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Title: RNA-Sequencing-Based Transcriptomic Analysis Reveals a Role for Annexin-A1 in Classical and Influenza A Virus-Induced Autophagy
Authors: Cui Jianzhou 
Morgan, Dhakshayini
Cheng, Dao Han
Foo, Sok Lin
Yap, Gracemary LR 
Ampomah, Patrick B
Arora, Suruchi 
Sachaphibulkij, Karishma 
Periaswamy, Balamurugan 
Fairhurst, Anna-Marie 
De Sessions, Paola Florez De
Lim, Lina HK 
Issue Date: 2020
Publisher: MDPI AG
Citation: Cui Jianzhou, Morgan, Dhakshayini, Cheng, Dao Han, Foo, Sok Lin, Yap, Gracemary LR, Ampomah, Patrick B, Arora, Suruchi, Sachaphibulkij, Karishma, Periaswamy, Balamurugan, Fairhurst, Anna-Marie, De Sessions, Paola Florez De, Lim, Lina HK (2020). RNA-Sequencing-Based Transcriptomic Analysis Reveals a Role for Annexin-A1 in Classical and Influenza A Virus-Induced Autophagy. Cells 9 (6) : 1399-1399. ScholarBank@NUS Repository.
Abstract: Influenza viruses have been shown to use autophagy for their survival. However, the proteins and mechanisms involved in the autophagic process triggered by the influenza virus are unclear. Annexin-A1 (ANXA1) is an immunomodulatory protein involved in the regulation of the immune response and Influenza A virus (IAV) replication. In this study, using clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 (CRISPR associated protein 9) deletion of ANXA1, combined with the next-generation sequencing, we systematically analyzed the critical role of ANXA1 in IAV infection as well as the detailed processes governing IAV infection, such as macroautophagy. A number of differentially expressed genes were uniquely expressed in influenza A virus-infected A549 parental cells and A549 ∆ANXA1 cells, which were enriched in the immune system and infection-related pathways. Gene ontology and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway revealed the role of ANXA1 in autophagy. To validate this, the effect of mechanistic target of rapamycin (mTOR) inhibitors, starvation and influenza infection on autophagy was determined, and our results demonstrate that ANXA1 enhances autophagy induced by conventional autophagy inducers and influenza virus. These results will help us to understand the underlying mechanisms of IAV infection and provide a potential therapeutic target for restricting influenza viral replication and infection.
Source Title: Cells
ISSN: 2073-4409
DOI: 10.3390/cells9061399
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