonomous Region, Jishou University, Jishou 416000, Hunan, PR China.
Trina MansourDivision of Biomedical Sciences, University of California, Riverside, Riverside, CA 92521-0121, United States.
Richard A LubenDivision of Biomedical Sciences, University of California, Riverside, Riverside, CA 92521-0121, United States; Department of Biochemistry, University of California, Riverside, Riverside, CA 92521-0121, United States.
Ameae M WalkerDivision of Biomedical Sciences, University of California, Riverside, Riverside, CA 92521-0121, United States. Electronic address: ameae.walker@ucr.edu.
University of California, Riverside · USJishou University · CN

Funding

Genetic approaches to study cytokine control of metabolismZ01DK061005 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HENNIGHAUSEN, LOTHAR · 2007 to 2008
$1.3M
S179D Prolactin: Inhibition of Prostate Cancer GrowthR01DK061005 · NIDDK · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI WALKER, AMEAE M · 2001 to 2004
$1.1M
Intramural NIH HHS Z01 DK061005NIDDK NIH HHS R01 DK061005
6 · The paper itself

Abstract

We have identified a new variant of human Stat5a, found at higher ratios to full-length Stat5a in invasive ductal carcinoma versus contiguous normal tissue. The variant, missing exon 5, inhibits p21 and Bax production and increases cell number. After prolactin stimulation, only full-length Stat5a interacts with the vitamin D and retinoid X receptors, whereas only Δ5 Stat5a interacts with activating protein 1-2 and specificity protein 1. Prolactin also oppositely regulates interaction of the two Stat5a forms with β-catenin. We propose that a change in splicing leading to upregulation of this new isoform is a pathogenic aspect of invasive ductal carcinoma.

Indexed as

Base SequenceBlotting, WesternBreast NeoplasmsCarcinoma, Ductal, BreastCell Line, TumorChromatin ImmunoprecipitationHumansMolecular Sequence DataProtein IsoformsReverse Transcriptase Polymerase Chain ReactionSignal TransductionSTAT5 Transcription FactorTranscription FactorsTransfectionTumor Suppressor ProteinsUp-RegulationProtein IsoformsSTAT5A protein, humanSTAT5 Transcription FactorTranscription FactorsTumor Suppressor ProteinsBreast cancerInteraction with other signaling/transcription factorsInvasive ductal carcinomaSplice variantStat5a

Identifiers

PMID24384092
PMCPMC3959904
OpenAlexW2090739374

What OpenQuestion holds

Textmetadata
LicenceTDM
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.