Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Elizabeta Gjoneska"'
Autor:
Ping-Chieh Pao, Debasis Patnaik, L. Ashley Watson, Fan Gao, Ling Pan, Jun Wang, Chinnakkaruppan Adaikkan, Jay Penney, Hugh P. Cam, Wen-Chin Huang, Lorena Pantano, Audrey Lee, Alexi Nott, Trongha X. Phan, Elizabeta Gjoneska, Sara Elmsaouri, Stephen J. Haggarty, Li-Huei Tsai
Publikováno v:
Nature Communications, Vol 11, Iss 1, Pp 1-17 (2020)
Defects in DNA repair have been linked to brain aging and neurodegenerative disorders. Here the authors reveal a role for HDAC1 in stimulating OGG1 activity to alleviate 8-oxoG lesions with implications in the aging brain and neurodegenerative diseas
Externí odkaz:
https://doaj.org/article/31affdab15104a389accac5fde35981f
Autor:
Hidekuni Yamakawa, Jemmie Cheng, Jay Penney, Fan Gao, Richard Rueda, Jun Wang, Satoko Yamakawa, Oleg Kritskiy, Elizabeta Gjoneska, Li-Huei Tsai
Publikováno v:
Cell Reports, Vol 20, Iss 6, Pp 1319-1334 (2017)
The histone deacetylase HDAC2, which negatively regulates synaptic gene expression and neuronal plasticity, is upregulated in Alzheimer’s disease (AD) patients and mouse models. Therapeutics targeting HDAC2 hold promise for ameliorating AD-related
Externí odkaz:
https://doaj.org/article/eb732d5409d948f581d34bbdeaf719e3
Autor:
Alexander Meissner, Andreas R. Pfenning, Philip L. De Jager, Tracy L. Young-Pearse, David A. Bennett, Jishu Xu, Cristin McCabe, Elizabeta Gjoneska, Hans-Ulrich Klein, Julie A. Schneider, Anna Tang, Bradley E. Bernstein, Robert V. Smith, Li-Huei Tsai, Sara Mostafavi, Sarah E. Sullivan, Belinda J. Kaskow
Publikováno v:
Nature neuroscience
Nature Neuroscience
Nature Neuroscience
Accumulation of tau and amyloid-β are two pathologic hallmarks of Alzheimer’s disease (AD). We conducted an epigenome-wide association study using the H3K9 acetylation (H3K9ac) mark in 669 aged human prefrontal cortices: in contrast to amyloid-β,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::11e699f60e53102cfc147beb23c6ae66
http://europepmc.org/articles/PMC6516529
http://europepmc.org/articles/PMC6516529
Autor:
Oleg Kritskiy, Fan Gao, Jun Wang, Li-Huei Tsai, Elizabeta Gjoneska, Satoko Yamakawa, Richard Rueda, Jay Penney, Hidekuni Yamakawa, Jemmie Cheng
Publikováno v:
Elsevier
Cell Reports, Vol 20, Iss 6, Pp 1319-1334 (2017)
Cell Reports, Vol 20, Iss 6, Pp 1319-1334 (2017)
The histone deacetylase HDAC2, which negatively regulates synaptic gene expression and neuronal plasticity, is upregulated in Alzheimer’s disease (AD) patients and mouse models. Therapeutics targeting HDAC2 hold promise for ameliorating AD-related
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2d9beacc679f537eb568f451d872e98a
https://doi.org/10.1016/j.celrep.2017.07.044
https://doi.org/10.1016/j.celrep.2017.07.044
Autor:
Elizabeta Gjoneska, Haitham Amal, Sarah M. Lewis, John S. Wishnok, Steven R. Tannenbaum, Guanyu Gong, Li-Huei Tsai
Publikováno v:
Translational Psychiatry
Translational Psychiatry, Vol 9, Iss 1, Pp 1-12 (2019)
Translational Psychiatry, Vol 9, Iss 1, Pp 1-12 (2019)
Mutations in the MAPT gene, which encodes the tau protein, are associated with several neurodegenerative diseases, including frontotemporal dementia (FTD), dementia with epilepsy, and other types of dementia. The missense mutation in the Mapt gene in
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::67920b766fbdf8d073ea140ca2614d43
https://doi.org/10.1038/s41398-019-0388-7
https://doi.org/10.1038/s41398-019-0388-7
Autor:
Alicia V. Zamudio, Paras S. Minhas, Li-Huei Tsai, Fan Gao, Peng Jin, Elizabeta Gjoneska, Jia Meng, Feiran Zhang, Yuan-Ta Lin, Jemmie Cheng, Alexi Nott, Tak Ko
Publikováno v:
Nature neuroscience
Mutations in MECP2 cause the neurodevelopmental disorder Rett syndrome (RTT). The RTT missense MECP2R306C mutation prevents MeCP2 from interacting with the NCoR/histone deacetylase 3 (HDAC3) complex; however, the neuronal function of HDAC3 is incompl
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b05f4398313aa566f28acbcde3f26fe0
https://doi.org/10.1038/nn.4347
https://doi.org/10.1038/nn.4347
Autor:
Julie A. Schneider, Cristin McCabe, Anna Tang, Bradley E. Bernstein, Robert V. Smith, Sarah E. Sullivan, Li-Huei Tsai, Tracy L. Young-Pearse, Alexander Meissner, Andreas R. Pfenning, Elizabeta Gjoneska, Sara Mostafavi, David A. Bennett, Philip L. De Jager, Hans-Ulrich Klein, Jishu Xu, Belinda J. Kaskow
SummaryAccumulation of tau and amyloid-β are two pathologic hallmarks of Alzheimer’s disease (AD). Here, we conducted an epigenome-wide association study using the H3K9 acetylation (H3K9Ac) mark in 669 aged human prefrontal cortices: in contrast t
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::df5e8ca1d943e09914d129ab63de3d12
Autor:
Trongha X. Phan, Ram Madabhushi, Sukhee Cho, Andreas R. Pfenning, Alexi Nott, Ling Pan, Fan Gao, Manolis Kellis, Satoko Yamakawa, Jinsoo Seo, Ryan T. Stott, Elizabeta Gjoneska, Ping-Chieh Pao, Richard Rueda, Hidekuni Yamakawa, Li-Huei Tsai
Publikováno v:
PMC
Neuronal activity causes the rapid expression of immediate early genes that are crucial for experience-driven changes to synapses, learning, and memory. Here, using both molecular and genome-wide next-generation sequencing methods, we report that neu
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f2ad16e34b4f9014e062eab1736916da
Autor:
Gerald Quon, Li-Huei Tsai, Elizabeta Gjoneska, Anshul Kundaje, Hansruedi Mathys, Andreas R. Pfenning, Manolis Kellis
Publikováno v:
Nature
PMC
PMC
Alzheimer’s disease (AD) is a severe age-related neurodegenerative disorder characterized by accumulation of amyloid-β plaques and neurofibrillary tangles, synaptic and neuronal loss, and cognitive decline. Several genes have been implicated in AD
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fbccffea5b64eaa74d52a65a7aa3aee1
https://doi.org/10.1038/nature14252
https://doi.org/10.1038/nature14252
Autor:
Jinsoo Seo, Jemmie Cheng, Dilip Dey, Tak Ko, Zhuyu Peng, Jay Penney, Richard Rueda, Chung Jong Yu, Hsin-Lan Wen, Blerta Milo, Hugh P. Cam, Elizabeta Gjoneska, Sara Elmsaouri, Waseem K. Raja, Li-Huei Tsai, Bruce A. Yankner, Fatema Abdurrob, Oleg Kritskiy, Heather M. Feldman, Fan Gao, Yuan-Ta Lin
Publikováno v:
PMC
The apolipoprotein E4 (APOE4) variant is the single greatest genetic risk factor for sporadic Alzheimer's disease (sAD). However, the cell-type-specific functions of APOE4 in relation to AD pathology remain understudied. Here, we utilize CRISPR/Cas9
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::069ca5b47112816edaac75539b2ac6c4
https://doi.org/10.1016/j.neuron.2018.05.008
https://doi.org/10.1016/j.neuron.2018.05.008