Evidence map›Paper›PMID 27995975›Full record

ArticleScientific reports2016

RNA activation of haploinsufficient Foxg1 gene in murine neocortex.

Cristina Fimiani, Elisa Goina, Qin Su, Guangping Gao, Antonello Mallamaci

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Genetic therapies for neurological diseases.Pharmacological reviews · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Approaches to Gene Modulation Therapy for ALS.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Review
  8. Multidimensional Functional Profiling of Human NeuropathogenicInternational journal of molecular sciences · 2022
    Article
  9. Review
  10. Article
  11. Review
  12. 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

5 authors at 2 institutions in 2 countries.

Cristina FimianiLab of Cerebral Cortex Development, SISSA, via Bonomea 265 - 34136 Trieste, Italy.
Elisa GoinaLab of Cerebral Cortex Development, SISSA, via Bonomea 265 - 34136 Trieste, Italy.
Qin SuViral Vector Core, University of Massachusetts Medical School - 368 Plantation Street, AS6-2049 - Worcester, MA 01605, USA.
Guangping GaoViral Vector Core, University of Massachusetts Medical School - 368 Plantation Street, AS6-2049 - Worcester, MA 01605, USA.
Antonello MallamaciLab of Cerebral Cortex Development, SISSA, via Bonomea 265 - 34136 Trieste, Italy.
Scuola Internazionale Superiore di Studi Avanzati · ITUniversity of Massachusetts Chan Medical School · US

Funding

Viral escape from AAV expressed transgenesP01AI100263 · NIAID · SCRIPPS FLORIDA · PI FARZAN, MICHAEL R. · 2012 to 2016
$11.9M
Oligodendrocyte-focused rAAV gene therapy strategies for Canavan disease and LeukodystrophiesR01NS076991 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Guangping Gao · 2012 to 2026
$5.7M
NIAID NIH HHS P01 AI100263NINDS NIH HHS R01 NS076991
6 · The paper itself

Abstract

More than one hundred distinct gene hemizygosities are specifically linked to epilepsy, mental retardation, autism, schizophrenia and neuro-degeneration. Radical repair of these gene deficits via genome engineering is hardly feasible. The same applies to therapeutic stimulation of the spared allele by artificial transactivators. Small activating RNAs (saRNAs) offer an alternative, appealing approach. As a proof-of-principle, here we tested this approach on the Rett syndrome-linked, haploinsufficient, Foxg1 brain patterning gene. We selected a set of artificial small activating RNAs (saRNAs) upregulating it in neocortical precursors and their derivatives. Expression of these effectors achieved a robust biological outcome. saRNA-driven activation (RNAa) was limited to neural cells which normally express Foxg1 and did not hide endogenous gene tuning. saRNAs recognized target chromatin through a ncRNA stemming from it. Gene upregulation required Ago1 and was associated to RNApolII enrichment throughout the Foxg1 locus. Finally, saRNA delivery to murine neonatal brain replicated Foxg1-RNAa in vivo.

Indexed as

3T3 CellsAnimalsArgonaute ProteinsCell LineEukaryotic Initiation FactorsForkhead Transcription FactorsHaploinsufficiencyHEK293 CellsHumansMiceMicroRNAsNeocortexNerve TissueNerve Tissue ProteinsRett SyndromeRNA InterferenceAgo1 protein, mouseArgonaute ProteinsEukaryotic Initiation FactorsForkhead Transcription FactorsFoxg1 protein, mouseMicroRNAsNerve Tissue ProteinsRNA Polymerase IIIRNA, Small Interfering

Identifiers

PMID27995975
PMCPMC5172352
OpenAlexW2565571358

What OpenQuestion holds

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LicenceCC BY
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.