Para-aminosalicylic acid acts as an alternative substrate of folate metabolism in Mycobacterium tuberculosis. - Wikidata - awgldk - TriplyDB

Para-aminosalicylic acid acts as an alternative substrate of folate metabolism in Mycobacterium tuberculosis.

Para-aminosalicylic acid acts as an alternative substrate of folate metabolism in Mycobacterium tuberculosis.

http://www.wikidata.org/entity/Q37220161

about

Whole-genome sequencing targets drug-resistant bacterial infections Learning from the past for TB drug discovery in the future Lipoamide Channel-Binding Sulfonamides Selectively Inhibit Mycobacterial Lipoamide Dehydrogenase Phylogenetic analysis of vitamin B12-related metabolism in Mycobacterium tuberculosis.New target prediction and visualization tools incorporating open source molecular fingerprints for TB Mobile 2.0 Mycobacterium tuberculosis folate metabolism and the mechanistic basis for para-aminosalicylic acid susceptibility and resistance Mycobacterium tuberculosis IMPDH in Complexes with Substrates, Products and Antitubercular Compounds An ancient riboswitch class in bacteria regulates purine biosynthesis and one-carbon metabolism Emerging Approaches to Tuberculosis Drug Development: At Home in the Metabolome.Tuberculosis Drug Development: History and Evolution of the Mechanism-Based Paradigm.Metabolomic strategies for the identification of new enzyme functions and metabolic pathways para-Aminosalicylic acid is a prodrug targeting dihydrofolate reductase in Mycobacterium tuberculosis Replacing sulfa drugs with novel DHPS inhibitors Identification of novel inhibitors of nonreplicating Mycobacterium tuberculosis using a carbon starvation model Genetic determinants involved in p-aminosalicylic acid resistance in clinical isolates from tuberculosis patients in northern China from 2006 to 2012 Target-based screen against a periplasmic serine protease that regulates intrabacterial pH homeostasis in Mycobacterium tuberculosis.The path of anti-tuberculosis drugs: from blood to lesions to mycobacterial cells.UDP-N-acetylmuramic acid l-alanine ligase (MurC) inhibition in a tolC mutant Escherichia coli strain leads to cell death Mycobacterium tuberculosis metabolism The molecular basis of antifolate resistance in Plasmodium falciparum: looking beyond point mutations.Opposing effects of target overexpression reveal drug mechanisms Genetic Approaches to Facilitate Antibacterial Drug Development.Effects of fluconazole on the metabolomic profile of Candida albicans.A Focused Screen Identifies Antifolates with Activity on Mycobacterium tuberculosis.Evolution of a thienopyrimidine antitubercular relying on medicinal chemistry and metabolomics insights.QSAR based therapeutic management of M. tuberculosis.A Biotin Biosynthesis Gene Restricted to Helicobacter.Ipso-hydroxylation and subsequent fragmentation: a novel microbial strategy to eliminate sulfonamide antibiotics.N-methylation of a bactericidal compound as a resistance mechanism in Mycobacterium tuberculosis.Mycobacterium tuberculosis Arylamine N-Acetyltransferase Acetylates and Thus Inactivates para-Aminosalicylic Acid Targeting intracellular p-aminobenzoic acid production potentiates the anti-tubercular action of antifolates.Binding pocket alterations in dihydrofolate synthase confer resistance to para-aminosalicylic acid in clinical isolates of Mycobacterium tuberculosis.The antimicrobial activity of nanoparticles: present situation and prospects for the future Characterizing the pocketome of Mycobacterium tuberculosis and application in rationalizing polypharmacological target selection.Mycobacterium tuberculosis evolutionary pathogenesis and its putative impact on drug development.Deletion of sigB Causes Increased Sensitivity to para-Aminosalicylic Acid and Sulfamethoxazole in Mycobacterium tuberculosis.Utility of the Biosynthetic Folate Pathway for Targets in Antimicrobial Discovery.Antibiotic resistance mechanisms in M. tuberculosis: an update.Bioluminescence for assessing drug potency against nonreplicating Mycobacterium tuberculosis.Anti-folates potentiate bactericidal effects of other antimicrobial agents.

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P2860

Para-aminosalicylic acid acts as an alternative substrate of folate metabolism in Mycobacterium tuberculosis.

http://www.wikidata.org/entity/Q37220161

description

2012 nî lūn-bûn

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2012年学术文章

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2012年學術文章

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name

Para-aminosalicylic acid acts ...... in Mycobacterium tuberculosis.

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Para-aminosalicylic acid acts ...... in Mycobacterium tuberculosis.

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Para-aminosalicylic acid acts ...... in Mycobacterium tuberculosis.

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Para-aminosalicylic acid acts ...... in Mycobacterium tuberculosis.

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Para-aminosalicylic acid acts ...... in Mycobacterium tuberculosis.

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Helena I Boshoff

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Kyu Y Rhee

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Sumit Chakraborty

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Todd Gruber

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P2860

Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence

Biochemical and structural characterization of the putative dihydropteroate synthase ortholog Rv1207 of Mycobacterium tuberculosis

Kinetics and ligand-binding preferences of Mycobacterium tuberculosis thymidylate synthases, ThyA and ThyX

The promoter of Rv0560c is induced by salicylate and structurally-related compounds in Mycobacterium tuberculosis

Cloning and expression of Mycobacterium tuberculosis and Mycobacterium leprae dihydropteroate synthase in Escherichia coli

Antifolate-induced depletion of intracellular glycine and purines inhibits thymineless death in E. coli.

Depletion of antibiotic targets has widely varying effects on growth

Conservation of the metabolomic response to starvation across two divergent microbes.

Mycobacterium tuberculosis thymidylate synthase gene thyX is essential and potentially bifunctional, while thyA deletion confers resistance to p-aminosalicylic acid.

Purification, crystallization and preliminary X-ray analysis of Mycobacterium tuberculosisfolylpolyglutamate synthase (MtbFPGS).

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88-91

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6115

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339

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Clifton E Barry

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2012-11-01T00:00:00Z

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23118010

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Akafuba bulwadde

Mycobacterium tuberculosis

aminosalicylic acid

2-hydroxy-7,8-dihydropteroate

4-aminosalicylate(1-)

P932

3792487

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