Инд. авторы: | Проскура А.Л., Вечкапова С.О., Запара Т.А., Ратушняк А.С. |
Заглавие: | Межбелковые взаимодействия хантингтина в гиппокампе |
Библ. ссылка: | Проскура А.Л., Вечкапова С.О., Запара Т.А., Ратушняк А.С. Межбелковые взаимодействия хантингтина в гиппокампе // Молекулярная биология. - 2017. - Т.51. - № 4. - С.734-742. - ISSN 0026-8984. |
Внешние системы: | DOI: 10.7868/S0026898417040152; РИНЦ: 29437533; PubMed: 28900094; SCOPUS: 2-s2.0-85044241850; |
Реферат: | rus: Белок хантингтин присутствует в цитоплазме нейронов, где он может взаимодействовать со структурными элементами синапсов. Болезнь Хантингтона развивается вследствие патологического увеличения полиглутаминового тракта в молекуле, что, вероятно, приводит к аберрантным межбелковым взаимодействиям. Механизм патогенеза до конца не исследован. На ранней стадии отмечено нарушение структуры синапсов и синаптической пластичности в гиппокампе. Цель данного исследования - теоретический анализ на основе интеграции экспериментальных данных вклада хантингтина в изменение синаптической пластичности. Показано, что белковые комплексы хантингтина включены в процессы поддержания эффективности синаптической передачи. Появление патогенной формы белка (polyQ-HTT), вероятно, приводит к дезорганизации межбелковых взаимодействий и нарушению динамики молекулярных процессов в синапсе. Выдвинуто предположение, что polyQ-HTT может вступать в конкурентные взаимодействия с белками постсинаптического уплотнения и регуляторами ремоделирования цитоскелета. eng: The huntingtin (HTT) protein is present in cytoplasm where it can interact with the structural elements of synapses. Huntington's disease is caused by a pathological expansion of a polyglutamine stretch in the protein molecule probably followed by aberrant protein interactions. The mechanism of Huntington's disease pathogenesis is not fully understood. In early stages the disruptions of hippocampal synaptic structure and plasticity are present. The aim of this study is the theoretical analysis based on the integration of experimental data of huntingtin contributing to the changes in synaptic plasticity. It was shown that HTT protein complexes are involved in the process of maintaining the efficiency of synaptic transmission. The emergence of the pathogenic form of the protein (polyQ-HTT) probably leads to the disruption of protein-protein interactions and disturbance of molecular processes dynamics at the synapse. It is suggested that polyQ-HTT may partake in the competitive interactions with postsynaptic density proteins and proteins, which are regulating the cyto-skeleton remodeling. |
Ключевые слова: | Protein Interaction Mapping; Protein Binding; Peptides; Neurons; Neuronal Plasticity; Nerve Tissue Proteins; Huntington Disease; Huntingtin Protein; Humans; Gene Expression; Cytoskeleton; Cytoskeletal Proteins; CA1 Region, Hippocampal; Animals; ultrastructure; synaptic transmission; synapse; protein analysis; pathology; nerve cell plasticity; nerve cell; metabolism; Huntington chorea; human; hippocampal CA1 region; genetics; gene expression; cytoskeleton; chemistry; animal; protein binding; postsynaptic density proteins; polyglutamine; peptide; nerve protein; huntingtin; HTT protein, human; cytoskeleton protein; synaptic plasticity; protein-protein interactions; huntingtin; hippocampus; хантингтин; Synapses; Synaptic Transmission; Interprotein interactions; hippocamp; synaptic plasticity; huntingtin; межбелковые взаимодействия; синаптическая пластичность; гиппокамп; |
Издано: | 2017 |
Физ. характеристика: | с.734-742 |
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