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Constanza J. Cortes
Researcher at Duke University
Publications - 31
Citations - 1380
Constanza J. Cortes is an academic researcher from Duke University. The author has contributed to research in topics: Spinal and bulbar muscular atrophy & Autophagy. The author has an hindex of 13, co-authored 24 publications receiving 1126 citations. Previous affiliations of Constanza J. Cortes include University of Chicago & University of Alabama at Birmingham.
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Journal ArticleDOI
S-nitrosylation and permeation through connexin 43 hemichannels in astrocytes: Induction by oxidant stress and reversal by reducing agents
TL;DR: It is demonstrated that MI increases the number of hemichannels on the cell surface assayed by biotinylation and Western blot, and that this change is followed by increased dephosphorylation and S-nitrosylation, presumably because of increase in open probability.
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Peripheral Androgen Receptor Gene Suppression Rescues Disease in Mouse Models of Spinal and Bulbar Muscular Atrophy
Andrew P. Lieberman,Zhigang Yu,Sue Murray,Raechel Peralta,Audrey Low,Shuling Guo,Xing Xian Yu,Constanza J. Cortes,C. Frank Bennett,Brett P. Monia,Albert R. La Spada,Albert R. La Spada,Gene Hung +12 more
TL;DR: It is concluded that polyQ-AR expression in the periphery is an important contributor to pathology in SBMA mice and that peripheral administration of therapeutics should be explored for SBMA patients.
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Polyglutamine-expanded androgen receptor interferes with TFEB to elicit autophagy defects in SBMA
Constanza J. Cortes,Helen C. Miranda,Harald Frankowski,Yakup Batlevi,Jessica E. Young,Amy Le,Nishi Ivanov,Bryce L. Sopher,Cassiano Carromeu,Alysson R. Muotri,Gwenn A. Garden,Albert R. La Spada +11 more
TL;DR: It is found that polyQ-AR reduced long-term protein turnover and impaired autophagic flux in motor neuron–like cells and diminishes TFEB function to impair autophagy and promote SBMA pathogenesis.
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Muscle expression of mutant androgen receptor accounts for systemic and motor neuron disease phenotypes in spinal and bulbar muscular atrophy.
Constanza J. Cortes,Shuo-Chien Ling,Ling T. Guo,Gene Hung,Taiji Tsunemi,Linda Ly,Seiya Tokunaga,Edith Lopez,Bryce L. Sopher,C. Frank Bennett,G. Diane Shelton,Don W. Cleveland,Albert R. La Spada +12 more
TL;DR: A BAC mouse model featuring a floxed first exon to permit cell-type-specific excision of human AR121Q reveals a crucial role for muscle expression of polyQ-AR in SBMA and suggest muscle-directed therapies as effective treatments.
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The many faces of autophagy dysfunction in Huntington's disease: from mechanism to therapy.
TL;DR: The utility of autophagy modulation as a treatment modality in HD is assessed, guidelines and caveats for future therapy development directed at the Autophagy pathway are suggested, and different targets and mechanistic pathways that might account for the autophagic abnormalities detected in HD are delineated.