Evidence map›Paper›PMID 26987686›Full record

ArticleImmunology and cell biology2016

Increased expression with differential subcellular location of cytidine deaminase APOBEC3G in human CD4(+) T-cell activation and dendritic cell maturation.

Harold Oliva, Rodrigo Pacheco, José M Martinez-Navio, Marta Rodríguez-García, Mar Naranjo-Gómez, Núria Climent, Carolina Prado, Cristina Gil, Montserrat Plana, Felipe García and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Immunology and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. 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

16 authors at 9 institutions in 3 countries.

Harold OlivaInstitut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)-AIDS Research Group and HIV Vaccine Development in Catalonia (HIVACAT), Hospital Clínic de Barcelona, Faculty of Medicine, University of Barcelona, Barcelona, Spain.
Rodrigo PachecoDepartamento de Ciencias Biológicas, Facultad de Ciencias Biológicas, Universidad Andres Bello, Santiago, Chile.
José M Martinez-NavioDepartment of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona, Barcelona, Spain.
Marta Rodríguez-GarcíaInstitut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)-AIDS Research Group and HIV Vaccine Development in Catalonia (HIVACAT), Hospital Clínic de Barcelona, Faculty of Medicine, University of Barcelona, Barcelona, Spain.
Mar Naranjo-GómezLIRAD (Laboratory of Immunobiology for Research and Diagnostic Applications), Institut d'Investigació Germans Trias-Pujol, Autonomous University of Barcelona, Badalona (Barcelona), Spain.
Núria ClimentInstitut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)-AIDS Research Group and HIV Vaccine Development in Catalonia (HIVACAT), Hospital Clínic de Barcelona, Faculty of Medicine, University of Barcelona, Barcelona, Spain.
Carolina PradoLaboratorio de Neuroinmunología, Fundación Ciencia and Vida, Santiago, Chile.
Cristina GilInstitut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)-AIDS Research Group and HIV Vaccine Development in Catalonia (HIVACAT), Hospital Clínic de Barcelona, Faculty of Medicine, University of Barcelona, Barcelona, Spain.
Montserrat PlanaInstitut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)-AIDS Research Group and HIV Vaccine Development in Catalonia (HIVACAT), Hospital Clínic de Barcelona, Faculty of Medicine, University of Barcelona, Barcelona, Spain.
Felipe GarcíaInstitut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)-AIDS Research Group and HIV Vaccine Development in Catalonia (HIVACAT), Hospital Clínic de Barcelona, Faculty of Medicine, University of Barcelona, Barcelona, Spain.
José M MiróInstitut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)-AIDS Research Group and HIV Vaccine Development in Catalonia (HIVACAT), Hospital Clínic de Barcelona, Faculty of Medicine, University of Barcelona, Barcelona, Spain.
Rafael FrancoDepartment of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona, Barcelona, Spain.
Francesc E BorrasIVECAT-Group, Institut d'Investigació Germans Trias i Pujol (IGTP), Badalona, Spain.
Naveenan NavaratnamMRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital Campus, London, UK.
José M GatellInstitut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)-AIDS Research Group and HIV Vaccine Development in Catalonia (HIVACAT), Hospital Clínic de Barcelona, Faculty of Medicine, University of Barcelona, Barcelona, Spain.
Teresa GallartInstitut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)-AIDS Research Group and HIV Vaccine Development in Catalonia (HIVACAT), Hospital Clínic de Barcelona, Faculty of Medicine, University of Barcelona, Barcelona, Spain.
Consorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESHospital Clínic de Barcelona · ESUniversitat de Barcelona · ESFundación Ciencia and Vida · CLHammersmith Hospital · GBHospital Universitari Germans Trias i Pujol · ESInstituto de Salud Carlos III · ESUniversidad Andrés Bello · CLUniversitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

APOBEC3G (apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3G; A3G) is an innate defense protein showing activity against retroviruses and retrotransposons. Activated CD4(+) T cells are highly permissive for HIV-1 replication, whereas resting CD4(+) T cells are refractory. Dendritic cells (DCs), especially mature DCs, are also refractory. We investigated whether these differences could be related to a differential A3G expression and/or subcellular distribution. We found that A3G mRNA and protein expression is very low in resting CD4(+) T cells and immature DCs, but increases strongly following T-cell activation and DC maturation. The Apo-7 anti-A3G monoclonal antibody (mAb), which was specifically developed, confirmed these differences at the protein level and disclosed that A3G is mainly cytoplasmic in resting CD4(+) T cells and immature DCs. Nevertheless, A3G translocates to the nucleus in activated-proliferating CD4(+) T cells, yet remaining cytoplasmic in matured DCs, a finding confirmed by immunoblotting analysis of cytoplasmic and nuclear fractions. Apo-7 mAb was able to immunoprecipitate endogenous A3G allowing to detect complexes with numerous proteins in activated-proliferating but not in resting CD4(+) T cells. The results show for the first time the nuclear translocation of A3G in activated-proliferating CD4(+) T cells.

Indexed as

Cell DifferentiationAnimalsAntibodies, MonoclonalAPOBEC-3G DeaminaseCD4-Positive T-LymphocytesCell LineCell NucleusDendritic CellsHumansImmunoprecipitationLymphocyte ActivationMice, Inbred BALB CMolecular WeightMonocytesProtein BindingRNA, MessengerAntibodies, MonoclonalAPOBEC-3G DeaminaseAPOBEC3G protein, humanRNA, Messenger

Identifiers

PMID26987686
OpenAlexW2297779845

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.