Evidence map›Paper›PMID 16892059›Full record

ArticleNature genetics2006

JAK signaling globally counteracts heterochromatic gene silencing.

Song Shi, Healani C Calhoun, Fan Xia, Jinghong Li, Long Le, Willis X Li

Open access · greenAbstract read
In one paragraph

Article in Nature genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

105 citing papers in PubMed, 174 citations in OpenAlex.

  1. CRIF counteracts oncogenic Ras and regulates heterochromatin.Molecular genetics and genomics : MGG · 2025
    Article
  2. Article
  3. Article
  4. Review
  5. JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025
    Review
  6. Epigenetic Regulation in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025
    Review
  7. Review
  8. Computational simulation of JAK/STAT signaling in somatic versus germline stem cells.Developmental dynamics : an official publication of the American Association of Anatomists · 2024
    Article
  9. Review
  10. Review
  11. Canonical and non-canonical functions of STAT in germline stem cell maintenance.Developmental dynamics : an official publication of the American Association of Anatomists · 2023
    Article
  12. Review
  13. Review
  14. Review
  15. The JAK/STAT signaling pathway: from bench to clinic.Signal transduction and targeted therapy · 2021
    Review
  16. Review
  17. Review
  18. Review
  19. Aging mechanisms-A perspective mostly fromAdvanced genetics (Hoboken, N.J.) · 2020
    Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Song ShiDepartment of Biomedical Genetics, University of Rochester Medical Center, Rochester, New York 14642, USA.
Healani C Calhoun
Fan Xia
Jinghong Li
Long Le
Willis X Li
University of Rochester Medical Center · US

Funding

Genetic Analysis of Intracellular Signaling CrosstalkR01GM065774 · NIGMS · UNIVERSITY OF ROCHESTER · PI LI, WILLIS X · 2002 to 2006
$1.3M
Epigenetic tumor induction by heterochromatin instabilityR01CA131326 · NCI · UNIVERSITY OF ROCHESTER · PI LI, WILLIS X · 2009 to 2013
$1.3M
Network Interaction between EGFR and TGFbeta PathwaysR01GM077046 · NIGMS · UNIVERSITY OF ROCHESTER · PI LI, WILLIS X · 2006 to 2009
$940k
NCI NIH HHS R01 CA131326NIGMS NIH HHS R01 GM065774NIGMS NIH HHS R01 GM077046NIGMS NIH HHS R01GM077046NIGMS NIH HHS R01GM65774
6 · The paper itself

Abstract

The JAK/STAT pathway has pleiotropic roles in animal development, and its aberrant activation is implicated in multiple human cancers. JAK/STAT signaling effects have been attributed largely to direct transcriptional regulation by STAT of specific target genes that promote tumor cell proliferation or survival. We show here in a Drosophila melanogaster hematopoietic tumor model, however, that JAK overactivation globally disrupts heterochromatic gene silencing, an epigenetic tumor suppressive mechanism. This disruption allows derepression of genes that are not direct targets of STAT, as evidenced by suppression of heterochromatin-mediated position effect variegation. Moreover, mutations in the genes encoding heterochromatin components heterochromatin protein 1 (HP1) and Su(var)3-9 enhance tumorigenesis induced by an oncogenic JAK kinase without affecting JAK/STAT signaling. Consistently, JAK loss of function enhances heterochromatic gene silencing, whereas overexpressing HP1 suppresses oncogenic JAK-induced tumors. These results demonstrate that the JAK/STAT pathway regulates cellular epigenetic status and that globally disrupting heterochromatin-mediated tumor suppression is essential for tumorigenesis induced by JAK overactivation.

Indexed as

Gene SilencingSignal TransductionAnimalsbeta-GalactosidaseDrosophilaDrosophila ProteinsFemaleHeterochromatinImmunohistochemistryJanus KinasesMutationProtein-Tyrosine KinasesSTAT Transcription FactorsTranscription Factorsbeta-GalactosidaseDrosophila ProteinsHeterochromatinhop protein, DrosophilaJanus KinasesProtein-Tyrosine KinasesStat92E protein, DrosophilaSTAT Transcription FactorsTranscription Factors

Identifiers

PMID16892059
PMCPMC3092431
OpenAlexW2001393635

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.