Heme oxygenase-1-derived carbon monoxide induces the Mycobacterium tuberculosis dormancy regulon
about
Pathogenesis, immunology, and diagnosis of latent Mycobacterium tuberculosis infectionThe emerging role of gasotransmitters in the pathogenesis of tuberculosisRedox homeostasis in mycobacteria: the key to tuberculosis control?2.3 A X-ray structure of the heme-bound GAF domain of sensory histidine kinase DosT of Mycobacterium tuberculosisStructural Insight into the Heme-based Redox Sensing by DosS from Mycobacterium tuberculosisCrystal Structure of Reduced MsAcg, a Putative Nitroreductase from Mycobacterium smegmatis and a Close Homologue of Mycobacterium tuberculosis AcgChemical probing suggests redox-regulation of the carbonic anhydrase activity of mycobacterial Rv1284Differential virulence and disease progression following Mycobacterium tuberculosis complex infection of the common marmoset (Callithrix jacchus)Mycobacterium tuberculosis transcriptional adaptation, growth arrest and dormancy phenotype development is triggered by vitamin CDosS responds to a reduced electron transport system to induce the Mycobacterium tuberculosis DosR regulonSelf-poisoning of Mycobacterium tuberculosis by targeting GlgE in an alpha-glucan pathwayCholesterol catabolism by Mycobacterium tuberculosis requires transcriptional and metabolic adaptationsMycobacterium tuberculosis WhiB3 maintains redox homeostasis by regulating virulence lipid anabolism to modulate macrophage responseThe Mycobacterium tuberculosis DosR regulon assists in metabolic homeostasis and enables rapid recovery from nonrespiring dormancyHeme oxygenase-1 promotes granuloma development and protects against dissemination of mycobacteria.Functional genetic diversity among Mycobacterium tuberculosis complex clinical isolates: delineation of conserved core and lineage-specific transcriptomes during intracellular survivalMycobacterium tuberculosis Induction of Heme Oxygenase-1 Expression Is Dependent on Oxidative Stress and Reflects Treatment Outcomes.Mycobacterium tuberculosis arrests host cycle at the G1/S transition to establish long term infectionThe DosS-DosT/DosR Mycobacterial Sensor System.To catch a killer. What can mycobacterial models teach us about Mycobacterium tuberculosis pathogenesis?Mycobacterium tuberculosis acg gene is required for growth and virulence in vivo.DevR (DosR) mimetic peptides impair transcriptional regulation and survival of Mycobacterium tuberculosis under hypoxia by inhibiting the autokinase activity of DevS sensor kinase.Individual Mycobacterium tuberculosis universal stress protein homologues are dispensable in vitro.Identification of trans- and cis-control elements involved in regulation of the carbon monoxide dehydrogenase genes in Mycobacterium sp. strain JC1 DSM 3803Appropriate DevR (DosR)-mediated signaling determines transcriptional response, hypoxic viability and virulence of Mycobacterium tuberculosisLatent tuberculosis infection: myths, models, and molecular mechanismsA high-resolution network model for global gene regulation in Mycobacterium tuberculosis.Linking the transcriptional profiles and the physiological states of Mycobacterium tuberculosis during an extended intracellular infectionEnergetics of Respiration and Oxidative Phosphorylation in Mycobacteria.New approaches in the diagnosis and treatment of latent tuberculosis infectionMetal limitation and toxicity at the interface between host and pathogenPlasma heme oxygenase-1 levels distinguish latent or successfully treated human tuberculosis from active disease.Role of haem oxygenase-1 in microbial host defence.The conserved hypothetical protein Rv0574c is required for cell wall integrity, stress tolerance, and virulence of Mycobacterium tuberculosis.A screen to identify small molecule inhibitors of protein-protein interactions in mycobacteria.cor, a novel carbon monoxide resistance gene, is essential for Mycobacterium tuberculosis pathogenesis.Induction of heme oxygenase-1 contributes to survival of Mycobacterium abscessus in human macrophages-like THP-1 cells.Virulence factor SenX3 is the oxygen-controlled replication switch of Mycobacterium tuberculosis.Mycobacterium tuberculosis response regulators, DevR and NarL, interact in vivo and co-regulate gene expression during aerobic nitrate metabolismComprehensive insights into Mycobacterium tuberculosis DevR (DosR) regulon activation switch.
P2860
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P2860
Heme oxygenase-1-derived carbon monoxide induces the Mycobacterium tuberculosis dormancy regulon
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
2008年论文
@zh
2008年论文
@zh-cn
name
Heme oxygenase-1-derived carbo ...... tuberculosis dormancy regulon
@ast
Heme oxygenase-1-derived carbo ...... tuberculosis dormancy regulon
@en
type
label
Heme oxygenase-1-derived carbo ...... tuberculosis dormancy regulon
@ast
Heme oxygenase-1-derived carbo ...... tuberculosis dormancy regulon
@en
prefLabel
Heme oxygenase-1-derived carbo ...... tuberculosis dormancy regulon
@ast
Heme oxygenase-1-derived carbo ...... tuberculosis dormancy regulon
@en
P2093
P2860
P50
P356
P1476
Heme oxygenase-1-derived carbo ...... tuberculosis dormancy regulon
@en
P2093
Anupam Agarwal
Jessy S Deshane
Subhashini Bolisetty
P2860
P304
18032-18039
P356
10.1074/JBC.M802274200
P407
P577
2008-04-09T00:00:00Z