ArticleVirology2014
Rotavirus infection induces G1 to S phase transition in MA104 cells via Ca⁺²/Calmodulin pathway.
Article in Virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- CD36 deficiency inhibits proliferation by cell cycle control in skeletal muscle cells.Frontiers in physiology · 2022Article
- Treading a HOSTile path: Mapping the dynamic landscape of host cell-rotavirus interactions to explore novel host-directed curative dimensions.Virulence · 2021Review
- Rotavirus Induces Epithelial-Mesenchymal Transition Markers by Transcriptional Suppression of miRNA-29b.Frontiers in microbiology · 2021Article
- Host Transcriptomic Response Following Administration of Rotavirus Vaccine in Infants' Mimics Wild Type Infection.Frontiers in immunology · 2020Article
- Progressive Rotavirus Infection Downregulates Redox-Sensitive Transcription Factor Nrf2 and Nrf2-Driven Transcription Units.Oxidative medicine and cellular longevity · 2020Article
- Signalome-wide assessment of host cell response to hepatitis C virus.Nature communications · 2017Article
- Article
- Rotavirus rewires host cell metabolic pathways toward glutamine catabolism for effective virus infection.Gut microbesArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viruses, obligate cellular parasites rely on host cellular functions and target the host cell cycle for their own benefit. In this study, effect of rotavirus infection on cell cycle machinery was explored. We found that rotavirus (RV) infection in MA104 cells induces the expression of cyclins and cyclin dependent kinases and down-regulates expression of CDK inhibitors, resulting in G1 to S phase transition. The rotavirus induced S phase accumulation was found to be concurrent with induction in expression of calmodulin and activation of CaMKI which is reported as inducer of G1-S phase transition. This cell cycle manipulation was found to be Ca(+2)/Calmodulin pathway dependent. The physiological relevance of G1 to S phase transition was established when viral gene expressions as well as viral titers were found to be increased in S phase synchronized cells and decreased in G0/G1 phase synchronized cells compared to unsynchronized cells during rotavirus infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.