Evidence map›Paper›PMID 9501246›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

The neural restrictive silencer element can act as both a repressor and enhancer of L1 cell adhesion molecule gene expression during postnatal development.

P Kallunki, G M Edelman, F S Jones

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 75 citations in OpenAlex.

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  15. A new binding motif for the transcriptional repressor REST uncovers large gene networks devoted to neuronal functions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  16. Article
  17. Article
  18. The C264Y missense mutation in the extracellular domain of L1 impairs protein trafficking in vitro and in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  19. Article
  20. Expression of brain-derived neurotrophic factor in cortical neurons is regulated by striatal target area.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    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.

P KallunkiDepartment of Neurobiology, The Scripps Research Institute and The Skaggs Institute for Chemical Biology, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
G M Edelman
F S Jones
Scripps Research Institute · US

Funding

CONTROL OF N-CAM BY HOX AND PAX GENES IN TRANSGENIC MICER01HD033576 · NICHD · SCRIPPS RESEARCH INSTITUTE · PI EDELMAN, GERALD · 1995 to 1998
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REGULATION OF GENE EXPRESSION OF NEURAL CAMSR01NS034493 · NINDS · SCRIPPS RESEARCH INSTITUTE · PI JONES, FREDERICK S · 1996 to 1998
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NICHD NIH HHS HD33576NINDS NIH HHS NS34493
6 · The paper itself

Abstract

The cell adhesion molecule L1 mediates axonal guidance during neural development and mutations in its gene result in severe neurological defects. In previous studies, we identified the promoter for the L1 gene and showed that a neural restrictive silencer element (NRSE) was critical for preventing ectopic expression of L1 during early embryonic development. In the present study, we have investigated the role of the NRSE in the regulation of L1 expression during postnatal development. In gel mobility shift experiments, the NRSE formed DNA-protein complexes with nuclear extracts prepared from the brains of postnatal mice. To examine the influence of the NRSE on postnatal patterns of L1 expression in vivo, we compared the expression of two lacZ transgene constructs, one containing the native L1 gene regulatory sequences (L1lacZ) and another (L1lacZDeltaN) lacking the NRSE. Newborn mice carrying the L1lacZDeltaN showed enhanced beta-galactosidase expression relative to L1lacZ in the brain and ectopic expression in nonneural tissues. In contrast to L1lacZ mice, however, L1lacZDeltaN mice showed an unexpected loss, during postnatal development and in the adult, of beta-galactosidase expression in several neural structures, including the neural retina, cerebellum, cortex, striatum, and hippocampus. These data support the conclusion that the NRSE not only plays a role in the silencing of L1 expression in nonneural tissues during early development but also can function as a silencer and an enhancer of L1 expression in the nervous system of postnatal and adult animals.

Indexed as

Enhancer Elements, GeneticRegulatory Sequences, Nucleic AcidAnimalsBrainGene Expression Regulation, DevelopmentalGenes, ReporterLeukocyte L1 Antigen ComplexMiceMice, TransgenicNerve Tissue ProteinsNeural Cell Adhesion MoleculesOlfactory PathwaysProtein BindingRecombinant ProteinsTissue DistributionLeukocyte L1 Antigen ComplexNerve Tissue ProteinsNeural Cell Adhesion MoleculesRecombinant Proteins

Identifiers

PMID9501246
PMCPMC19725
OpenAlexW2153932747

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.