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Article

Genetic deletion of transglutaminase 2 does not rescue the phenotypic deficits observed in R6/2 and zQ175 mouse models of Huntington's disease.

PloS one - 1 Jan 2014

Menalled Liliana B, Kudwa Andrea E, Oakeshott Steve, Farrar Andrew, Paterson Neil, Filippov Igor, Miller Sam, Kwan Mei, Olsen Michael, Beltran Jose, Torello Justin, Fitzpatrick Jon, Mushlin Richard, Cox Kimberly, McConnell Kristi, Mazzella Matthew, He Dansha, Osborne Georgina F, Al-Nackkash Rand, Bates Gill P, Tuunanen Pasi, Lehtimaki Kimmo, Brunner Dani, Ghavami Afshin, Ramboz Sylvie, Park Larry, Macdonald Douglas, Munoz-Sanjuan Ignacio, Howland David

Abstract excerpt

Huntington's disease (HD) is an autosomal dominant, progressive neurodegenerative disorder caused by expansion of CAG repeats in the huntingtin gene. Tissue transglutaminase 2 (TG2), a multi-functional enzyme, was found to be increased both in HD patients and in mouse models of the disease. Furth...

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Identifiers

PMID: 24955833
DOI: 10.1371/journal.pone.0099520
PMCID: PMC4067284

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-24955833-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

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Genetic deletion of transglutaminase 2 does not rescue the phenotypic deficits observed in R6/2 and zQ175 mouse models of Huntington's disease.PMID 24955833Read ↗

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