Evidence map›Paper›PMID 21943404›Full record

ArticleCell & bioscience2011

Transient knockdown and overexpression reveal a developmental role for the zebrafish enosf1b gene.

Steve Finckbeiner, Pin-Joe Ko, Blake Carrington, Raman Sood, Kenneth Gross, Bruce Dolnick, Janice Sufrin, Paul Liu

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

12 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Use of Zebrafish Models to Boost Research in Rare Genetic Diseases.International journal of molecular sciences · 2021
    Review
  6. Article
  7. Review
  8. Comparative Proteomic Analysis of Yak Follicular Fluid during Estrus.Asian-Australasian journal of animal sciences · 2016
    Article
  9. Article
  10. Article
  11. Article
  12. 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 2 institutions in 1 country.

Steve FinckbeinerOncogenesis and Development Section, National Human Genome Research Institute, 49 Convent Drive, Bethesda MD, 20892, USA. pliu@mail.nih.gov.
Pin-Joe Ko
Blake Carrington
Raman Sood
Kenneth Gross
Bruce Dolnick
Janice Sufrin
Paul Liu
National Human Genome Research Institute · USRoswell Park Comprehensive Cancer Center · US

Funding

GENETIC ANALYSIS OF ZEBRAFISH EMBRYO DEVELOPMENTZIAHG000102 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI LIU, PAUL · 2009 to 2025
$17.1M
NHGRI/DIR Zebrafish CoreZIGHG200351 · NHGRI · NATIONAL HUMAN GENOME RESEARCH INSTITUTE · PI SOOD, RAMAN · 2010 to 2014
$3.9M
6 · The paper itself

Abstract

backgroundDespite detailed in vivo knowledge of glycolytic enolases and many bacterial non-enolase members of the superfamily, little is known about the in vivo function of vertebrate non-enolase enolase superfamily members (ENOSF1s). Results of previous studies suggest involvement of the β splice form of ENOSF1 in breast and colon cancers. This study used the zebrafish (Danio rerio) as a vertebrate model of ENOSF1β function.

resultsWhole mount in situ hybridization (WISH) showed that zebrafish ENOSF1β (enosf1b) is zygotic and expressed ubiquitously through the first 24 hours post fertilization (hpf). After 24 hpf, enosf1b expression is restricted to the notochord. Embryos injected with enosf1b-EGFP mRNA grew slower than EGFP mRNA-injected embryos but caught up to the EGFP-injected embryos by 48 hpf. Embryos injected with ATG or exon 10 enosf1b mRNA-targeting morpholinos had kinked notochords, shortened anterior-posterior axes, and circulatory edema. WISH for ntl or pax2a expression showed that embryos injected with either morpholino have deformed notochord and pronephros. TUNEL staining revealed increased apoptosis in the peri-notochord region.

conclusionsThis study is the first report of ENOSF1 function in a vertebrate and shows that ENOSF1 is required for embryonic development. Increased apoptosis following enosf1b knockdown suggests a potential survival advantage for increased ENOSF1β expression in human cancers.

Identifiers

PMID21943404
PMCPMC3197473
OpenAlexW2127192432

What OpenQuestion holds

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LicenceCC BY
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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.