Glucose phosphorylation is required for Mycobacterium tuberculosis persistence in mice.
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TB drug development: immunology at the tableMycobacterial genes essential for the pathogen's survival in the hostNew insights into TB physiology suggest untapped therapeutic opportunitiesSurface hydrolysis of sphingomyelin by the outer membrane protein Rv0888 supports replication of Mycobacterium tuberculosis in macrophagesInactivation of fructose-1,6-bisphosphate aldolase prevents optimal co-catabolism of glycolytic and gluconeogenic carbon substrates in Mycobacterium tuberculosisInduction of a stringent metabolic response in intracellular stages of Leishmania mexicana leads to increased dependence on mitochondrial metabolismMycobacterium tuberculosis exploits asparagine to assimilate nitrogen and resist acid stress during infectionMetabolic Perspectives on PersistenceManipulation of the mononuclear phagocyte system by Mycobacterium tuberculosis.The Sculpting of the Mycobacterium tuberculosis Genome by Host Cell-Derived PressuresMycobacterium tuberculosis metabolismThe tuberculosis drug discovery and development pipeline and emerging drug targets.Deficiency of the novel exopolyphosphatase Rv1026/PPX2 leads to metabolic downshift and altered cell wall permeability in Mycobacterium tuberculosisTwo enzymes with redundant fructose bisphosphatase activity sustain gluconeogenesis and virulence in Mycobacterium tuberculosis.E1 of α-ketoglutarate dehydrogenase defends Mycobacterium tuberculosis against glutamate anaplerosis and nitroxidative stress.Central Role of Pyruvate Kinase in Carbon Co-catabolism of Mycobacterium tuberculosis.Oxadiazoles Have Butyrate-Specific Conditional Activity against Mycobacterium tuberculosisA central role for aspartate in Mycobacterium tuberculosis physiology and virulence.Mycobacterium tuberculosis nitrogen assimilation and host colonization require aspartate.Triosephosphate isomerase is dispensable in vitro yet essential for Mycobacterium tuberculosis to establish infection.Tuberculosis drug discovery and emerging targets.Nitrogen metabolism in Mycobacterium tuberculosis physiology and virulence.Neglected diseases prioritized in Brazil under the perspective of metabolomics: A review.Integration of Metabolomics and Transcriptomics Reveals a Complex Diet of Mycobacterium tuberculosis during Early Macrophage Infection.Metabolic crosstalk between host and pathogen: sensing, adapting and competing.Amino acid capture and utilization within the Mycobacterium tuberculosis phagosome.Rv2031c of Mycobacterium tuberculosis: a master regulator of Rv2028-Rv2031 (HspX) operon.To Eat and to Be Eaten: Mutual Metabolic Adaptations of Immune Cells and Intracellular Bacterial Pathogens upon Infection.Lactate oxidation facilitates growth of Mycobacterium tuberculosis in human macrophages.Mycobacterium tuberculosis Proteome Response to Antituberculosis Compounds Reveals Metabolic "Escape" Pathways That Prolong Bacterial Survival.Fumarase Deficiency Causes Protein and Metabolite Succination and Intoxicates Mycobacterium tuberculosis.Acetate Dissimilation and Assimilation in Mycobacterium tuberculosis Depend on Carbon Availability.Metabolomics of Mycobacterium tuberculosis.Allosteric regulation of the partitioning of glucose-1-phosphate between glycogen and trehalose biosynthesis in Mycobacterium tuberculosis.Allosteric pyruvate kinase-based "logic gate" synergistically senses energy and sugar levels in Mycobacterium tuberculosis.Metabolic adaptation of two in silico mutants of Mycobacterium tuberculosis during infection.Multifaceted remodeling by vitamin C boosts sensitivity of Mycobacterium tuberculosis subpopulations to combination treatment by anti-tubercular drugs.Ultrastructural Analysis of Cell Envelope and Accumulation of Lipid Inclusions in Clinical Mycobacterium tuberculosis Isolates from Sputum, Oxidative Stress, and Iron Deficiency.Metabolic principles of persistence and pathogenicity in Mycobacterium tuberculosis.Glutamate mediated metabolic neutralization mitigates propionate toxicity in intracellular Mycobacterium tuberculosis.
P2860
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P2860
Glucose phosphorylation is required for Mycobacterium tuberculosis persistence in mice.
description
2013 nî lūn-bûn
@nan
2013 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2013 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
name
Glucose phosphorylation is required for Mycobacterium tuberculosis persistence in mice.
@ast
Glucose phosphorylation is required for Mycobacterium tuberculosis persistence in mice.
@en
Glucose phosphorylation is required for Mycobacterium tuberculosis persistence in mice.
@nl
type
label
Glucose phosphorylation is required for Mycobacterium tuberculosis persistence in mice.
@ast
Glucose phosphorylation is required for Mycobacterium tuberculosis persistence in mice.
@en
Glucose phosphorylation is required for Mycobacterium tuberculosis persistence in mice.
@nl
prefLabel
Glucose phosphorylation is required for Mycobacterium tuberculosis persistence in mice.
@ast
Glucose phosphorylation is required for Mycobacterium tuberculosis persistence in mice.
@en
Glucose phosphorylation is required for Mycobacterium tuberculosis persistence in mice.
@nl
P2093
P2860
P1433
P1476
Glucose phosphorylation is required for Mycobacterium tuberculosis persistence in mice.
@en
P2093
Carolina Trujillo
Joeli Marrero
Kyu Y Rhee
Sabine Ehrt
P2860
P304
P356
10.1371/JOURNAL.PPAT.1003116
P577
2013-01-10T00:00:00Z