Reciprocal changes in phosphorylation and methylation of mammalian brain sodium channels in response to seizures

Je Hyun Baek; Moran Rubinstein; Todd Scheuer; James Trimmer

doi:10.1074/jbc.M114.562785

Reciprocal changes in phosphorylation and methylation of mammalian brain sodium channels in response to seizures

Je Hyun Baek, Moran Rubinstein, Todd Scheuer, James Trimmer

Physiology and Membrane Biology

Research output: Contribution to journal › Article › peer-review

35 Scopus citations

Abstract

Background: Sodium channels underlie neuronal excitability and are regulated by seizures. Results: Mass spectrometric analysis of brain sodium channels revealed novel phosphorylation and methylation sites that decreased and increased, respectively, after seizures. Inducing methylation increased sodium channel activity. Conclusion: Reciprocal phosphorylation and methylation after seizures will alter sodium channel function. Significance: Such regulation would impact neuronal excitability.

Original language	English (US)
Pages (from-to)	15363-15373
Number of pages	11
Journal	Journal of Biological Chemistry
Volume	289
Issue number	22
DOIs	https://doi.org/10.1074/jbc.M114.562785
State	Published - May 30 2014

ASJC Scopus subject areas

Biochemistry
Cell Biology
Molecular Biology

Access to Document

10.1074/jbc.M114.562785

Fingerprint Dive into the research topics of 'Reciprocal changes in phosphorylation and methylation of mammalian brain sodium channels in response to seizures'. Together they form a unique fingerprint.

Cite this

@article{fb8447d484fe43f5ab61ca81a452085f,

title = "Reciprocal changes in phosphorylation and methylation of mammalian brain sodium channels in response to seizures",

abstract = "Background: Sodium channels underlie neuronal excitability and are regulated by seizures. Results: Mass spectrometric analysis of brain sodium channels revealed novel phosphorylation and methylation sites that decreased and increased, respectively, after seizures. Inducing methylation increased sodium channel activity. Conclusion: Reciprocal phosphorylation and methylation after seizures will alter sodium channel function. Significance: Such regulation would impact neuronal excitability.",

author = "Baek, {Je Hyun} and Moran Rubinstein and Todd Scheuer and James Trimmer",

year = "2014",

month = may,

day = "30",

doi = "10.1074/jbc.M114.562785",

language = "English (US)",

volume = "289",

pages = "15363--15373",

journal = "Journal of Biological Chemistry",

issn = "0021-9258",

publisher = "American Society for Biochemistry and Molecular Biology Inc.",

number = "22",

}

TY - JOUR

T1 - Reciprocal changes in phosphorylation and methylation of mammalian brain sodium channels in response to seizures

AU - Baek, Je Hyun

AU - Rubinstein, Moran

AU - Scheuer, Todd

AU - Trimmer, James

PY - 2014/5/30

Y1 - 2014/5/30

N2 - Background: Sodium channels underlie neuronal excitability and are regulated by seizures. Results: Mass spectrometric analysis of brain sodium channels revealed novel phosphorylation and methylation sites that decreased and increased, respectively, after seizures. Inducing methylation increased sodium channel activity. Conclusion: Reciprocal phosphorylation and methylation after seizures will alter sodium channel function. Significance: Such regulation would impact neuronal excitability.

AB - Background: Sodium channels underlie neuronal excitability and are regulated by seizures. Results: Mass spectrometric analysis of brain sodium channels revealed novel phosphorylation and methylation sites that decreased and increased, respectively, after seizures. Inducing methylation increased sodium channel activity. Conclusion: Reciprocal phosphorylation and methylation after seizures will alter sodium channel function. Significance: Such regulation would impact neuronal excitability.

UR - http://www.scopus.com/inward/record.url?scp=84901724023&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84901724023&partnerID=8YFLogxK

U2 - 10.1074/jbc.M114.562785

DO - 10.1074/jbc.M114.562785

M3 - Article

C2 - 24737319

AN - SCOPUS:84901724023

VL - 289

SP - 15363

EP - 15373

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 22

ER -