Evidence map›Paper›PMID 35714598›Full record

ArticleStem cell reports2022

Zika virus induces FOXG1 nuclear displacement and downregulation in human neural progenitors.

Giulia Lottini, Matteo Baggiani, Giulia Chesi, Beatrice D'Orsi, Paola Quaranta, Michele Lai, Laura Pancrazi, Marco Onorati, Mauro Pistello, Giulia Freer and 1 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Tricyclic Pyrrole-Based Compounds as Zika Virus Inhibitors.International journal of molecular sciences · 2026
    Article
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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

11 authors at 2 institutions in 1 country.

Giulia LottiniCentro Retrovirus, Department of Translational Research, University of Pisa, Pisa 56127, Italy; Department of Medical Biotechnologies, University of Siena, Siena 53100, Italy.
Matteo BaggianiUnit of Cell and Developmental Biology, Department of Biology, University of Pisa, Pisa 56127, Italy.
Giulia ChesiCentro Retrovirus, Department of Translational Research, University of Pisa, Pisa 56127, Italy.
Beatrice D'OrsiInstitute of Neuroscience, Italian National Research Council (CNR), Via Moruzzi, 1, Pisa 56124, Italy; Centro Pisano ricerca e implementazione clinica Flash Radiotherapy (CPFR@CISUP), Presidio S. Chiara, ed.18 via Roma, 67, Pisa 56126, Italy.
Paola QuarantaCentro Retrovirus, Department of Translational Research, University of Pisa, Pisa 56127, Italy.
Michele LaiCentro Retrovirus, Department of Translational Research, University of Pisa, Pisa 56127, Italy.
Laura PancraziInstitute of Neuroscience, Italian National Research Council (CNR), Via Moruzzi, 1, Pisa 56124, Italy.
Marco OnoratiUnit of Cell and Developmental Biology, Department of Biology, University of Pisa, Pisa 56127, Italy.
Mauro PistelloCentro Retrovirus, Department of Translational Research, University of Pisa, Pisa 56127, Italy.
Giulia FreerCentro Retrovirus, Department of Translational Research, University of Pisa, Pisa 56127, Italy.
Mario CostaInstitute of Neuroscience, Italian National Research Council (CNR), Via Moruzzi, 1, Pisa 56124, Italy; Centro Pisano ricerca e implementazione clinica Flash Radiotherapy (CPFR@CISUP), Presidio S. Chiara, ed.18 via Roma, 67, Pisa 56126, Italy; Laboratory of Biology "Bio@SNS", Scuola Normale Superiore, Piazza dei Cavalieri, Pisa 56124, Italy. Electronic address: costa@in.cnr.it.
University of Pisa · ITNational Research Council · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Congenital alterations in the levels of the transcription factor Forkhead box g1 (FOXG1) coding gene trigger "FOXG1 syndrome," a spectrum that recapitulates birth defects found in the "congenital Zika syndrome," such as microcephaly and other neurodevelopmental conditions. Here, we report that Zika virus (ZIKV) infection alters FOXG1 nuclear localization and causes its downregulation, thus impairing expression of genes involved in cell replication and apoptosis in several cell models, including human neural progenitor cells. Growth factors, such as EGF and FGF2, and Thr271 residue located in FOXG1 AKT domain, take part in the nuclear displacement and apoptosis protection, respectively. Finally, by progressive deletion of FOXG1 sequence, we identify the C-terminus and the residues 428-481 as critical domains. Collectively, our data suggest a causal mechanism by which ZIKV affects FOXG1, its target genes, cell cycle progression, and survival of human neural progenitors, thus contributing to microcephaly.

Indexed as

MicrocephalyNeural Stem CellsZika VirusZika Virus InfectionDown-RegulationForkhead Transcription FactorsHumansNerve Tissue ProteinsForkhead Transcription FactorsFOXG1 protein, humanNerve Tissue Proteinsautismbrain cancercongenital brain malformationsFGF2FOXG1hiPSCsmicrocephalyneural stem cellsneurodevelopmentneurotropic virusZika virus

Identifiers

PMID35714598
PMCPMC9287670
OpenAlexW4283013448

What OpenQuestion holds

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LicenceCC BY
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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.