Mechanism of cell cycle regulation and cell proliferation during human viral infection

Panda, Mamta; Kalita, Elora; Rao, Abhishek; Prajapati, Vijay Kumar

doi:10.1016/bs.apcsb.2022.11.013

Cited by 4 publications

(1 citation statement)

References 116 publications

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“…Because of this dependence, viruses have evolved a myriad of mechanisms for exploiting host cell functions. Many viruses subvert the host cell cycle in order to increase their replication [ 7 , 8 , 9 ]. For example, severe acute respiratory syndrome coronavirus (SARS-CoV) and the mouse hepatitis virus (MHV) are known to induce a cell cycle arrest in infected host cells [ 10 , 11 , 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

P53-Independent G1-Cell Cycle Arrest Increases SARS-CoV-2 RNA Replication

Husser,

Kwon,

Andersson

et al. 2024

Microorganisms

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While having already killed more than 7 million of people worldwide in 4 years, SARS-CoV-2, the etiological agent of COVID-19, is still circulating and evolving. Understanding the pathogenesis of the virus is of capital importance. It was shown that in vitro and in vivo infection with SARS-CoV-2 can lead to cell cycle arrest but the effect of the cell cycle arrest on the virus infection and the associated mechanisms are still unclear. By stopping cells in the G1 phase as well as targeting several pathways involved using inhibitors and small interfering RNAs, we were able to determine that the cell cycle arrest in the late G1 is beneficial for SARS-CoV-2 replication. This cell cycle arrest is independent of p53 but is dependent on the CDC25A-CDK2/cyclin E pathway. These data give a new understanding in SARS-CoV-2 pathogenesis and highlight some possible targets for the development of novel therapeutic approaches.

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Section: Introductionmentioning

confidence: 99%

P53-Independent G1-Cell Cycle Arrest Increases SARS-CoV-2 RNA Replication

Husser,

Kwon,

Andersson

et al. 2024

Microorganisms

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The study on the mechanism of miR-29a in SPPV infection

Ding,

Ma,

Zhang

et al. 2024

Virology

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The Molecular Docking and Molecular Dynamic Effects of Omeprazole on CDKs 2, 4, and 6 as a Potential CDK Inhibitor in Cancer Treatment

Jamali,

Mohseni,

Zareei

et al. 2025

CCTR

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Introduction: Cyclin-dependent kinases (CDKs) are serine/threonine kinase proteins that regulate the cell cycle through phosphorylation and dephosphorylation. These proteins are a main target in cancer therapy. This study investigated the effect of omeprazole on CDK2, CDK4, and CDK6 through simulation studies. Methods: To investigate the interaction between omeprazole and CDK2, 4, and 6, the threedimensional structure of omeprazole was obtained from PubChem, and the structures of CDK2, 4, and 6 were acquired from RCSB servers. The proteins were then simulated for 50 nanoseconds using the GROMACS 2021 platform before the docking process. Next, Autodock v.4.2.6 software was used to bind omeprazole as a ligand to these proteins, and a molecular dynamics simulation of the resulting protein-ligand complex was conducted using GROMACS after the docking process. Results: Omeprazole exhibited a high affinity for interacting with CDK2, 4, and 6, mainly occurring in the ATP binding site of CDK4. However, the docking of omeprazole in the CDKs induced conformational changes in their structures, which could potentially affect their function and lead to cell cycle arrest. Conclusion: Omeprazole, which is a proton pump inhibitor, can induce cell cycle arrest by interacting with the ATP-binding site of CDK4. Moreover, it can also induce conformational changes in CDK2, CDK4, and CDK6 through high-affinity interactions with specific amino acid residues.

show abstract

Mechanism of cell cycle regulation and cell proliferation during human viral infection

Cited by 4 publications

References 116 publications

P53-Independent G1-Cell Cycle Arrest Increases SARS-CoV-2 RNA Replication

P53-Independent G1-Cell Cycle Arrest Increases SARS-CoV-2 RNA Replication

The study on the mechanism of miR-29a in SPPV infection

The Molecular Docking and Molecular Dynamic Effects of Omeprazole on CDKs 2, 4, and 6 as a Potential CDK Inhibitor in Cancer Treatment

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