Evidence map›Paper›PMID 20501334›Full record

ArticleDevelopmental biology2010

Characterization of a dominant-active STAT that promotes tumorigenesis in Drosophila.

Laura A Ekas, Timothy J Cardozo, Maria Sol Flaherty, Elizabeth A McMillan, Foster C Gonsalves, Erika A Bach

Abstract read
In one paragraph

Article in Developmental biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.4field-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

38 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Frontiers in immunology · 2023
    Article
  11. Neuroscience insights · 2023
    Article
  12. Article
  13. Article
  14. Tumor models in various Drosophila tissues.WIREs mechanisms of disease · 2021
    Review
  15. The S1A protease family membersmicroPublication biology · 2021
    Article
  16. Article
  17. Article
  18. Article
  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

6 authors at 1 institution in 1 country.

Laura A EkasPharmacology Department, New York University School of Medicine, New York, New York 10016-6402, USA.
Timothy J Cardozo
Maria Sol Flaherty
Elizabeth A McMillan
Foster C Gonsalves
Erika A Bach
New York University · US

Funding

Eludicating the Molecular Mechanisms That Regulate Stem Cell Numbers in VivoR01GM085075 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BACH, ERIKA A · 2009 to 2023
$4.3M
Training in Pharmacological SciencesT32GM066704 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BACH, ERIKA A · 2004 to 2018
$2.6M
NIGMS NIH HHS 1R01GM085075NIGMS NIH HHS R01 GM085075NIGMS NIH HHS T32 GM066704NIGMS NIH HHS T32 GM066704-03
6 · The paper itself

Abstract

Little is known about the molecular mechanisms by which STAT proteins promote tumorigenesis. Drosophila is an ideal system for investigating this issue, as there is a single STAT (Stat92E), and its hyperactivation causes overgrowths resembling human tumors. Here we report the first identification of a dominant-active Stat92E protein, Stat92E(DeltaNDeltaC), which lacks both N- and C-termini. Mis-expression of Stat92E(DeltaNDeltaC)in vivo causes melanotic tumors, while in vitro it transactivates a Stat92E-luciferase reporter in the absence of stimulation. These gain-of-function phenotypes require phosphorylation of Y(711) and dimer formation with full-length Stat92E. Furthermore, a single point mutation, an R(442P) substitution in the DNA-binding domain, abolishes Stat92E function. Recombinant Stat92E(R442P) translocates to the nucleus following activation but fails to function in all assays tested. Interestingly, R(442) is conserved in most STATs in higher organisms, suggesting conservation of function. Modeling of Stat92E indicates that R(442) may contact the minor groove of DNA via invariant TC bases in the consensus binding element bound by all STAT proteins. We conclude that the N- and C- termini function unexpectedly in negatively regulating Stat92E activity, possibly by decreasing dimer dephosphorylation or increasing stability of DNA interaction, and that Stat92E(R442) has a nuclear function by altering dimer:DNA binding.

Indexed as

AnimalsDrosophilaPhosphorylationProteinsTrans-ActivatorsTranscription FactorsProteinsTrans-ActivatorsTranscription Factors

Identifiers

PMID20501334
PMCPMC2914209
OpenAlexW2066783571

What OpenQuestion holds

Textmetadata
LicenceTDM
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.