Evidence map›Paper›PMID 8577753›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1996

Neuronal abnormalities in microtubule-associated protein 1B mutant mice.

W Edelmann, M Zervas, P Costello, L Roback, I Fischer, J A Hammarback, N Cowan, P Davies, B Wainer, R Kucherlapati

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 152 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Photoreceptor Compartment-Specific TULP1 Interactomes.International journal of molecular sciences · 2021
    Article
  8. Article
  9. Article
  10. Genomic and phenotypic delineation of congenital microcephaly.Genetics in medicine : official journal of the American College of Medical Genetics · 2019
    Article
  11. Article
  12. Review
  13. Article
  14. Building Blocks of Functioning Brain: Cytoskeletal Dynamics in Neuronal Development.International review of cell and molecular biology · 2016
    Review
  15. Article
  16. Review
  17. Mutations in the microtubule-associated protein 1A (Map1a) gene cause Purkinje cell degeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    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

10 authors at 4 institutions in 1 country.

W EdelmannDepartment of Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
M Zervas
P Costello
L Roback
I Fischer
J A Hammarback
N Cowan
P Davies
B Wainer
R Kucherlapati
Albert Einstein College of Medicine · USYeshiva University · USNew York University · USWake Forest University · US

Funding

MAMMALIAN TUBULIN ISOTYPES &THEIR INTERACTION WITH MAPSR01AG009989 · NIA · NEW YORK UNIVERSITY · PI COWAN, NICHOLAS · 1991 to 1995
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HUMAN GENOME DISSECTION BY HOMOLOGOUS RECOMBINATIONR01HG000380 · NHGRI · YESHIVA UNIVERSITY · PI KUCHERLAPATI, RAJU S · 1991 to 1993
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NHGRI NIH HHS HG00380NIA NIH HHS AG09989NICHD NIH HHS HD31601
6 · The paper itself

Abstract

Microtubules play an important role in establishing cellular architecture. Neuronal microtubules are considered to have a role in dendrite and axon formation. Different portions of the developing and adult brain microtubules are associated with different microtubule-associated proteins (MAPs). The roles of each of the different MAPs are not well understood. One of these proteins, MAP1B, is expressed in different portions of the brain and has been postulated to have a role in neuronal plasticity and brain development. To ascertain the role of MAP1B, we generated mice which carry an insertion in the gene by gene-targeting methods. Mice which are homozygous for the modification die during embryogenesis. The heterozygotes exhibit a spectrum of phenotypes including slower growth rates, lack of visual acuity in one or both eyes, and motor system abnormalities. Histochemical analysis of the severely affected mice revealed that their Purkinje cell dendritic processes are abnormal, do not react with MAP1B antibodies, and show reduced staining with MAP1A antibodies. Similar histological and immunochemical changes were observed in the olfactory bulb, hippocampus, and retina, providing a basis for the observed phenotypes.

Indexed as

AnimalsAntibodies, MonoclonalBase SequenceBrainDNA PrimersFetal DeathGenes, LethalHeterozygoteHomozygoteImmunohistochemistryMiceMice, Mutant StrainsMicrotubule-Associated ProteinsMolecular Sequence DataMutagenesis, InsertionalNeuronsAntibodies, MonoclonalDNA Primersmicrotubule-associated protein 1BMicrotubule-Associated Proteins

Identifiers

PMID8577753
PMCPMC40069
OpenAlexW1986235843

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.