Evidence map›Paper›PMID 22457349›Full record

Trial reportThe Journal of biological chemistry2012

L-MPZ, a novel isoform of myelin P0, is produced by stop codon readthrough.

Yoshihide Yamaguchi, Akiko Hayashi, Celia W Campagnoni, Akio Kimura, Takashi Inuzuka, Hiroko Baba

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.5field-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

42 citing papers in PubMed, 57 citations in OpenAlex.

  1. RNAViruses · 2026
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  9. Nonsense suppression therapies in human genetic diseases.Cellular and molecular life sciences : CMLS · 2021
    Review
  10. Stop codon read-through of mammalianThe Journal of biological chemistry · 2020
    Article
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  14. Review
  15. Review
  16. Detection of ALDH3B2 in Human Placenta.International journal of molecular sciences · 2019
    Article
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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 3 institutions in 2 countries.

Yoshihide YamaguchiDepartment of Molecular Neurobiology, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo 192-0392, Japan. Electronic address: yoshiy@toyaku.ac.jp.
Akiko HayashiDepartment of Molecular Neurobiology, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo 192-0392, Japan.
Celia W CampagnoniSemel Institute for Neuroscience and Human Behavior, University of California at Los Angeles, Los Angeles, California 90095.
Akio KimuraDepartment of Neurology and Geriatrics, Graduate School of Medicine, Gifu University, Gifu 501-1194, Japan.
Takashi InuzukaDepartment of Neurology and Geriatrics, Graduate School of Medicine, Gifu University, Gifu 501-1194, Japan.
Hiroko BabaDepartment of Molecular Neurobiology, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo 192-0392, Japan.
Tokyo University of Pharmacy and Life Sciences · JPGifu University · JPUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myelin protein zero (P0 or MPZ) is a major myelin protein (∼30 kDa) expressed in the peripheral nervous system (PNS) in terrestrial vertebrates. Several groups have detected a P0-related 36-kDa (or 35-kDa) protein that is expressed in the PNS as an antigen for the serum IgG of patients with neuropathy. The molecular structure and function of this 36-kDa protein are, however, still unknown. We hypothesized that the 36-kDa protein may be derived from P0 mRNA by stop codon readthrough. We found a highly conserved region after the regular stop codon in predicted sequences from the 3'-UTR of P0 in higher animals. MS of the 36-kDa protein revealed that both P0 peptides and peptides deduced from the P0 3'-UTR sequence were found among the tryptic fragments. In transfected cells and in an in vitro transcription/translation system, the 36-kDa molecule was also produced from the identical mRNA that produced P0. We designated this 36-kDa molecule as large myelin protein zero (L-MPZ), a novel isoform of P0 that contains an additional domain at the C terminus. In the PNS, L-MPZ was localized in compact myelin. In transfected cells, just like P0, L-MPZ was localized at cell-cell adhesion sites in the plasma membrane. These results suggest that L-MPZ produced by the stop codon readthrough mechanism is potentially involved in myelination. Since this is the first finding of stop codon readthrough in a common mammalian protein, detailed analysis of L-MPZ expression will help to understand the mechanism of stop codon readthrough in mammals.

Indexed as

AnimalsChronic DiseaseCodon, TerminatorDemyelinating DiseasesFemaleGene Expression RegulationHeLa CellsHumansMiceMiddle AgedMyelin P0 ProteinMyelin SheathNIH 3T3 CellsProtein IsoformsRatsRats, WistarCodon, TerminatorMPZ protein, humanMpz protein, mouseMpz protein, ratMyelin P0 ProteinProtein Isoforms

Identifiers

PMID22457349
PMCPMC3366853
OpenAlexW1997459647

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.