Abstract
Hackett et al. identify a role for the anti-inflammatory miR-21 in limiting host glycolysis during tuberculosis (TB) infection to favor bacterial replication. This occurs by targeting a pro-glycolytic isoform at the rate-limiting step in glycolysis, PFK-M, a process antagonized by the host Th1-cytokine IFN-γ, to promote full macrophage activation and antimicrobial function.
| Original language | English |
|---|---|
| Pages (from-to) | 124-136.e4 |
| Journal | Cell Reports |
| Volume | 30 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 7 Jan 2020 |
| Externally published | Yes |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- glycolysis
- interferon gamma
- interleukin-1b
- macrophage
- metabolic reprogramming
- microRNA
- miR-21
- mycobacterium tuberculosis
- phosphofructokinase
- tuberculosis
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