Evidence map›Paper›PMID 10398534›Full record

ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists1999

Misexpression of a bHLH gene, cNSCL1, results in abnormal brain development.

C M Li, R T Yan, S Z Wang

Open access · greenAbstract read
In one paragraph

Article in Developmental dynamics : an official publication of the American Association of Anatomists, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Enhanced retinal ganglion cell differentiation by ath5 and NSCL1 coexpression.Investigative ophthalmology & visual science · 2004
    Article
  8. A role of ath5 in inducing neuroD and the photoreceptor pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
  9. neurogenin2 elicits the genesis of retinal neurons from cultures of nonneural cells.Proceedings of the National Academy of Sciences of the United States of America · 2001
    Article
  10. 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

3 authors at 1 institution in 1 country.

C M LiDepartment of Ophthalmology, University of Alabama at Birmingham School of Medicine, Birmingham, Alabama 35233, USA.
R T Yan
S Z Wang
University of Alabama at Birmingham · US

Funding

MOLECULAR BIOLOGY OF RETINAL DEVELOPMENTR01EY011640 · NEI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, SHU-ZHEN · 1997 to 2016
$4.1M
NEI NIH HHS EY11640NEI NIH HHS R01 EY011640PHS HHS PD98047
6 · The paper itself

Abstract

NSCL1 is a basic helix-loop-helix transcription factor involved in the development of the nervous system. To elucidate its role in neurogenesis, we cloned chick NSCL1 (cNSCL1) and examined its expression pattern and the effect of its misexpression on brain development. cNSCL1 was predominantly expressed during active neurogenesis. Double-labeling experiments showed that proliferating neuroblasts in the ventricular zone lacked cNSCL1 expression and cells expressing cNSCL1 were located just outside the ventricular zone. Retroviral misexpression of cNSCL1 in chick embryos produced a brain with abnormal structure. While the forebrain of the embryonic day-12 (E12) brain appeared normal, the tectum was enlarged. The enlargement was likely due to an increase in cell proliferation, since more radioactivity was detected in this region of the brain after [3H]thymidine labeling at E9. The cerebellum, on the other hand, was reduced in size. Fewer cells were labeled with BrdU in the external granule layer (a secondary germinal layer required for cerebellum development) in experimental embryos than in the controls, suggesting that misexpression of cNSCL1 might interfere with cell proliferation in the external granular layer. Our data indicate that regulated expression of cNSCL1 is required for normal brain development. They also imply that cNSCL1 might be involved in preventing some postmitotic cells from reentering the cell cycle during neurogenesis. Dev Dyn 1999;215:238-247.

Indexed as

Gene Expression Regulation, DevelopmentalAmino Acid SequenceAnimalsApoptosisBasic Helix-Loop-Helix ProteinsBrainCell CycleCerebellumChick EmbryoDNA-Binding ProteinsGenetic VectorsHelix-Loop-Helix MotifsHumansIn Situ HybridizationMicroinjectionsMolecular Sequence DataBasic Helix-Loop-Helix ProteinsDNA-Binding ProteinsNerve Tissue ProteinsNHLH1 protein, human

Identifiers

PMID10398534
PMCPMC1764459
OpenAlexW2060551776

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.