Zobrazeno 1 - 10
of 33
pro vyhledávání: '"Aya Ito-Ishida"'
Autor:
Christopher S. Ward, Teng-Wei Huang, Jose A. Herrera, Rodney C. Samaco, Christopher M. McGraw, Diana E. Parra, E. Melissa Arvide, Aya Ito-Ishida, Xiangling Meng, Kerstin Ure, Huda Y. Zoghbi, Jeffrey L. Neul
Publikováno v:
Frontiers in Neurology, Vol 11 (2020)
Rett Syndrome (RTT) is a neurodevelopmental disorder caused by loss of function of the transcriptional regulator Methyl-CpG-Binding Protein 2 (MeCP2). In addition to the characteristic loss of hand function and spoken language after the first year of
Externí odkaz:
https://doaj.org/article/068530e644a94a5095446b5ab905b4e5
Publikováno v:
Scientific Reports, Vol 8, Iss 1, Pp 1-10 (2018)
Abstract Patients and rodents with cerebellar damage display ataxic gaits characterized by impaired coordination of limb movements. Here, gait ataxia in mice with a null mutation of the gene for the cerebellin 1 precursor protein (cbln1-null mice) wa
Externí odkaz:
https://doaj.org/article/11de74f53cf24782ae498ca9920ca840
Autor:
Kerstin Ure, Hui Lu, Wei Wang, Aya Ito-Ishida, Zhenyu Wu, Ling-jie He, Yehezkel Sztainberg, Wu Chen, Jianrong Tang, Huda Y Zoghbi
Publikováno v:
eLife, Vol 5 (2016)
The postnatal neurodevelopmental disorder Rett syndrome, caused by mutations in MECP2, produces a diverse array of symptoms, including loss of language, motor, and social skills and the development of hand stereotypies, anxiety, tremor, ataxia, respi
Externí odkaz:
https://doaj.org/article/d6aeea3afa9144a29bfb8adb4ffb6ae6
Autor:
Huda Y. Zoghbi, Roy V. Sillitoe, Yaling Sun, Yukiteru Ono, Aya Ito-Ishida, Junichi Iwakiri, Jian Zhou, Michisuke Yuzaki, Steven Andrew Baker
Publikováno v:
J Neurosci
Methyl-CpG binding protein 2 (MeCP2) is a nuclear protein critical for normal brain function, and both depletion and overexpression of MeCP2 lead to severe neurodevelopmental disease, Rett syndrome (RTT) andMECP2multiplication disorder, respectively.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d65d02a7c8e5e10db168fe0539b32c93
https://europepmc.org/articles/PMC7643291/
https://europepmc.org/articles/PMC7643291/
Autor:
Aya Ito-Ishida
Publikováno v:
Bio-Protocol, Vol 3, Iss 12 (2013)
This protocol will be useful to introduce the genes of interest into the cerebellar granule cells at early stages of development. Since the granule cell precursors are localized in the external granule layer before migration, DNA plasmids can be spec
Externí odkaz:
https://doaj.org/article/2c25164bcb564e3996545efa5aff8901
Autor:
Laura A. Lavery, Steven Andrew Baker, Huda Y. Zoghbi, Yingyao Shao, Aya Ito-Ishida, Hari Krishna Yamalanchili, Ji-Yoen Kim, Laura Dean Heckman, Zhandong Liu, Laura Marie Lombardi, Yaling Sun
Publikováno v:
Nature neuroscience
Previous studies suggested that MeCP2 competes with linker histone H1, but this hypothesis has never been tested in vivo. Here, we performed chromatin immunoprecipitation followed by sequencing (ChIP-seq) of Flag-tagged-H1.0 in mouse forebrain excita
Autor:
Aya Ito-Ishida, Baker, Steven A., Sillitoe, Roy V., Yaling Sun, Jian Zhou, Yukiteru Ono, Junichi Iwakiri, Michisuke Yuzaki, Zoghbi, Huda Y.
Publikováno v:
Journal of Neuroscience; 2020, Vol. 40 Issue 45, p8746-8766, 21p
Autor:
Ling-jie He, Jianrong Tang, Kerstin Ure, Benjamin R. Arenkiel, Wei Wang, Xiangling Meng, Dinghui Yu, Yaling Sun, Stelios M. Smirnakis, Sara E Kee, Daoyun Ji, Ryan T. Ash, Aya Ito-Ishida, Huda Y. Zoghbi, Shuang Hao, Bin Tang, Hui Lu
Publikováno v:
Neuron. 91:739-747
Loss- and gain-of-function mutations in methyl-CpG-binding protein 2 (MECP2) underlie two distinct neurological syndromes with strikingly similar features, but the synaptic and circuit-level changes mediating these shared features are undefined. Here
Publikováno v:
Scientific Reports
Scientific Reports, Vol 8, Iss 1, Pp 1-10 (2018)
Scientific Reports, Vol 8, Iss 1, Pp 1-10 (2018)
Patients and rodents with cerebellar damage display ataxic gaits characterized by impaired coordination of limb movements. Here, gait ataxia in mice with a null mutation of the gene for the cerebellin 1 precursor protein (cbln1-null mice) was investi