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HIV-1 Tat activates Akt/mTORC1 pathway and AICDA expression by downregulating its transcriptional inhibitors in B cellsстатья
Статья опубликована в высокорейтинговом журнале
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 9 апреля 2021 г.
- Авторы: Akbay B., Germini D., Bissenbaev A.K., Musinova Y.R., Sheval E.V., Vassetzky Y., Dokudovskaya S.
- Журнал: International Journal of Molecular Sciences
- Том: 22
- Номер: 4
- Год издания: 2021
- Издательство: MDPI
- Местоположение издательства: Basel, Switzerland
- Номер статьи: 1588
- DOI: 10.3390/ijms22041588
- Аннотация: HIV-1 infects T cells, but the most frequent AIDS-related lymphomas are of B-cell origin. Molecular mechanisms of HIV-1-induced oncogenic transformation of B cells remain largely unknown. HIV-1 Tat protein may participate in this process by penetrating and regulating gene expression in B cells. Both immune and cancer cells can reprogram communications between extracellular signals and intracellular signaling pathways via the Akt/mTORC1 pathway, which plays a key role in the cellular response to various stimuli including viral infection. Here, we investigated the role of HIV-1 Tat on the modulation of the Akt/mTORC1 pathway in B cells. We found that HIV-1 Tat activated the Akt/mTORC1 signaling pathway; this leads to aberrant activation of activation-induced cytidine deaminase (AICDA) due to inhibition of the AICDA transcriptional repressors c-Myb and E2F8. These perturbations may ultimately lead to an increased genomic instability and proliferation that might cause B cell malignancies.
- Добавил в систему: Шеваль Евгений Валерьевич