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Ajoy Basak

Researcher at University of Ottawa

Publications -  116
Citations -  6823

Ajoy Basak is an academic researcher from University of Ottawa. The author has contributed to research in topics: Furin & Proprotein convertase. The author has an hindex of 39, co-authored 113 publications receiving 6424 citations. Previous affiliations of Ajoy Basak include Ottawa Hospital & Ottawa Hospital Research Institute.

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The secretory proprotein convertase neural apoptosis-regulated convertase 1 (NARC-1): Liver regeneration and neuronal differentiation

TL;DR: The properties of a proteinase K-like subtilase, neural apoptosis-regulated convertase 1 (NARC-1), representing the ninth member of the secretory subtilases family, are described, suggesting that NARC- 1 is implicated in the differentiation of cortical neurons.
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Impaired Repression at a 5-Hydroxytryptamine 1A Receptor Gene Polymorphism Associated with Major Depression and Suicide

TL;DR: The data indicate that NUDR is a repressor of the 5-HT1A receptor in raphe cells the function of which is abrogated by a promoter polymorphism, suggesting a novel transcriptional model in which the G(-1019) allele derepresses 5- HT1A autoreceptor expression to reduce serotonergic neurotransmission, predisposing to depression and suicide.
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Mammalian subtilisin/kexin isozyme SKI-1: A widely expressed proprotein convertase with a unique cleavage specificity and cellular localization

TL;DR: In vitro studies suggest that SKI-1 is a Ca2+-dependent serine proteinase exhibiting a wide pH optimum for cleavage of pro-brain-derived neurotrophic factor and phylogenetically ancestral human, rat, and mouse type I membrane-bound proteinase called subtilisin/kexin-isozyme-1 (SKI- 1).
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Akt-Mediated Cisplatin Resistance in Ovarian Cancer: Modulation of p53 Action on Caspase-Dependent Mitochondrial Death Pathway

TL;DR: It is shown that CDDP induces mitochondrial p53 accumulation, the mitochondrial release of Smac, cytochrome c, and HTR/Omi, and apoptosis in chemosensitive but not in resistant ovarian cancer cells, and inhibition of Akt facilitated Smac release and sensitized chemoresistant cells to CDDP in a p53-dependent manner.