Back to search

Article

C-Terminal Domain of <i>Mycobacterium tuberculosis</i> Glutamate Decarboxylase determines the bacterial stress-adaptive metabolic state that steers macrophage polarisation supporting intracellular persistence

2026-05-06

Abstract excerpt

Mycobacterium tuberculosis ( Mtb ) adapts metabolically to survive hostile conditions within alveolar macrophages, but whether specific enzyme-driven metabolic states of Mtb link stress adaptation to host immunomodulation remains unclear. Using LC-MRM/MS metabolite profiling and metabolic modeling, we previously identified elevated γ-aminobutyric acid (GABA) production via the GABA shunt during adaptation to oxi...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work
c9c89773-8adc-5a88-8f14-5075568ddd2d
DOI
10.64898/2026.05.05.722917
Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest
Interactive article relationship graphSelect a related publication card to move it into the centre and load its closest explainable connections. Solid lines are source-backed structured connections. Dashed lines are semantic discovery signals and are not scientific evidence.
C-Terminal Domain of <i>Mycobacterium tuberculosis</i> Glutamate Decarboxylase determines the bacterial stress-adaptive metabolic state that steers macrophage polarisation supporting intracellular persistenceDOI 10.64898/2026.05.05.722917
A new stress-response pathway in <i>Mycobacterium tuberculosis</i>Semantic proximity
Glutamine is required for M1-like polarization in response to <i>Mycobacterium tuberculosis</i> infectionSemantic proximity
Genetic and metabolic regulation of <i>Mycobacterium tuberculosis</i> acid growth arrestSemantic proximity
Phagosomal acidification coordinates a lipid–redox program underlying antibiotic tolerance in Mycobacterium tuberculosisSemantic proximity
Compromised Metabolic Reprogramming Is an Early Indicator of CD8+ T Cell Dysfunction during Chronic Mycobacterium tuberculosis InfectionSemantic proximity
Fatty acid oxidation impairs macrophage effector functions that control <i>Mycobacterium tuberculosis</i>Semantic proximity
Down-regulation of malate synthase in Mycobacterium tuberculosis H37Ra leads to reduced stress tolerance, persistence and survival in macrophages.Semantic proximity
Metabolomics of Central Carbon Metabolism in <i>Mycobacterium tuberculosis</i>Semantic proximity
Glutamine Is Required for M1-like Polarization of Macrophages in Response to Mycobacterium tuberculosis InfectionSemantic proximity
Uncovering the Roles of <i>Mycobacterium tuberculosis melH</i> in Redox and Bioenergetic Homeostasis: Implications for Antitubercular TherapySemantic proximity
IRG1 controls host responses to restrict <i>Mycobacterium tuberculosis</i> infectionSemantic proximity
Glyoxylate detoxification is an essential function of malate synthase required for carbon assimilation in Mycobacterium tuberculosis.Semantic proximity
Select a neighboring publication to make it the new centre.