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

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

Keywords

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

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Molecular Medicine

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