Abul Bashar Mir Md. Khademul Islam

This study shows that medium-chain fatty acid exposure in non-transformed mammary glands induces aging-like changes linked to breast cancer risk.

The paper shows that lipid metabolism, specifically through OA, shifts metabolic pathways in breast cells, increasing SAM and 2-HG, which contribute to oncogenic properties and epigenetic changes.

This study shows that E2F binding to the metabolic gene Pgk affects glycolytic flux, mitochondrial morphology, and lifespan in Drosophila.

This study examines how SARS-CoV-2 mutations affect host miRNA binding and viral IRES structure, revealing potential impacts on immune pathways and viral function.

This study identifies how SARS-CoV-2 proteins interact with host signaling pathways and epigenetic factors to evade immune responses and contribute to disease pathophysiology.

The paper identifies that viral miRNAs target host apoptosis-related genes to suppress cell death, enhancing viral survival.

This study analyzes RNA-seq data from lung biopsy cells of COVID-19 patients to identify molecular mechanisms underlying lung injury, highlighting impaired surfactant metabolism and mitochondrial dysfunction.

This study identifies a role for C. elegans I{kappa}B homologs in chromatin regulation, showing they bind histones, Polycomb proteins, and alter chromatin marks, suggesting ancestral I{kappa}B functions in development.

The paper identifies 21 differentially expressed lncRNAs in SARS-CoV-2 infection that interact with host genes and microRNAs, influencing viral proliferation and immune response.

The paper constructs a single-cell RNA-seq atlas of Drosophila muscle precursors to identify transcriptional signatures and a novel gene involved in muscle divergence.

This study analyzes transcriptomic profiles and SARS-CoV-2 isolates from Bangladeshi COVID-19 patients, revealing unique mutations and immune responses in nasopharyngeal samples compared to lung cells.

The paper identifies miRNA pattern differences between SARS-CoV, SARS-CoV-2, and global SARS-CoV-2 isolates, linking them to pathogenicity and clinical outcomes.