Type 2 Transglutaminase, mitochondria and Huntington's disease: Menage a trois

Sara Altuntas, Manuela D'Eletto, Federica Rossin, Laura Diaz Hidalgo, Maria Grazia Farrace, Laura Falasca, Lucia Piredda, Stefania Cocco, Pier Giorgio Mastroberardino, Mauro Piacentini, Michelangelo Campanella

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Mitochondria produce the bulk of cellular energy and work as decisional "hubs" for cellular responses by integrating different input signals. The determinant in the physiopathology of mammals, they attract major attention, nowadays, for their contribution to brain degeneration. How they can withstand or succumb to insults leading to neuronal death is an object of great attention increasing the need for a better understanding of the interplay between inner and outer mitochondrial pathways residing in the cytosol. Of the latter, those dictating protein metabolism and therefore influencing the quality function and control of the organelle are of our most immediate interest and here we describe the Transglutaminase type 2 (TG2) contribution to mitochondrial function, dysfunction and neurodegeneration. Besides reviewing the latest evidences we share also the novel ones on the IF1 pathway depicting a molecular conduit governing mitochondrial turnover and homeostasis relevant to envisaging preventive and therapeutic strategies to respectively predict and counteract deficiencies associated with deregulated mitochondrial function in neuropathology.

Original languageEnglish
Pages (from-to)97-104
Number of pages8
JournalMitochondrion
Issue numberPart A
DOIs
Publication statusPublished - Nov 1 2014

Fingerprint

Mitochondrial Turnover
Huntington Disease
Quality Control
Organelles
Cytosol
Mammals
Mitochondria
Homeostasis
Brain
Proteins
Therapeutics
Neuropathology
transglutaminase 2

Keywords

  • IF<inf>1</inf>
  • Mitochondria
  • Mitophagy
  • Neurodegeneration
  • TG2

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Molecular Medicine

Cite this

Type 2 Transglutaminase, mitochondria and Huntington's disease : Menage a trois. / Altuntas, Sara; D'Eletto, Manuela; Rossin, Federica; Hidalgo, Laura Diaz; Farrace, Maria Grazia; Falasca, Laura; Piredda, Lucia; Cocco, Stefania; Mastroberardino, Pier Giorgio; Piacentini, Mauro; Campanella, Michelangelo.

In: Mitochondrion, No. Part A, 01.11.2014, p. 97-104.

Research output: Contribution to journalArticle

Altuntas, S, D'Eletto, M, Rossin, F, Hidalgo, LD, Farrace, MG, Falasca, L, Piredda, L, Cocco, S, Mastroberardino, PG, Piacentini, M & Campanella, M 2014, 'Type 2 Transglutaminase, mitochondria and Huntington's disease: Menage a trois', Mitochondrion, no. Part A, pp. 97-104. https://doi.org/10.1016/j.mito.2014.09.008
Altuntas S, D'Eletto M, Rossin F, Hidalgo LD, Farrace MG, Falasca L et al. Type 2 Transglutaminase, mitochondria and Huntington's disease: Menage a trois. Mitochondrion. 2014 Nov 1;(Part A):97-104. https://doi.org/10.1016/j.mito.2014.09.008
Altuntas, Sara ; D'Eletto, Manuela ; Rossin, Federica ; Hidalgo, Laura Diaz ; Farrace, Maria Grazia ; Falasca, Laura ; Piredda, Lucia ; Cocco, Stefania ; Mastroberardino, Pier Giorgio ; Piacentini, Mauro ; Campanella, Michelangelo. / Type 2 Transglutaminase, mitochondria and Huntington's disease : Menage a trois. In: Mitochondrion. 2014 ; No. Part A. pp. 97-104.
@article{f0e0df6f1a834337a9ae900fa6c07ffe,
title = "Type 2 Transglutaminase, mitochondria and Huntington's disease: Menage a trois",
abstract = "Mitochondria produce the bulk of cellular energy and work as decisional {"}hubs{"} for cellular responses by integrating different input signals. The determinant in the physiopathology of mammals, they attract major attention, nowadays, for their contribution to brain degeneration. How they can withstand or succumb to insults leading to neuronal death is an object of great attention increasing the need for a better understanding of the interplay between inner and outer mitochondrial pathways residing in the cytosol. Of the latter, those dictating protein metabolism and therefore influencing the quality function and control of the organelle are of our most immediate interest and here we describe the Transglutaminase type 2 (TG2) contribution to mitochondrial function, dysfunction and neurodegeneration. Besides reviewing the latest evidences we share also the novel ones on the IF1 pathway depicting a molecular conduit governing mitochondrial turnover and homeostasis relevant to envisaging preventive and therapeutic strategies to respectively predict and counteract deficiencies associated with deregulated mitochondrial function in neuropathology.",
keywords = "IF<inf>1</inf>, Mitochondria, Mitophagy, Neurodegeneration, TG2",
author = "Sara Altuntas and Manuela D'Eletto and Federica Rossin and Hidalgo, {Laura Diaz} and Farrace, {Maria Grazia} and Laura Falasca and Lucia Piredda and Stefania Cocco and Mastroberardino, {Pier Giorgio} and Mauro Piacentini and Michelangelo Campanella",
year = "2014",
month = "11",
day = "1",
doi = "10.1016/j.mito.2014.09.008",
language = "English",
pages = "97--104",
journal = "Mitochondrion",
issn = "1567-7249",
publisher = "Elsevier",
number = "Part A",

}

TY - JOUR

T1 - Type 2 Transglutaminase, mitochondria and Huntington's disease

T2 - Menage a trois

AU - Altuntas, Sara

AU - D'Eletto, Manuela

AU - Rossin, Federica

AU - Hidalgo, Laura Diaz

AU - Farrace, Maria Grazia

AU - Falasca, Laura

AU - Piredda, Lucia

AU - Cocco, Stefania

AU - Mastroberardino, Pier Giorgio

AU - Piacentini, Mauro

AU - Campanella, Michelangelo

PY - 2014/11/1

Y1 - 2014/11/1

N2 - Mitochondria produce the bulk of cellular energy and work as decisional "hubs" for cellular responses by integrating different input signals. The determinant in the physiopathology of mammals, they attract major attention, nowadays, for their contribution to brain degeneration. How they can withstand or succumb to insults leading to neuronal death is an object of great attention increasing the need for a better understanding of the interplay between inner and outer mitochondrial pathways residing in the cytosol. Of the latter, those dictating protein metabolism and therefore influencing the quality function and control of the organelle are of our most immediate interest and here we describe the Transglutaminase type 2 (TG2) contribution to mitochondrial function, dysfunction and neurodegeneration. Besides reviewing the latest evidences we share also the novel ones on the IF1 pathway depicting a molecular conduit governing mitochondrial turnover and homeostasis relevant to envisaging preventive and therapeutic strategies to respectively predict and counteract deficiencies associated with deregulated mitochondrial function in neuropathology.

AB - Mitochondria produce the bulk of cellular energy and work as decisional "hubs" for cellular responses by integrating different input signals. The determinant in the physiopathology of mammals, they attract major attention, nowadays, for their contribution to brain degeneration. How they can withstand or succumb to insults leading to neuronal death is an object of great attention increasing the need for a better understanding of the interplay between inner and outer mitochondrial pathways residing in the cytosol. Of the latter, those dictating protein metabolism and therefore influencing the quality function and control of the organelle are of our most immediate interest and here we describe the Transglutaminase type 2 (TG2) contribution to mitochondrial function, dysfunction and neurodegeneration. Besides reviewing the latest evidences we share also the novel ones on the IF1 pathway depicting a molecular conduit governing mitochondrial turnover and homeostasis relevant to envisaging preventive and therapeutic strategies to respectively predict and counteract deficiencies associated with deregulated mitochondrial function in neuropathology.

KW - IF<inf>1</inf>

KW - Mitochondria

KW - Mitophagy

KW - Neurodegeneration

KW - TG2

UR - http://www.scopus.com/inward/record.url?scp=84911413293&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84911413293&partnerID=8YFLogxK

U2 - 10.1016/j.mito.2014.09.008

DO - 10.1016/j.mito.2014.09.008

M3 - Article

C2 - 25262960

AN - SCOPUS:84911413293

SP - 97

EP - 104

JO - Mitochondrion

JF - Mitochondrion

SN - 1567-7249

IS - Part A

ER -