Evidence map›Paper›PMID 20847228›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011

Unphosphorylated STAT and heterochromatin protect genome stability.

Shian-Jang Yan, Su Jun Lim, Song Shi, Pranabananda Dutta, Willis X Li

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. CRIF counteracts oncogenic Ras and regulates heterochromatin.Molecular genetics and genomics : MGG · 2025
    Article
  3. Review
  4. Article
  5. Review
  6. 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
  7. Article
  8. Article
  9. Article
  10. Aging mechanisms-A perspective mostly fromAdvanced genetics (Hoboken, N.J.) · 2020
    Article
  11. Review
  12. Article
  13. Review
  14. DetectingInternational journal of molecular sciences · 2019
    Article
  15. Article
  16. Article
  17. Article
  18. The molecular details of cytokine signaling via the JAK/STAT pathway.Protein science : a publication of the Protein Society · 2018
    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

5 authors at 1 institution in 1 country.

Shian-Jang YanDepartment of Biomedical Genetics, University of Rochester Medical Center, 601 Elmwood Ave., KMRB 2-9654, Rochester, NY 14642, USA.
Su Jun Lim
Song Shi
Pranabananda Dutta
Willis X Li
University of Rochester Medical Center · US

Funding

CANCER RESEARCH TRAINING-EXPERIMENTAL THERAPY MODELST32CA009363 · NCI · UNIVERSITY OF ROCHESTER · PI LAND, HARTMUT · 1985 to 2013
$2.9M
Epigenetic tumor induction by heterochromatin instabilityR01CA131326 · NCI · UNIVERSITY OF ROCHESTER · PI LI, WILLIS X · 2009 to 2013
$1.3M
NCI NIH HHS R01 CA131326NCI NIH HHS T32 CA009363NCI NIH HHS T32CA009363
6 · The paper itself

Abstract

Heterochromatin is a form of highly compacted chromatin associated with epigenetic gene silencing and chromosome organization. We have previously shown that unphosphorylated nuclear signal transducer and activator of transcription (STAT) physically interacts with heterochromatin protein 1 (HP1) to promote heterochromatin stability. To understand whether STAT and heterochromatin are important for maintenance of genome stability, we genetically manipulated the levels of unphosphorylated STAT and HP1 [encoded by Su(var)205] in Drosophila and examined the effects on chromosomal morphology and resistance to DNA damage under conditions of genotoxic stress. Here we show that, compared with wild-type controls, Drosophila mutants with reduced levels of unphosphorylated STAT or heterochromatin are more sensitive to radiation-induced cell cycle arrest, have higher levels of spontaneous and radiation-induced DNA damage, and exhibit defects in chromosomal compaction and segregation during mitosis. Conversely, animals with increased levels of heterochromatin exhibit less DNA damage and increased survival rate after irradiation. These results suggest that maintaining genome stability by heterochromatin formation and correct chromosomal packaging is essential for normal cellular functions and for survival of animals under genotoxic stress.

Indexed as

Genomic InstabilityAnimalsAnimals, Genetically ModifiedCell CycleChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneChromosome BreakageChromosomes, InsectDNA DamageDrosophila melanogasterDrosophila ProteinsEmbryo, NonmammalianFemaleHeterochromatinHistonesImmunohistochemistryChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneDrosophila ProteinsHeterochromatinHistonesRepressor ProteinsStat92E protein, DrosophilaSTAT Transcription FactorsSu(var)205 protein, DrosophilaSu(var)3-9 protein, Drosophila

Identifiers

PMID20847228
PMCPMC3005427
OpenAlexW1989156362

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.