Diane Merry

Affiliations: 
Biochemistry and Molecular Biology Thomas Jefferson University, Philadelphia, PA, United States 
Area:
Molecular Biology
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"Diane Merry"
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Publications

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Richardson K, Sengupta M, Sujkowski A, et al. (2024) A phenotypically robust model of spinal and bulbar muscular atrophy in Drosophila. Journal of Neuroscience Research. 102: e25278
Garcia Castro DR, Mazuk JR, Heine EM, et al. (2023) Increased SIRT3 combined with PARP inhibition rescues motor function of SBMA mice. Iscience. 26: 107375
Sengupta M, Pluciennik A, Merry DE. (2022) The role of ubiquitination in spinal and bulbar muscular atrophy. Frontiers in Molecular Neuroscience. 15: 1020143
Molotsky E, Liu Y, Lieberman AP, et al. (2022) Neuromuscular junction pathology is correlated with differential motor unit vulnerability in spinal and bulbar muscular atrophy. Acta Neuropathologica Communications. 10: 97
Pluciennik A, Liu Y, Molotsky E, et al. (2020) Deubiquitinase USP7 contributes to the pathogenicity of spinal and bulbar muscular atrophy. The Journal of Clinical Investigation
Arnold FJ, Merry DE. (2019) Molecular Mechanisms and Therapeutics for SBMA/Kennedy's Disease. Neurotherapeutics : the Journal of the American Society For Experimental Neurotherapeutics
Arnold FJ, Pluciennik A, Merry DE. (2019) Impaired Nuclear Export of Polyglutamine-Expanded Androgen Receptor in Spinal and Bulbar Muscular Atrophy. Scientific Reports. 9: 119
Yersak JM, Montie HL, Chevalier-Larsen ES, et al. (2017) The 11S Proteasomal Activator REGγ Impacts Polyglutamine-Expanded Androgen Receptor Aggregation and Motor Neuron Viability through Distinct Mechanisms. Frontiers in Molecular Neuroscience. 10: 159
Bott LC, Salomons FA, Maric D, et al. (2016) The polyglutamine-expanded androgen receptor responsible for spinal and bulbar muscular atrophy inhibits the APC/C(Cdh1) ubiquitin ligase complex. Scientific Reports. 6: 27703
Zboray L, Pluciennik A, Curtis D, et al. (2015) Preventing the Androgen Receptor N/C Interaction Delays Disease Onset in a Mouse Model of SBMA. Cell Reports
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