Dopamine neuron-specific LRRK2 G2019S effects on gene expression revealed by translatome profiling

Autor: Judit Pallos, Sophia Jeng, Shannon McWeeney, Ian Martin

Publikováno v: Neurobiology of Disease, Vol 155, Iss , Pp 105390- (2021)

Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of late-onset Parkinson's disease. The pathogenic G2019S mutation enhances LRRK2 kinase activity and induces neurodegeneration in C. elegans, Drosophila and rodent model

Externí odkaz: https://doaj.org/article/93e0b204a1e64b8b9e07c115910a596e

Histone deacetylase (HDAC) inhibitors targeting HDAC3 and HDAC1 ameliorate polyglutamine-elicited phenotypes in model systems of Huntington's disease

Autor: Haiqun Jia, Judit Pallos, Vincent Jacques, Alice Lau, Bin Tang, Andrew Cooper, Adeela Syed, Judith Purcell, Yi Chen, Shefali Sharma, Gavin R. Sangrey, Shayna B. Darnell, Heather Plasterer, Ghazaleh Sadri-Vakili, Joel M. Gottesfeld, Leslie M. Thompson, James R. Rusche, J. Lawrence Marsh, Elizabeth A. Thomas

Publikováno v: Neurobiology of Disease, Vol 46, Iss 2, Pp 351-361 (2012)

We have previously demonstrated amelioration of Huntington's disease (HD)-related phenotypes in R6/2 transgenic mice in response to treatment with the novel histone deacetylase (HDAC) inhibitor 4b. Here we have measured the selectivity profiles of 4b

Externí odkaz: https://doaj.org/article/ef4bd67eeef24038b1106af8a3c56e6d

SUMO-2 and PIAS1 Modulate Insoluble Mutant Huntingtin Protein Accumulation

Autor: Marian DiFiglia, David Reverter, Tamás Raskó, Joan S. Steffan, Joseph Ochaba, Jaclyn R. Gareau, Ya-Zhen Zhu, Alex Mas Monteys, Erich E. Wanker, Thomas Peter Nicholson, Gillian P. Bates, Wan Song, Barbara L. Apostol, Christopher D. Lima, Jacqueline G. O’Rourke, Judit Pallos, Mary Dasso, John H. Lee, Malini Vashishtha, Katalin Illes, J. Lawrence Marsh, Beverly L. Davidson, Leslie M. Thompson, Lisa Mee

Publikováno v: Recercat. Dipósit de la Recerca de Catalunya
instname
Dipòsit Digital de Documents de la UAB
Universitat Autònoma de Barcelona
Cell reports
Cell Reports
Cell Reports; Vol 4
Cell Reports, Vol 4, Iss 2, Pp 362-375 (2013)
Recercat: Dipósit de la Recerca de Catalunya
Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
O’Rourke, Jacqueline Gire; Gareau, Jaclyn R.; Ochaba, Joseph; Song, Wan; Raskó, Tamás; Reverter, David; et al.(2013). SUMO-2 and PIAS1 Modulate Insoluble Mutant Huntingtin Protein Accumulation. Cell Reports, 4(2), 362-375. doi: 10.1016/j.celrep.2013.06.034. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/0ww148xb

SUMMARY A key feature in Huntington disease (HD) is the accumulation of mutant Huntingtin (HTT) protein, which may be regulated by posttranslational modifications. Here, we define the primary sites of SUMO modification in the amino-terminal domain of

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::517096cf1e2043fe4d5dc48600a7e7ce
https://doi.org/10.1016/j.celrep.2013.06.034

Inhibition of specific HDACs and sirtuins suppresses pathogenesis in a Drosophila model of Huntington’s disease

Autor: Tamas Lukacsovich, J. Lawrence Marsh, Judith Purcell, Joan S. Steffan, László Bodai, Leslie M. Thompson, Judit Pallos

Publikováno v: Pallos, J; Bodai, L; Lukacsovich, T; Purcell, JM; Steffan, JS; Thompson, LM; et al.(2008). Inhibition of specific HDACs and sirtuins suppresses pathogenesis in a Drosophila model of Huntington's disease. Human Molecular Genetics, 17(23), 3767-3775. doi: 10.1093/hmg/ddn273. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/18j70154

Huntington's disease (HD) is associated with transcriptional dysregulation, and multiple studies with histone deacetylase (HDAC) inhibitors suggest that global approaches for restoring transcriptional balance and appropriate protein acetylation are t

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5464a422f7a6cb45fef0f6d0c53af37c
https://doi.org/10.1093/hmg/ddn273

[General Articles] Altered Protein Acetylation in Polyglutamine Diseases

Autor: László Bodai, J. L. Marsh, Judit Pallos, Leslie M. Thompson

Publikováno v: Current Medicinal Chemistry. 10:2577-2587

Polyglutamine diseases are hereditary neurodegenerative disorders caused by the expansion of a CAG repeat in the disease gene. A dominant gain of function is associated with these expanded alleles. The resulting elongated polyglutamine repeats are th

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::a6db70450e7b02713206b0e30ce17425
https://doi.org/10.2174/0929867033456530