Mojnu Miah
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Researcher
Also affiliated: Jatiya Kabi Kazi Nazrul Islam University (2025); Bangladesh Council of Scientific and Industrial Research (2025); International Centre for Diarrhoeal Disease Research (1993–2024); Bangladesh Agricultural University (2021–2025); Winthrop Rockefeller Foundation (2024–2025)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Mojnu Miah's research focuses on viral infections, with a significant emphasis on SARS-CoV-2 and influenza viruses. His work has investigated the molecular mechanisms and epidemiology of these viruses, including the identification of mutations affecting diagnostic tests and the monitoring of variants in wastewater. Miah has also explored the effectiveness of diagnostic assays in resource-limited settings and contributed to vaccine development strategies against SARS-CoV-2 variants.
Beyond coronaviruses and influenza, his research extends to other viral pathogens, such as rotavirus and avian influenza strains. Miah has conducted epidemiological studies on avian influenza in live bird markets in Bangladesh, examining patterns and risk factors associated with virus circulation in both avian populations and potentially humans. His scholarship metrics include an h-index of 12, with 42 publications and 598 total citations.
Metrics
- h-index: 12
- Publications: 41
- Citations: 602
Selected Publications
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Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation (2026)
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DNA secondary structures in <i>BCL2</i> and <i>MYC</i> elicit activation-induced cytidine deaminase binding and activity (2026)
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Low detection of H5N1 virus in commercial chickens with a low-level of vaccination coverage against H5N1 virus infection in Bangladesh (2024)
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Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing (2024)
Collaboration Network
Top Collaborators
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing
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