Zobrazeno 1 - 10
of 10
pro vyhledávání: '"Joy X Lei"'
Autor:
Rugao Liu, Joy X. Lei, Chun Luo, Xun Lan, Liying Chi, Panyue Deng, Saobo Lei, Othman Ghribi, Qing Yan Liu
Publikováno v:
Neurobiology of Disease, Vol 45, Iss 3, Pp 902-912 (2012)
Though loss of function in CBP/p300, a family of CREB-binding proteins, has been causally associated with a variety of human neurological disorders, such as Rubinstein–Taybi syndrome, Huntington's disease and drug addiction, the role of EP300 inter
Externí odkaz:
https://doaj.org/article/52421cde94394ecb9c24a83cf7635d5b
Autor:
Joy X Lei, Liying Chi, Qing Yan Liu, Rugao Liu, Xun Lan, Othman Ghribi, Chun Luo, Saobo Lei, Panyue Deng
Publikováno v:
Neurobiology of Disease, Vol 45, Iss 3, Pp 902-912 (2012)
Though loss of function in CBP/p300, a family of CREB-binding proteins, has been causally associated with a variety of human neurological disorders, such as Rubinstein–Taybi syndrome, Huntington's disease and drug addiction, the role of EP300 inter
Autor:
Qing Yan, Liu, Roger, Koukiekolo, Dong Ling, Zhang, Brandon, Smith, Dao, Ly, Joy X, Lei, Othman, Ghribi
Publikováno v:
American journal of neurodegenerative disease. 5(1)
Alzheimer’s disease (AD) is the most common neurodegenerative disorder, characterized by cognitive impairment and dementia, resulting from progressive synaptic dysfunction, loss and neuronal cell death. Inclusion body myositis (IBM) is a skeletal m
Autor:
Qing Yan, Liu, Marilyn N Vera, Chang, Joy X, Lei, Roger, Koukiekolo, Brandon, Smith, Dongling, Zhang, Othman, Ghribi
Publikováno v:
American journal of neurodegenerative disease. 3(1)
Alzheimer’s disease (AD) is the most common neurodegenerative disorder characterized by the presence of extracellular plaques of β-amyloid peptides and intracellular tangles of hyperphosphorylated tau proteins in the brain. The vast majority of ca
Publikováno v:
Alzheimer's & Dementia. 6
Autor:
Maria Ribecco-Lutkiewicz, Caroline Sodja, Hung Fang, Joy X Lei, Erin Twomey, Brandon Smith, Yan Li, Iain McKinnell, Mahmud Bani-Yaghoub, Marianna Sikorska
Myosin phosphatase target subunit 1 (MYPT1), together with catalytic subunit of type1 delta isoform (PP1cdelta) and a small 20-kDa regulatory unit (M20), form a heterotrimeric holoenzyme, myosin phosphatase (MP), which is responsible for regulating t
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ea63c22fff678299dcc693d4b575d8bc
https://doi.org/10.1016/j.yexcr.2009.09.001
https://doi.org/10.1016/j.yexcr.2009.09.001
Autor:
Joy X Lei, Qing Yan Liu, Marianna Sikorska, Claudie Charlebois, Caroline Sodja, J LeBlanc, P R Walker, Dao Ly, S Hirohashi, T Yamada
Publikováno v:
Cell death and differentiation. 11(6)
DNaseY, a Ca(2+)- and Mg(2+)-dependent endonuclease, has been implicated in apoptotic DNA degradation; however, the molecular mechanisms controlling its involvement in this process have not been fully elucidated. We have obtained evidence from yeast
Autor:
Qing Yan Liu, Boleslaw Lach, Joel Martin, Hui Shen, Lawrence T. Malek, Maria Ribecco-Lutkiewicz, Roy Sooknanan, P. Roy Walker, Joy X Lei, Marianna Sikorska
Publikováno v:
BMC Genomics
BMC Genomics, Vol 7, Iss 1, p 286 (2006)
BMC Genomics, Vol 7, Iss 1, p 286 (2006)
Background Alzheimer's disease (AD) is a complex disorder that involves multiple biological processes. Many genes implicated in these processes may be present in low abundance in the human brain. DNA microarray analysis identifies changed genes that
Publikováno v:
Molecular Neurodegeneration, Vol 3, Iss 1, p 4 (2008)
Molecular Neurodegeneration
Molecular Neurodegeneration
Background Alterations in multiple cellular pathways contribute to the development of chronic neurodegeneration such as a sporadic Alzheimer's disease (AD). These, in turn, involve changes in gene expression, amongst which are genes regulating protei
Publikováno v:
Molecular Neurodegeneration
Molecular Neurodegeneration, Vol 6, Iss 1, p 9 (2011)
Molecular Neurodegeneration, Vol 6, Iss 1, p 9 (2011)
Background Molecular changes in multiple biological processes contribute to the development of chronic neurodegeneration such as late onset Alzheimer's disease (LOAD). To discover how these changes are reflected at the level of gene expression, we us