Keyword search (4,164 papers available)

"Mallick J" Authored Publications:

Title Authors PubMed ID
1 Hof1 plays a checkpoint related role in MMS induced DNA damage response in Candida albicans. Feng J, Islam A, Bean B, Feng J, Sparapani S, Shrivastava M, Goyal A, Omran RP, Mallick J, Whiteway M 31940254
BIOLOGY
2 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
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 Integration of Growth and Cell Size via the TOR Pathway and the Dot6 Transcription Factor in Candida albicans. Chaillot J, Tebbji F, Mallick J, Sellam A 30593490
BIOLOGY
5 MAP Kinase Regulation of the Candida albicans Pheromone Pathway. Rastghalam G, Omran RP, Alizadeh M, Fulton D, Mallick J, Whiteway M 30787119
BIOLOGY
6 The evolutionary rewiring of the ribosomal protein transcription pathway modifies the interaction of transcription factor heteromer Ifh1-Fhl1 (interacts with forkhead 1-forkhead-like 1) with the DNA-binding specificity element. Mallick J, Whiteway M 23625919
BIOLOGY
7 Mms21: A Putative SUMO E3 Ligase in Candida albicans That Negatively Regulates Invasiveness and Filamentation, and Is Required for the Genotoxic and Cellular Stress Response. Islam A, Tebbji F, Mallick J, Regan H, Dumeaux V, Omran RP, Whiteway M 30530734
PERFORM

 

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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