Evidence map›Paper›PMID 24497979›Full record

ArticlePloS one2014

Identification of STAT5A and STAT5B target genes in human T cells.

Takahiro Kanai, Scott Seki, Jennifer A Jenks, Arunima Kohli, Trupti Kawli, Dorrelyn Patacsil Martin, Michael Snyder, Rosa Bacchetta, Kari C Nadeau

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 19% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

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  20. Asymmetrically Substituted m-Terphenyl Phosphates Inhibit the Transcription Factor STAT5a.Chembiochem : a European journal of chemical biology · 2022
    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

9 authors at 1 institution in 2 countries.

Takahiro KanaiDivision of Immunology and Allergy, Department of Pediatrics, School of Medicine, Stanford University, Stanford, California, United States of America.
Scott SekiDivision of Immunology and Allergy, Department of Pediatrics, School of Medicine, Stanford University, Stanford, California, United States of America.
Jennifer A JenksDivision of Immunology and Allergy, Department of Pediatrics, School of Medicine, Stanford University, Stanford, California, United States of America.
Arunima KohliDivision of Immunology and Allergy, Department of Pediatrics, School of Medicine, Stanford University, Stanford, California, United States of America.
Trupti KawliDepartment of Genetics, School of Medicine, Stanford University, Stanford, California, United States of America.
Dorrelyn Patacsil MartinDepartment of Genetics, School of Medicine, Stanford University, Stanford, California, United States of America.
Michael SnyderDepartment of Genetics, School of Medicine, Stanford University, Stanford, California, United States of America.
Rosa BacchettaDivision of Immunology and Allergy, Department of Pediatrics, School of Medicine, Stanford University, Stanford, California, United States of America ; San Raffaele Telethon Institute for Gene Therapy (HSR-TIGET), San Raffaele Scientific Institute, Milan, Italy.
Kari C NadeauDivision of Immunology and Allergy, Department of Pediatrics, School of Medicine, Stanford University, Stanford, California, United States of America.
Stanford University · US

Funding

Telethon TGT11A04
6 · The paper itself

Abstract

Signal transducer and activator of transcription (STAT) comprises a family of universal transcription factors that help cells sense and respond to environmental signals. STAT5 refers to two highly related proteins, STAT5A and STAT5B, with critical function: their complete deficiency is lethal in mice; in humans, STAT5B deficiency alone leads to endocrine and immunological problems, while STAT5A deficiency has not been reported. STAT5A and STAT5B show peptide sequence similarities greater than 90%, but subtle structural differences suggest possible non-redundant roles in gene regulation. However, these roles remain unclear in humans. We applied chromatin immunoprecipitation followed by DNA sequencing using human CD4(+) T cells to detect candidate genes regulated by STAT5A and/or STAT5B, and quantitative-PCR in STAT5A or STAT5B knock-down (KD) human CD4(+) T cells to validate the findings. Our data show STAT5A and STAT5B play redundant roles in cell proliferation and apoptosis via SGK1 interaction. Interestingly, we found a novel, unique role for STAT5A in binding to genes involved in neural development and function (NDRG1, DNAJC6, and SSH2), while STAT5B appears to play a distinct role in T cell development and function via DOCK8, SNX9, FOXP3 and IL2RA binding. Our results also suggest that one or more co-activators for STAT5A and/or STAT5B may play important roles in establishing different binding abilities and gene regulation behaviors. The new identification of these genes regulated by STAT5A and/or STAT5B has major implications for understanding the pathophysiology of cancer progression, neural disorders, and immune abnormalities.

Indexed as

Active Transport, Cell NucleusBase SequenceBinding SitesCD4-Positive T-LymphocytesCells, CulturedConsensus SequenceHumansProtein MultimerizationSTAT5 Transcription FactorTranscriptional ActivationTranscriptomeTumor Suppressor ProteinsSTAT5A protein, humanSTAT5B protein, humanSTAT5 Transcription FactorTumor Suppressor Proteins

Identifiers

PMID24497979
PMCPMC3907443
OpenAlexW1988177782

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.