Evidence map›Paper›PMID 26169829›Full record

ArticleMolecular and cellular biology2015

Impact of the N-Terminal Domain of STAT3 in STAT3-Dependent Transcriptional Activity.

Tiancen Hu, Jennifer E Yeh, Luca Pinello, Jaison Jacob, Srinivas Chakravarthy, Guo-Cheng Yuan, Rajiv Chopra, David A Frank

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

32 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Cellular signaling meets bacterial infection: the integrative role of STAT3.Frontiers in cellular and infection microbiology · 2026
    Review
  3. STAT3 SH2 Domain Aspartic Acid 661 Mutations Activate Immune Gene Programs.Journal of cellular and molecular medicine · 2026
    Article
  4. Review
  5. Article
  6. Article
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  8. Article
  9. Review
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  11. Review
  12. Review
  13. Review
  14. Article
  15. Targeting key transcriptional factor STAT3 in colorectal cancer.Molecular and cellular biochemistry · 2021
    Review
  16. STAT3 Is an Upstream Regulator ofInternational journal of molecular sciences · 2021
    Article
  17. Epigenetic Signaling of Cancer Stem Cells During Inflammation.Frontiers in cell and developmental biology · 2021
    Review
  18. Review
  19. Article
  20. 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.

Tiancen HuCenter for Proteomic Chemistry, Novartis Institutes for BioMedical Research, Cambridge, Massachusetts, USA Postdoctoral Program, Novartis Institutes for BioMedical Research, Cambridge, Massachusetts, USA.
Jennifer E YehDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA.
Luca PinelloDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA.
Jaison JacobCenter for Proteomic Chemistry, Novartis Institutes for BioMedical Research, Cambridge, Massachusetts, USA.
Srinivas ChakravarthyBiophysical Collaborative Access Team/Illinois Institute of Technology, Sector 18ID (Advanced Photon Source, Argonne National Laboratory), Lemont, Illinois, USA.
Guo-Cheng YuanDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA.
Rajiv ChopraCenter for Proteomic Chemistry, Novartis Institutes for BioMedical Research, Cambridge, Massachusetts, USA rajiv.chopra@novartis.com david_frank@dfci.harvard.edu.
David A FrankDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA Biophysical Collaborative Access Team/Illinois Institute of Technology, Sector 18ID (Advanced Photon Source, Argonne National Laboratory), Lemont, Illinois, USA Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA rajiv.chopra@novartis.com david_frank@dfci.harvard.edu.
Harvard University · USArgonne National Laboratory · USIllinois Institute of Technology · US

Funding

Molecular, Cellular, & Developmental Dynamics PhD ProgramT32GM007226 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI VAN VACTOR, DAVID L. · 1985 to 2021
$14.4M
Time resolved SAXS studies on the RP2/Arl3 complex pp.484-485P41GM103622 · NIGMS · ILLINOIS INSTITUTE OF TECHNOLOGY · PI IRVING, THOMAS C · 2012 to 2020
$11.9M
Dual STAT3/NF-kB Inhibitors for Targeted Cancer TherapyR01CA160979 · NCI · DANA-FARBER CANCER INST · PI FRANK, DAVID A. · 2012 to 2016
$1.8M
Defining the CD44-STAT3 axis in the pathogenesis of triple-negative breast cancerF30CA180340 · NCI · HARVARD MEDICAL SCHOOL · PI YEH, JENNIFER ELYNN · 2013 to 2016
$162k
NCI NIH HHS F30 CA180340NCI NIH HHS F30 CA180340-01NCI NIH HHS R01 CA160979NCI NIH HHS R01-CA160979NIGMS NIH HHS P41 GM103622NIGMS NIH HHS T32 GM007226NIGMS NIH HHS T32GM007226
6 · The paper itself

Abstract

The transcription factor STAT3 is constitutively active in many cancers, where it mediates important biological effects, including cell proliferation, differentiation, survival, and angiogenesis. The N-terminal domain (NTD) of STAT3 performs multiple functions, such as cooperative DNA binding, nuclear translocation, and protein-protein interactions. However, it is unclear which subsets of STAT3 target genes depend on the NTD for transcriptional regulation. To identify such genes, we compared gene expression in STAT3-null mouse embryonic fibroblasts (MEFs) stably expressing wild-type STAT3 or STAT3 from which NTD was deleted. NTD deletion reduced the cytokine-induced expression of specific STAT3 target genes by decreasing STAT3 binding to their regulatory regions. To better understand the potential mechanisms of this effect, we determined the crystal structure of the STAT3 NTD and identified a dimer interface responsible for cooperative DNA binding in vitro. We also observed an Ni(2+)-mediated oligomer with an as yet unknown biological function. Mutations on both dimer and Ni(2+)-mediated interfaces affected the cytokine induction of STAT3 target genes. These studies shed light on the role of the NTD in transcriptional regulation by STAT3 and provide a structural template with which to design STAT3 NTD inhibitors with potential therapeutic value.

Indexed as

Transcription, GeneticAmino Acid SequenceAnimalsBase SequenceCells, CulturedCrystallography, X-RayLeukemia Inhibitory FactorMiceModels, MolecularMolecular Sequence DataProtein BindingProtein MultimerizationProtein Structure, SecondaryProtein Structure, TertiarySTAT3 Transcription FactorTranscriptional ActivationLeukemia Inhibitory FactorLif protein, mouseStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID26169829
PMCPMC4561728
OpenAlexW2155396299

What OpenQuestion holds

Textmetadata
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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.