Suvendra N. Bhattacharyya

The paper identifies HuR as a miRNA sensor that uncouples miRNAs from Ago2 and promotes their storage on lipid droplets to buffer miRNA activity in mammalian cells.

The paper shows that activated macrophages export miRNAs cooperatively, with miR-122 enhancing the export of miR-146a via HuR-mediated endosomal entry.

The paper shows that HuD replaces HuR in regulating miRNA export during neuronal differentiation, promoting differentiation by altering miRNA activity.

This paper isolates and quantifies mRNAs from subcellular phase-separated structures in brain cells to study how amyloid proteins affect mRNA dynamics in neurons and glial cells.

The paper shows that specific miRNAs, including miR-122, are reversibly shuttled to mitochondria in stressed hepatic cells, where they regulate apoptosis-related gene expression and cytosolic miRNA levels.

This paper identifies Syntaxin5's role in miRNA export and pathogen clearance by showing its RNA-binding and SNARE domain functions in macrophages.

This study shows amyloid beta oligomers enhance Ago2 phase separation to RNA processing bodies by promoting miRNA-mRNA targeting, while HuR counteracts this effect.

The paper develops an in vitro assay to study miRNA packaging into endosomes and shows that HuR-miRNA complexes activate RalA GTPase to facilitate miRNA import and export.

The paper identifies primary miRNAs that coordinate the biogenesis of secondary miRNAs to regulate immune response in activated macrophages.

The paper identifies that Rheb-mTOR activation restores miR-146 activity in glial cells, reducing amyloid beta-induced cytokine production and rescuing cognitive impairment in a rat Alzheimer's model.

The paper shows that GW182 proteins restrict the export of used miRNAs via extracellular vesicles in cancer cells, independent of HuR, and that this process is linked to miRNA turnover and cellular senescence.

The paper investigates how mitochondrial dysfunction affects miRNA trafficking and export by altering eIF4E compartmentalization and mTORC1 activity in mammalian cells.