Evidence map›Paper›PMID 17510282›Full record

ArticleGenes & development2007

Unphosphorylated STAT3 accumulates in response to IL-6 and activates transcription by binding to NFkappaB.

Jinbo Yang, Xudong Liao, Mukesh K Agarwal, Laura Barnes, Philip E Auron, George R Stark

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 368 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
368citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

368 citing papers in PubMed, 1 synthesis or guideline pooled it, 609 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Neuroinflammation and Disease: Pathways and Opportunities.Annual review of pharmacology and toxicology · 2026
    Review
  12. Cellular signaling meets bacterial infection: the integrative role of STAT3.Frontiers in cellular and infection microbiology · 2026
    Review
  13. Review
  14. Review
  15. NovelImmune network · 2025
    Article
  16. AhR and STAT3: A Dangerous Duo in Chemical Carcinogenesis.International journal of molecular sciences · 2025
    Review
  17. Article
  18. Review
  19. Article
  20. Article

308 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Jinbo YangDepartment of Molecular Genetics, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Xudong Liao
Mukesh K Agarwal
Laura Barnes
Philip E Auron
George R Stark
Cleveland Clinic · USCase Comprehensive Cancer CenterUniversity of Pittsburgh · US

Funding

TELOMERASE INACTIVATION BY RNASE L SIGNALS CELL DEATHP01CA062220 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI LI, XIAOXIA, STARK, GEORGE ROBERT · 1994 to 2020
$35.6M
NCI NIH HHS P01 CA062220NCI NIH HHS P01 CA 62220PHS HHS R01 A144122
6 · The paper itself

Abstract

gp130-linked cytokines such as interleukin-6 (IL-6) stimulate the formation of tyrosine-phosphorylated signal transducer and activator of transcription 3 (P-STAT3), which activates many genes, including the STAT3 gene itself. The resulting increase in the concentration of unphosphorylated STAT3 (U-STAT3) drives a second wave of expression of genes such as RANTES, IL6, IL8, MET, and MRAS that do not respond directly to P-STAT3. Thus, U-STAT3 sustains cytokine-dependent signaling at late times through a mechanism completely distinct from that used by P-STAT3. Many U-STAT3-responsive genes have kappaB elements that are activated by a novel transcription factor complex formed when U-STAT3 binds to unphosphorylated NFkappaB (U-NFkappaB), in competition with IkappaB. The U-STAT3/U-NFkappaB complex accumulates in the nucleus with help from the nuclear localization signal of STAT3, activating a subset of kappaB-dependent genes. Additional genes respond to U-STAT3 through an NFkappaB-independent mechanism. The role of signal-dependent increases in U-STAT3 expression in regulating gene expression is likely to be important in physiological responses to gp130-linked cytokines and growth factors that activate STAT3, and in cancers that have constitutively active P-STAT3.

Indexed as

Gene Expression RegulationTranscription, GeneticBinding SitesBiomarkersBreastCell NucleusCells, CulturedChemokine CCL5Chromatin ImmunoprecipitationEpithelial CellsGene Expression ProfilingHumansImmunoprecipitationInterleukin-6NF-kappa BNuclear Localization SignalsBiomarkersChemokine CCL5Interleukin-6NF-kappa BNuclear Localization SignalsSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID17510282
PMCPMC1877751
OpenAlexW2103422355

What OpenQuestion holds

Textmetadata
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.