Evidence map›Paper›PMID 40196584›Full record

ArticlebioRxiv : the preprint server for biology2025

RAB5c controls the assembly of non-canonical autophagy machinery to promote phagosome maturation and microbicidal function of macrophages.

Edismauro Garcia Freitas-Filho, Isabella Zaidan, Marlon Fortes-Rocha, Daniel Leonardo Alzamora-Terrel, Carolina Bifano, Patrícia Alves de Castro, Renan Eugênio Araujo Piraine, Camila Figueiredo Pinzan, Caroline Patine de Rezende, Emilio Boada-Romero and 4 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

14 authors.

Edismauro Garcia Freitas-FilhoDepartamento de Biologia Celular e Molecular e Bioagentes Patogênicos, Faculdade de Medicina de Ribeirão Preto (FMRP), Universidade de São Paulo (USP), Ribeirão Preto, SP, Brazil.ORCID 0000-0002-1910-1085
Isabella ZaidanDepartamento de Biologia Celular e Molecular e Bioagentes Patogênicos, Faculdade de Medicina de Ribeirão Preto (FMRP), Universidade de São Paulo (USP), Ribeirão Preto, SP, Brazil.
Marlon Fortes-RochaDepartamento de Biologia Celular e Molecular e Bioagentes Patogênicos, Faculdade de Medicina de Ribeirão Preto (FMRP), Universidade de São Paulo (USP), Ribeirão Preto, SP, Brazil.
Daniel Leonardo Alzamora-TerrelDepartamento de Biologia Celular e Molecular e Bioagentes Patogênicos, Faculdade de Medicina de Ribeirão Preto (FMRP), Universidade de São Paulo (USP), Ribeirão Preto, SP, Brazil.
Carolina BifanoDepartamento de Biologia Celular e Molecular e Bioagentes Patogênicos, Faculdade de Medicina de Ribeirão Preto (FMRP), Universidade de São Paulo (USP), Ribeirão Preto, SP, Brazil.
Patrícia Alves de CastroDepartamento de Ciências Farmacêuticas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, USP, Ribeirão Preto, Brazil.
Renan Eugênio Araujo PiraineDepartamento de Bioquímica e Imunologia, FMRP, USP, Ribeirão Preto, SP, Brazil.
Camila Figueiredo PinzanDepartamento de Ciências Farmacêuticas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, USP, Ribeirão Preto, Brazil.
Caroline Patine de RezendeDepartamento de Bioquímica e Imunologia, FMRP, USP, Ribeirão Preto, SP, Brazil.
Emilio Boada-RomeroDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Fausto Bruno Dos Reis AlmeidaDepartamento de Bioquímica e Imunologia, FMRP, USP, Ribeirão Preto, SP, Brazil.
Gustavo Henrique GoldmanDepartamento de Ciências Farmacêuticas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, USP, Ribeirão Preto, Brazil.
Oliver FloreySignalling Programme, Babraham Institute, Cambridge, UK.
Larissa Dias CunhaDepartamento de Biologia Celular e Molecular e Bioagentes Patogênicos, Faculdade de Medicina de Ribeirão Preto (FMRP), Universidade de São Paulo (USP), Ribeirão Preto, SP, Brazil.

Funding

Deciphering the phenotypic and genomic traits that underlie the evolution of pathogenicity differences among Aspergillus fumigatus and its close relativesR01AI153356 · NIAID · VANDERBILT UNIVERSITY · PI Antonis Rokas · 2022 to 2026
$3.5M
NIAID NIH HHS R01 AI153356
6 · The paper itself

Abstract

Non-canonical conjugation of ATG8 proteins, including LC3, to single membranes implicates the autophagy machinery in cell functions unrelated to metabolic stress. One such pathway is LC3-associated phagocytosis (LAP), which aids in phagosome maturation and subsequent signaling upon cargo uptake mediated by certain innate immunity-associated receptors. Here, we show that a specific isoform of RAB5 GTPases, the molecular switches controlling early endosome traffic, is necessary for LAP. We demonstrate that RAB5c regulates phagosome recruitment and function of complexes required for phosphatidylinositol-3-phosphate [PI(3)P] and reactive oxygen species (ROS) generation by macrophages. RAB5c facilitates phagosome translocation of the V-ATPase transmembrane core, which is needed for ATG16L1 binding and consequent LC3 conjugation. RAB5c depletion impaired macrophage elimination of the fungal pathogen

Indexed as

Aspergillus fumigatusLC3-associated phagocytosisNon-canonical autophagyRAB5c GTPase

Identifiers

PMID40196584
PMCPMC11974809

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.