Keyword search (4,163 papers available)

"Choudhury BI" Authored Publications:

Title Authors PubMed ID
1 Chemogenomic Profiling of the Fungal Pathogen Candida albicans. Chen Y, Mallick J, Maqnas A, Sun Y, Choudhury BI, Côte P, Yan L, Ni TJ, Li Y, Zhang D, Rodríguez-Ortiz R, Lv QZ, Jiang YY, Whiteway M 29203491
BIOLOGY
2 Evolutionary Transition of GAL Regulatory Circuit from Generalist to Specialist Function in Ascomycetes. Choudhury BI, Whiteway M 29395731
BIOLOGY
3 Erratum for Chen et al., "Chemogenomic Profiling of the Fungal Pathogen Candida albicans". Chen Y, Mallick J, Maqnas A, Sun Y, Choudhury BI, Côte P, Yan L, Ni TJ, Li Y, Zhang D, Rodríguez-Ortiz R, Lv QZ, Jiang YY, Whiteway M 29588354
BIOLOGY
4 Functional androdioecy in critically endangered Gymnocladus assamicus (Leguminosae) in the Eastern Himalayan Region of Northeast India. Choudhury BI, Khan ML, Dayanandan S 24586267
BIOLOGY
5 Patterns of nucleotide diversity and phenotypes of two domestication related genes (OsC1 and Wx) in indigenous rice varieties in Northeast India. Choudhury BI, Khan ML, Dayanandan S 24935343
BIOLOGY
6 Genetic relatedness among indigenous rice varieties in the Eastern Himalayan region based on nucleotide sequences of the Waxy gene. Choudhury BI, Khan ML, Dayanandan S 25547027
CSFG
7 Rewiring of the Ppr1 Zinc Cluster Transcription Factor from Purine Catabolism to Pyrimidine Biogenesis in the Saccharomycetaceae. Tebung WA, Choudhury BI, Tebbji F, Morschhäuser J, Whiteway M 27321996
BIOLOGY

 

Title:Chemogenomic Profiling of the Fungal Pathogen Candida albicans.
Authors:Chen Y,  Mallick J,  Maqnas A,  Sun Y,  Choudhury BI,  Côte P,  Yan L,  Ni TJ,  Li Y,  Zhang D,  Rodríguez-Ortiz R,  Lv QZ,  Jiang YY,  Whiteway M
Link:https://www.ncbi.nlm.nih.gov/pubmed/29203491?dopt=Abstract
DOI:10.1128/AAC.02365-17
Publication:Antimicrobial agents and chemotherapy
Keywords:Candida albicans;  drug interactions;  genome analysis; 
PMID:29203491 Category:Antimicrob Agents Chemother Date Added:2019-06-07
Dept Affiliation: BIOLOGY
1 Biology Department, Concordia University, Montreal, Canada.
2 Center for New Drug Research, School of Pharmacy, Second Military Medical University, Shanghai, People's Republic of China.
3 Department of Organic Chemistry, School of Pharmacy, Second Military Medical University, Shanghai, People's Republic of China.
4 CONACYT, Institute of Neurobiology, UNAM, Juriquilla Campus, Querétaro, Mexico.
5 Biology Department, Concordia University, Montreal, Canada malcolm.whiteway@concordia.ca.

Description:

Chemogenomic Profiling of the Fungal Pathogen Candida albicans.

Antimicrob Agents Chemother. 2018 02;62(2):

Authors: Chen Y, Mallick J, Maqnas A, Sun Y, Choudhury BI, Côte P, Yan L, Ni TJ, Li Y, Zhang D, Rodríguez-Ortiz R, Lv QZ, Jiang YY, Whiteway M

Abstract

There is currently a small number of classes of antifungal drugs, and these drugs are known to target a very limited set of cellular functions. We derived a set of approximately 900 nonessential, transactivator-defective disruption strains from the tetracycline-regulated GRACE collection of strains of the fungal pathogen Candida albicans This strain set was screened against classic antifungal drugs to identify gene inactivations that conferred either enhanced sensitivity or increased resistance to the compounds. We examined two azoles, fluconazole and posaconazole; two echinocandins, caspofungin and anidulafungin; and a polyene, amphotericin B. Overall, the chemogenomic profiles within drug classes were highly similar, but there was little overlap between classes, suggesting that the different drug classes interacted with discrete networks of genes in C. albicans We also tested two pyridine amides, designated GPI-LY7 and GPI-C107; these drugs gave very similar profiles that were distinct from those of the echinocandins, azoles, or polyenes, supporting the idea that they target a distinct cellular function. Intriguingly, in cases where these gene sets can be compared to genetic disruptions conferring drug sensitivity in other fungi, we find very little correspondence in genes. Thus, even though the drug targets are the same in the different species, the specific genetic profiles that can lead to drug sensitivity are distinct. This implies that chemogenomic screens of one organism may be poorly predictive of the profiles found in other organisms and that drug sensitivity and resistance profiles can differ significantly among organisms even when the apparent target of the drug is the same.

PMID: 29203491 [PubMed]




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