Evidence map›Paper›PMID 33818279›Full record

ArticleAutophagy2022

A NOVEL NOX/PHOX-CD38-NAADP-TFEB AXIS IMPORTANT FOR MACROPHAGE ACTIVATION DURING BACTERIAL PHAGOCYTOSIS.

Mehran Najibi, Havisha H Honwad, Joseph A Moreau, Stephanie M Becker, Javier E Irazoqui

Open access · greenAbstract read
In one paragraph

Article in Autophagy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. HIV-1 gp120-induced lysosomal stress responses are controlled by TRPML1 redox sensors.Redox report : communications in free radical research · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Microbiology spectrum · 2024
    Article
  11. Article
  12. Article
  13. NAADP-Mediated CaHandbook of experimental pharmacology · 2023
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Molecular design of a pathogen activated, self-assembling mechanopharmaceutical device.Journal of controlled release : official journal of the Controlled Release Society · 2022
    Review
  19. Article
  20. NADSignal transduction and targeted therapy · 2020
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Mehran NajibiDepartment of Microbiology and Physiological Systems and Program in Innate Immunity, University of Massachusetts Medical School, Worcester, USA.
Havisha H HonwadDepartment of Microbiology and Physiological Systems and Program in Innate Immunity, University of Massachusetts Medical School, Worcester, USA.
Joseph A MoreauDepartment of Microbiology and Physiological Systems and Program in Innate Immunity, University of Massachusetts Medical School, Worcester, USA.
Stephanie M BeckerDepartment of Microbiology and Physiological Systems and Program in Innate Immunity, University of Massachusetts Medical School, Worcester, USA.ORCID 0000-0003-0565-5930
Javier E IrazoquiDepartment of Microbiology and Physiological Systems and Program in Innate Immunity, University of Massachusetts Medical School, Worcester, USA.ORCID 0000-0001-6553-1329
University of Massachusetts Chan Medical School · US

Funding

Role of MiT Transcription Factors in Host Defense Against Bacterial InfectionR01GM101056 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI IRAZOQUI, JAVIER ELBIO · 2012 to 2022
$3.9M
NIGMS NIH HHS R01 GM101056
6 · The paper itself

Abstract

Macrophage activation in the presence of bacterial cells and molecules entails complex programs of gene expression. How such triggers elicit specific gene expression programs is incompletely understood. We previously discovered that TFEB (transcription factor EB) is a key contributor to macrophage activation during bacterial phagocytosis. However, the mechanism linking phagocytosis of bacterial cells to TFEB activation and downstream pro-inflammatory cytokine induction remained unknown. We found that macrophages lacking both TFEB and TFE3 (transcription factor E3) were unable to mount a pro-inflammatory phenotype in response to bacterial infection. The NOX/PHOX (NADPH oxidase)-dependent oxidative burst was required for nuclear translocation of TFEB during phagocytosis of Gram-positive or -negative bacteria, and reactive oxygen species (ROS) were sufficient to trigger TFEB activation in a CD38- and NAADP (nicotinic acid adenine dinucleotide phosphate)-dependent manner. Consistent with the Ca

Indexed as

AutophagyMacrophage ActivationBacteriaBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsNADPPhagocytosisReactive Oxygen SpeciesBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsNAADPNADPReactive Oxygen SpeciesCD38il1αil1βil6innate immunityphagocytereactive oxygen speciestfe3tfebtnfα

Identifiers

PMID33818279
PMCPMC8865266
OpenAlexW3146706804

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.