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Santosh K. Katiyar

Researcher at Drexel University

Publications -  33
Citations -  1868

Santosh K. Katiyar is an academic researcher from Drexel University. The author has contributed to research in topics: Candida glabrata & Echinocandin. The author has an hindex of 21, co-authored 33 publications receiving 1747 citations.

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A naturally occurring proline-to-alanine amino acid change in Fks1p in Candida parapsilosis, Candida orthopsilosis, and Candida metapsilosis accounts for reduced echinocandin susceptibility.

TL;DR: Investigation of the role of a naturally occurring Pro-to-Ala substitution at amino acid position 660 (P660A), immediately distal to the highly conserved hot spot 1 region of Fks1p, in the reduced-echinocandin-susceptibility phenotype indicates that a Naturally occurring P660A substitution from the C. parapsilosis group accounts for the reduced susceptibility phenotype.
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Antiprotozoal activities of benzimidazoles and correlations with beta-tubulin sequence.

TL;DR: In vitro susceptibility data for Trichomonas vaginalis and G. lamblia is presented and in vitro activity of benzimidazoles against additional protozoan parasites is examined: little or no activity was observed against Entamoeba histolytica, Leishmania major, and AcanthamoebA polyphaga.
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Phylogenetic Analysis of β-Tubulin Sequences from Amitochondrial Protozoa

TL;DR: Phylogenetic analysis of rRNA sequences from these amitochondrial organisms suggests that G. lamblia, T. vaginalis, and microsporidia are near the base of the eukaryotic tree, while E. histolytica clusters with mitochondria-containing species.
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Candida albicans and Candida glabrata clinical isolates exhibiting reduced echinocandin susceptibility.

TL;DR: It is reported that the mutation F641Y is associated with RES in a C. albicans isolate, and Y641-equivalent Fks residues were identified in intrinsically RES Fusarium species and Candida guilliermondii.
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Antifungal activity in Saccharomyces cerevisiae is modulated by calcium signalling.

TL;DR: Evidence is presented that azole activity versus Saccharomyces cerevisiae is also modulated by Ca2+‐regulated signalling, and a model to explain the role of Ca2-regulated signalling in azole/terbinafine tolerance is proposed.