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317 results on '"Dong, Xiaoyun"'

35. Fast Segmentation-Based Object Tracking Model for Autonomous Vehicles

Author

Dong, Xiaoyun, Niu, Jianwei, Cui, Jiahe, Fu, Zongkai, Ouyang, Zhenchao, Goos, Gerhard, Founding Editor, Hartmanis, Juris, Founding Editor, Bertino, Elisa, Editorial Board Member, Gao, Wen, Editorial Board Member, Steffen, Bernhard, Editorial Board Member, Woeginger, Gerhard, Editorial Board Member, Yung, Moti, Editorial Board Member, and Qiu, Meikang, editor

Published
2020
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37. DAEimp: Denoising Autoencoder-Based Imputation of Sleep Heart Health Study for Identification of Cardiovascular Diseases

Author

Dong, Xiaoyun, Zhang, Jingjing, Wang, Gang, Xia, Yong, Goos, Gerhard, Founding Editor, Hartmanis, Juris, Founding Editor, Bertino, Elisa, Editorial Board Member, Gao, Wen, Editorial Board Member, Steffen, Bernhard, Editorial Board Member, Woeginger, Gerhard, Editorial Board Member, Yung, Moti, Editorial Board Member, Lin, Zhouchen, editor, Wang, Liang, editor, Yang, Jian, editor, Shi, Guangming, editor, Tan, Tieniu, editor, Zheng, Nanning, editor, Chen, Xilin, editor, and Zhang, Yanning, editor

Published
2019
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42. Differential Light-induced Responses in Sectorial Inherited Retinal Degeneration*

Author

Ramon, Eva, Cordomí, Arnau, Aguilà, Mònica, Srinivasan, Sundaramoorthy, Dong, Xiaoyun, Moore, Anthony T, Webster, Andrew R, Cheetham, Michael E, and Garriga, Pere

Subjects
Neurodegenerative, Eye Disease and Disorders of Vision, Rare Diseases, Genetics, Neurosciences, Aetiology, 2.1 Biological and endogenous factors, Eye, Adult, Animals, COS Cells, Cell Line, Tumor, Chlorocebus aethiops, Female, Humans, Kinetics, Middle Aged, Mutation, Missense, Protein Stability, Protein Transport, Retinitis Pigmentosa, Rhodopsin, G-protein-coupled Receptor, Light Exposure, Protein Structure, Retinal Degeneration, Signal Transduction, Transducin, Visual Pigments, Chemical Sciences, Biological Sciences, Medical and Health Sciences, Biochemistry & Molecular Biology
Abstract

Retinitis pigmentosa (RP) is a group of genetically and clinically heterogeneous inherited degenerative retinopathies caused by abnormalities of photoreceptors or retinal pigment epithelium in the retina leading to progressive sight loss. Rhodopsin is the prototypical G-protein-coupled receptor located in the vertebrate retina and is responsible for dim light vision. Here, novel M39R and N55K variants were identified as causing an intriguing sector phenotype of RP in affected patients, with selective degeneration in the inferior retina. To gain insights into the molecular aspects associated with this sector RP phenotype, whose molecular mechanism remains elusive, the mutations were constructed by site-directed mutagenesis, expressed in heterologous systems, and studied by biochemical, spectroscopic, and functional assays. M39R and N55K opsins had variable degrees of chromophore regeneration when compared with WT opsin but showed no gross structural misfolding or altered trafficking. M39R showed a faster rate for transducin activation than WT rhodopsin with a faster metarhodopsinII decay, whereas N55K presented a reduced activation rate and an altered photobleaching pattern. N55K also showed an altered retinal release from the opsin binding pocket upon light exposure, affecting its optimal functional response. Our data suggest that these sector RP mutations cause different protein phenotypes that may be related to their different clinical progression. Overall, these findings illuminate the molecular mechanisms of sector RP associated with rhodopsin mutations.

Published
2014

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