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Gaurav Datta

Researcher at University of North Dakota

Publications -  18
Citations -  238

Gaurav Datta is an academic researcher from University of North Dakota. The author has contributed to research in topics: Plasmodium falciparum & Hemozoin. The author has an hindex of 8, co-authored 18 publications receiving 159 citations. Previous affiliations of Gaurav Datta include International Centre for Genetic Engineering and Biotechnology.

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Disruption of cellular homeostasis induces organelle stress and triggers apoptosis like cell-death pathways in malaria parasite

TL;DR: It is shown that persistent cellular stress and organelle dysfunction because of disruption of cellular homeostasis in human malaria parasite Plasmodium falciparum, leads to apoptosis-like cell death, establishing one of the possible mechanisms of instigation of cell death by organelle stress in PlasModium.
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The prokaryotic ClpQ protease plays a key role in growth and development of mitochondria in Plasmodium falciparum

TL;DR: It is shown that the dominant negative effect of PfClpQ(mut) disrupted transcription of mitochondrial genome encoded genes, which in turn blocked normal development and functioning of the mitochondria in the parasite.
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A role for adaptor protein complex 1 in protein targeting to rhoptry organelles in Plasmodium falciparum

TL;DR: A role for the AP-1 complex in rhoptry protein trafficking in P. falciparum is suggested by treatment with AlF4, which resulted in a shift to a predominantly ER-associated compartment and consequent decrease in co-localization with the Golgi marker GRASP.
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HIV-1 gp120 Promotes Lysosomal Exocytosis in Human Schwann Cells.

TL;DR: The results suggest that gp120-induced lysosome exocytosis and release of ATP from Schwann cells and DRG neurons contribute to the pathogenesis of HIV-1 associated neuropathy.
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Morphine-Induced Modulation of Endolysosomal Iron Mediates Upregulation of Ferritin Heavy Chain in Cortical Neurons.

TL;DR: It is demonstrated that iron mediates morphine-induced FHC upregulation and consequent dendritic spine deficits and implicate endolysosomal iron efflux to the cytoplasm in these effects.