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A polyalanine tract expansion in Arx forms intranuclear inclusions and results in increased cell death.
Nasrallah, Ilya M; Minarcik, Jeremy C; Golden, Jeffrey A.
Afiliação
  • Nasrallah IM; Neuroscience Program, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
J Cell Biol ; 167(3): 411-6, 2004 Nov 08.
Article em En | MEDLINE | ID: mdl-15533998
A growing number of human disorders have been associated with expansions of a tract of a single amino acid. Recently, polyalanine (polyA) tract expansions in the Aristaless-related homeobox (ARX) protein have been identified in a subset of patients with infantile spasms and mental retardation. How alanine expansions in ARX, or any other transcription factor, cause disease have not been determined. We generated a series of polyA expansions in Arx and expressed these in cell culture and brain slices. Transfection of these constructs results in nuclear protein aggregation, filamentous nuclear inclusions, and an increase in cell death. These inclusions are ubiquitinated and recruit Hsp70. Coexpressing Hsp70 decreases the percentage of cells with nuclear inclusions. Finally, we show that expressing mutant Arx in mouse brains results in neuronal nuclear inclusion formation. Our data suggest expansions in one of the ARX polyA tracts results in nuclear protein aggregation and an increase in cell death; likely underlying the pathogenesis of the associated infantile spasms and mental retardation.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Peptídeos / Fatores de Transcrição / Morte Celular / Proteínas de Homeodomínio / Corpos de Inclusão Intranuclear Tipo de estudo: Etiology_studies / Prognostic_studies Limite: Animals / Humans / Infant Idioma: En Ano de publicação: 2004 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Peptídeos / Fatores de Transcrição / Morte Celular / Proteínas de Homeodomínio / Corpos de Inclusão Intranuclear Tipo de estudo: Etiology_studies / Prognostic_studies Limite: Animals / Humans / Infant Idioma: En Ano de publicação: 2004 Tipo de documento: Article