Special Feature

User Panel

My Panel

My Panel

Bookmark Science Articles

Recent News
Bookmark / Share This Science Site

Regulation of the Inositol 1,4,5-Trisphosphate Receptor Type I by O-GlcNAc Glycosylation.

Regulation of the Inositol 1,4,5-Trisphosphate Receptor Type I by O-GlcNAc Glycosylation. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

  • Abstract Text of This Paper
  • Journal Published
  • MeSH Keywords of This Abstract
  • Chemicals and Substances Used in this Paper
  • Grants and Granting Agency of this Research
  • Database Accession Numbers Used in this Paper
  • Related Papers
  • Related Research Tags
  • Rate this Research Paper
  • Regulation of the Inositol 1,4,5-Trisphosphate Receptor Type I by O-GlcNAc Glycosylation. Abstract Text:

    juliana rengifoJuliana Rengifo,craig j gibsonCraig J Gibson,eva winklerEva Winkler,thibault collinThibault Collin,barbara e ehrlichBarbara E Ehrlich,juliana rengifoJuliana Rengifo,craig j gibsonCraig J Gibson,eva winklerEva Winkler,thibault collinThibault Collin,barbara e ehrlichBarbara E Ehrlich,juliana rengifoJuliana Rengifo,craig j gibsonCraig J Gibson,eva winklerEva Winkler,thibault collinThibault Collin,barbara e ehrlichBarbara E Ehrlich,

    The inositol 1,4,5-trisphosphate (InsP(3)) receptor type I (InsP(3)R-I) is the principle channel for intracellular calcium (Ca(2+)) release in many cell types, including central neurons. It is regulated by endogenous compounds like Ca(2+) and ATP, by protein partners, and by posttranslational modification. We report that the InsP(3)R-I is modified by O-linked glycosylation of serine or threonine residues with beta-N-acetylglucosamine (O-GlcNAc). The level of O-GlcNAcylation can be altered in vitro by the addition of the enzymes which add [OGT (O-GlcNActransferase)] or remove (O-GlcNAcase) this sugar or by loading cells with UDP-GlcNAc. We monitored the effects of this modification on InsP(3)R function at the single-channel level and on intracellular Ca(2+) transients. Single-channel activity was monitored with InsP(3)R incorporated into bilayers; Ca(2+) signaling was monitored using cells loaded with a Ca(2+)-sensitive fluorophore. We found that channel activity was decreased by the addition of O-GlcNAc and that this decrease was reversed by removal of the sugar. Similarly, cells loaded with UDP-GlcNAc had an attenuated response to uncaging of InsP(3). These results show that O-GlcNAcylation is an important regulator of the InsP(3)R-I and suggest a mechanism for neuronal dysfunction under conditions in which O-GlcNAc is high, such as diabetes or physiological stress.

    Regulation of the Inositol 1,4,5-Trisphosphate Receptor Type I by O-GlcNAc Glycosylation. Publishing Authors By Initials

    j rengifoJ Rengifo,cj gibsonCJ Gibson,e winklerE Winkler,t collinT Collin,be ehrlichBE Ehrlich,j rengifoJ Rengifo,cj gibsonCJ Gibson,e winklerE Winkler,t collinT Collin,be ehrlichBE Ehrlich,j rengifoJ Rengifo,cj gibsonCJ Gibson,e winklerE Winkler,t collinT Collin,be ehrlichBE Ehrlich,

    For similar abstracts research abstracts see: abstracts research

    PUBMED ID PMID:

    MEDLINE DATE:

    Regulation of the Inositol 1,4,5-Trisphosphate Receptor Type I by O-GlcNAc Glycosylation. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: The Journal of neuroscience : the official journal

    VOLUME: 27

    Page Numbers: 13813-21

    Journal Abbreviation: J. Neurosci.

    ISSN: 1529-2401

    DAY: 12

    MONTH: Dec

    YEAR: 2007

    Regulation of the Inositol 1,4,5-Trisphosphate Receptor Type I by O-GlcNAc Glycosylation. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8102140

    Regulation of the Inositol 1,4,5-Trisphosphate Receptor Type I by O-GlcNAc Glycosylation. Keywords Mesh Terms:

    KEYWORDS:

    MESH TERMS:

    Chemical & Substance for Abstract: Regulation of the Inositol 1,4,5-Trisphosphate Receptor Type I by O-GlcNAc Glycosylation. Information

    Substance Name:

    Registry Number:

    Grant and Affiliation Information for Regulation of the Inositol 1,4,5-Trisphosphate Receptor Type I by O-GlcNAc Glycosylation.

    AFFILIATION: Department of Pharmacology and Cellular and Molecular Physiology, Yale University, New Haven, Connecticut 06520, and Laboratoire de Physiologie Cérébrale, Université Paris 5, 75006 Paris, France.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY:

    GRANT:

    ACRONYM:

    MEDLINETA: J Neurosci

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

    Regulation of the Inositol 1,4,5-Trisphosphate Receptor Type I by O-GlcNAc Glycosylation Related Publications

     

    Molecular Station USER Menu

    Welcome to Molecular Station!

    You have to register before you can post on our forums or use our advanced features. Register Now! Its Free and Fast!

    Already registered? Login now below.

    User Name:

    Password:

    Already registered and Forgot your password? Click below to recover it.

    Recover Lost Password

    Join now - it's fast and free!

    Molecular Station is THE largest network of researchers, scientists and science lovers anywhere!

    Research Terms of Usage and Disclaimer
    Home
    Features

    Protocols

    DNA Forum

    Science Forum

    DNA Forum
    Biology Forum

    Science News


    [CaRP] XML error: Invalid document end at line 2

    For more click here:Science News