Evidence map›Paper›PMID 17502419›Full record

ArticleThe Journal of cell biology2007

Myelin protein zero/P0 phosphorylation and function require an adaptor protein linking it to RACK1 and PKC alpha.

Ana-Maria Gaboreanu, Ronald Hrstka, Wenbo Xu, Michael Shy, John Kamholz, Jack Lilien, Janne Balsamo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Neurodegenerative Disorder Risk in Krabbe Disease Carriers.International journal of molecular sciences · 2022
    Article
  5. Article
  6. Mechanisms and Treatments in Demyelinating CMT.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Sc65 is a novel endoplasmic reticulum protein that regulates bone mass homeostasis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014
    Article
  12. Article
  13. Article
  14. P0 protein is required for and can induce formation of schmidt-lantermann incisures in myelin internodes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008
    Article
  15. Article
  16. Review
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

7 authors at 2 institutions in 1 country.

Ana-Maria GaboreanuDepartment of Biological Sciences, The University of Iowa, Iowa City, IA 52242, USA.
Ronald Hrstka
Wenbo Xu
Michael Shy
John Kamholz
Jack Lilien
Janne Balsamo
University of Iowa · USWayne State University · US

Funding

PO-Mediated Signaling and MyelinationR01NS043168 · NINDS · UNIVERSITY OF IOWA · PI LILIEN, JACK E · 2003 to 2006
$1.0M
NINDS NIH HHS NS043168NINDS NIH HHS R01 NS043168
6 · The paper itself

Abstract

Point mutations in the cytoplasmic domain of myelin protein zero (P0; the major myelin protein in the peripheral nervous system) that alter a protein kinase Calpha (PKCalpha) substrate motif (198HRSTK201) or alter serines 199 and/or 204 eliminate P0-mediated adhesion. Mutation in the PKCalpha substrate motif (R198S) also causes a form of inherited peripheral neuropathy (Charcot Marie Tooth disease [CMT] 1B), indicating that PKCalpha-mediated phosphorylation of P0 is important for myelination. We have now identified a 65-kD adaptor protein that links P0 with the receptor for activated C kinase 1 (RACK1). The interaction of p65 with P0 maps to residues 179-197 within the cytoplasmic tail of P0. Mutations or deletions that abolish p65 binding reduce P0 phosphorylation and adhesion, which can be rescued by the substitution of serines 199 and 204 with glutamic acid. A mutation in the p65-binding sequence G184R occurs in two families with CMT, and mutation of this residue results in the loss of both p65 binding and adhesion function.

Indexed as

Adaptor Proteins, Signal TransducingAmino Acid SequenceAnimalsGTP-Binding ProteinsHumansL CellsMiceMolecular Sequence DataMyelin P0 ProteinNeoplasm ProteinsPhosphorylationProtein Kinase C-alphaRatsReceptors, Cell SurfaceReceptors for Activated C KinaseTwo-Hybrid System TechniquesAdaptor Proteins, Signal TransducingGTP-Binding ProteinsMyelin P0 ProteinNeoplasm ProteinsProtein Kinase C-alphaRACK1 protein, humanReceptors, Cell SurfaceReceptors for Activated C Kinase

Identifiers

PMID17502419
PMCPMC2064215
OpenAlexW2075632207

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.