Literature DB >> 31677786

Ultrasensitive quantitative measurement of huntingtin phosphorylation at residue S13.

Cristina Cariulo1, Margherita Verani1, Paola Martufi1, Raffaele Ingenito2, Marco Finotto2, Sean M Deguire3, Daniel J Lavery4, Leticia Toledo-Sherman4, Ramee Lee5, Elizabeth M Doherty4, Thomas F Vogt6, Celia Dominguez4, Hilal A Lashuel3, Lara Petricca1, Andrea Caricasole1.   

Abstract

Huntington's disease (HD) is a progressive neurodegenerative disorder caused by an expansion of a CAG triplet repeat (encoding for a polyglutamine tract) within the first exon of the huntingtin gene. Expression of the mutant huntingtin (mHTT) protein can result in the production of N-terminal fragments with a robust propensity to form oligomers and aggregates, which may be causally associated with HD pathology. Several lines of evidence indicate that N17 phosphorylation or pseudophosphorylation at any of the residues T3, S13 or S16, alone or in combination, modulates mHTT aggregation, subcellular localization and toxicity. Consequently, increasing N17 phosphorylation has been proposed as a potential therapeutic approach. However, developing genetic/pharmacological tools to quantify these phosphorylation events is necessary in order to subsequently develop tool modulators, which is difficult given the transient and incompletely penetrant nature of such post-translational modifications. Here we describe the first ultrasensitive sandwich immunoassay that quantifies HTT phosphorylated at residue S13 and demonstrate its utility for specific analyte detection in preclinical models of HD.
Copyright © 2019. Published by Elsevier Inc.

Entities:  

Keywords:  Huntington’s disease; Immunoassay; Neurodegeneration; Phosphorylation; Post-translational modifications

Mesh:

Substances:

Year:  2019        PMID: 31677786     DOI: 10.1016/j.bbrc.2019.09.097

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


  3 in total

Review 1.  How Do Post-Translational Modifications Influence the Pathomechanistic Landscape of Huntington's Disease? A Comprehensive Review.

Authors:  Beata Lontay; Andrea Kiss; László Virág; Krisztina Tar
Journal:  Int J Mol Sci       Date:  2020-06-16       Impact factor: 5.923

2.  TBK1 phosphorylates mutant Huntingtin and suppresses its aggregation and toxicity in Huntington's disease models.

Authors:  Ramanath Narayana Hegde; Anass Chiki; Lara Petricca; Paola Martufi; Nicolas Arbez; Laurent Mouchiroud; Johan Auwerx; Christian Landles; Gillian P Bates; Malvindar K Singh-Bains; Mike Dragunow; Maurice A Curtis; Richard Lm Faull; Christopher A Ross; Andrea Caricasole; Hilal A Lashuel
Journal:  EMBO J       Date:  2020-08-05       Impact factor: 11.598

3.  Site-Specific Phosphorylation of Huntingtin Exon 1 Recombinant Proteins Enabled by the Discovery of Novel Kinases.

Authors:  Anass Chiki; Jonathan Ricci; Ramanath Hegde; Luciano A Abriata; Andreas Reif; Driss Boudeffa; Hilal A Lashuel
Journal:  Chembiochem       Date:  2020-10-13       Impact factor: 3.164

  3 in total

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