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Blocking of Doublecortin-like Kinase 1-regulated SARS-CoV-2 Replication Cycle Restores Cell Signaling Network

Abstract

Severe COVID-19 and post-acute sequelae often afflict patients with underlying co-morbidities. There is a pressing need for highly effective treatment, particularly in light of the emergence of SARS-CoV-2 variants. In a previous study, we demonstrated that DCLK1, a protein associated with cancer stem cells, is highly expressed in the lungs of COVID-19 patients and enhances viral production and hyperinflammatory responses. In this study, we report the pivotal role of DCLK1-regulated mechanisms in driving SARS-CoV-2 replication-transcription processes and pathogenic signaling. Notably, pharmacological inhibition of DCLK1 kinase during SARS-CoV-2 effectively impedes these processes and counteracts virus-induced alternations in global cell signaling. These findings hold significant potential for immediate application in treating COVID-19.

Citing Articles

From Inflammation to Oncogenesis: Tracing Serum DCLK1 and miRNA Signatures in Chronic Liver Diseases.

Moore L, Qu D, Sureban S, Mitchell S, Pitts K, Cooper N Int J Mol Sci. 2024; 25(12).

PMID: 38928187 PMC: 11203803. DOI: 10.3390/ijms25126481.

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