Zobrazeno 1 - 10
of 16
pro vyhledávání: '"Weirui Guo"'
Publikováno v:
Journal of Clinical and Translational Science, Vol 7, Pp 127-127 (2023)
OBJECTIVES/GOALS: SLC6A1-Related Neurodevelopmental Disorder (SLC6A1-NDD) is a leading genetic cause of epilepsy and autism. Haploinsufficiency of SLC6A1 leads to reduced uptake of GABA from the synaptic cleft, and increased extracellular GABA in mic
Externí odkaz:
https://doaj.org/article/823f4ecf022e4bd2837747a2af5ce1de
Publikováno v:
Cell Reports, Vol 13, Iss 10, Pp 2297-2311 (2015)
Abnormal metabotropic glutamate receptor 5 (mGluR5) function, as a result of disrupted scaffolding with its binding partner Homer, contributes to the pathophysiology of fragile X syndrome, a common inherited form of intellectual disability and autism
Externí odkaz:
https://doaj.org/article/26574830c75a4001b41783eb43d6c7c2
Autor:
Pu Ge, Chunyan Han, Reyila, Abudurousuli, Diyue Liu, Wenying Hong, Jiaxin Liu, Jinzi Zhang, Xiao Han, Xialei Li, Mengjie Huang, Siyuan Fan, Kaierdebieke, Ayidana, Xiaoyu Wu, Xiaolu Huang, Weirui Guo, Siyu Liu, Ying Bian
Publikováno v:
Medicine; Sep2023, Vol. 102 Issue 35, p1-12, 12p
Autor:
Weirui Guo1, Yanbo Chen2, Xiaohong Zhou1 xuqi@pumc.edu.cn, Kar, Amar3, Ray, Payal4, Xiaoping Chen4, Rao, Elizabeth J.5, Mengxue Yang6, Haihong Ye6, Li Zhu6, Jianghong Liu6, Meng Xu7, Yanlian Yang7, Chen Wang7, David Zhang4, Bigio, Eileen H.7, Mesulam, Marsel7, Yan Shen7, Qi Xu7, Kazuo Fushimi4
Publikováno v:
Nature Structural & Molecular Biology. Jul2011, Vol. 18 Issue 7, p822-830. 9p. 1 Black and White Photograph, 7 Graphs.
Publikováno v:
Human molecular genetics. 26(2)
The Myocyte Enhancer Factor 2 (MEF2) transcription factors suppress an excitatory synapse number by promoting degradation of the synaptic scaffold protein, postsynaptic density protein 95 (PSD-95), a process that is deficient in the mouse model of Fr
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::13de4a91b81b472ef162dc514365623a
https://pubmed.ncbi.nlm.nih.gov/28025327
https://pubmed.ncbi.nlm.nih.gov/28025327
Autor:
Kimberly M. Huber, Weirui Guo, Katie A. Collins, Gemma Molinaro, Richard Paylor, Paul F. Worley, Karen K. Szumlinski, Seth A. Hays
Publikováno v:
The Journal of neuroscience : the official journal of the Society for Neuroscience, vol 36, iss 7
Guo, W; Molinaro, G; Collins, KA; Hays, SA; Paylor, R; Worley, PF; et al.(2016). Selective disruption of metabotropic glutamate receptor 5-homer interactions mimics phenotypes of fragile X syndrome in mice. Journal of Neuroscience, 36(7), 2131-2147. doi: 10.1523/JNEUROSCI.2921-15.2016. UC Santa Barbara: Retrieved from: http://www.escholarship.org/uc/item/15q912kf
Guo, W; Molinaro, G; Collins, KA; Hays, SA; Paylor, R; Worley, PF; et al.(2016). Selective disruption of metabotropic glutamate receptor 5-homer interactions mimics phenotypes of fragile X syndrome in mice. Journal of Neuroscience, 36(7), 2131-2147. doi: 10.1523/JNEUROSCI.2921-15.2016. UC Santa Barbara: Retrieved from: http://www.escholarship.org/uc/item/15q912kf
Altered function of the Gq-coupled, Group 1 metabotropic glutamate receptors, specifically mGlu5, is implicated in multiple mouse models of autism and intellectual disability. mGlu5 dysfunction has been most well characterized in the fragile X syndro
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::86ab89a09915a45fa08184acfa04861b
https://europepmc.org/articles/PMC4756152/
https://europepmc.org/articles/PMC4756152/
Autor:
Weirui Guo, Kimberly M. Huber, Jia Hua Hu, Jay R. Gibson, Katie A. Collins, Nien Pei Tsai, Shari G. Birnbaum, Jennifer A. Ronesi, Paul F. Worley, Seth A. Hays
Publikováno v:
Nature Neuroscience. 15:431-440
Enhanced metabotropic glutamate receptor subunit 5 (mGluR5) function is causally associated with the pathophysiology of fragile X syndrome, a leading inherited cause of intellectual disability and autism. Here we provide evidence that altered mGluR5-
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::32e3ffe2782c6f0fcc1df9b14e8c7658
https://doi.org/10.1038/nn.3033
https://doi.org/10.1038/nn.3033
Autor:
David Luowei Zhang, Li Zhu, Amar N. Kar, Xiaohong Zhou, Yanbo Chen, Mengxue Yang, Jianghong Liu, Qi Xu, Yan Shen, Yanlian Yang, M.-Marsel Mesulam, Chen Wang, Payal Ray, Jane Y. Wu, Haihong Ye, Meng Xu, Elizabeth J. Rao, Weirui Guo, Xiaoping Chen, Kazuo Fushimi, Eileen H. Bigio
Publikováno v:
Nature Structural & Molecular Biology. 18:822-830
Mutations in TARDBP, encoding TAR DNA-binding protein-43 (TDP-43), are associated with TDP-43 proteinopathies, including amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). We compared wild-type TDP-43 and an ALS-associa
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c6f717cb9e36452b12cb0aa63f1bcb9e
https://doi.org/10.1038/nsmb.2053
https://doi.org/10.1038/nsmb.2053
Autor:
Yehong Wan, P. Jeffrey Conn, Weirui Guo, Nicole Calakos, Srishti Bhagat, Kristen K. Ade, Justin K. O’Hare, Harold C. Hamann, Kimberly M. Huber, Sunil Kumar, William C. Wetsel, Ramona M. Rodriguiz, Kafui Dzirasa, Anna Quian
Publikováno v:
Biological psychiatry. 80(7)
Background Development of treatments for obsessive-compulsive disorder (OCD) is hampered by a lack of mechanistic understanding about this prevalent neuropsychiatric condition. Although circuit changes such as elevated frontostriatal activity are lin
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1a8445f82dbb6f8e64055b710a7f2233
https://pubmed.ncbi.nlm.nih.gov/27601339
https://pubmed.ncbi.nlm.nih.gov/27601339
Publikováno v:
Protein & Cell. 1:419-421
1 Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, Beijing 100101, China 2 Center for Bioinformatics, National Laboratory of Protein Engineering and Plant Genetic Engineering, College of Life Sciences, Peking University, Beijing 1
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3b6983e7bd3a8731f8863c1735a124eb
https://doi.org/10.1007/s13238-010-0056-4
https://doi.org/10.1007/s13238-010-0056-4