@article{99e3e00c722a42c3b92d6fa71d4c135b,
title = "STAT3 isoforms differentially affect ACE2 expression: A potential target for COVID-19 therapy",
abstract = "The SARS-coronavirus 2 is the aetiologic agent COVID-19. ACE2 has been identified as a cell entry receptor for the virus. Therefore, trying to understand how the gene is controlled has become a major goal. We silenced the expression of STAT3α and STAT3β, and found that while silencing STAT3α causes an increase in ACE2 expression, silencing STAT3β causes the opposite effect. Studying the role of STAT3 in ACE2 expression will shed light on the molecular events that contribute to the progression of the disease and that the different roles of STAT3α and STAT3β in that context must be taken in consideration. Our results place STAT3 in line with additional potential therapeutic targets for treating COVID-19 patients.",
keywords = "ACE2, COVID-19, SARS-CoV-2, STAT3 isoforms, STAT3α, STAT3β",
author = "Inbal Shamir and Mor Abutbul-Amitai and Haya Abbas-Egbariya and Metsada Pasmanik-Chor and Gideon Paret and Yael Nevo-Caspi",
note = "Publisher Copyright: {\textcopyright} 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd",
year = "2020",
month = nov,
doi = "10.1111/jcmm.15838",
language = "אנגלית",
volume = "24",
pages = "12864--12868",
journal = "Journal of Cellular and Molecular Medicine",
issn = "1582-1838",
publisher = "Wiley-Blackwell Publishing Ltd",
number = "21",
}
