Evidence map›Paper›PMID 35508131›Full record

ArticleCell reports2022

Loss-of-function variants in the schizophrenia risk gene SETD1A alter neuronal network activity in human neurons through the cAMP/PKA pathway.

Shan Wang, Jon-Ruben van Rhijn, Ibrahim Akkouh, Naoki Kogo, Nadine Maas, Anna Bleeck, Irene Santisteban Ortiz, Elly Lewerissa, Ka Man Wu, Chantal Schoenmaker and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
12.5field-weighted citation impact, top 1% 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

46 citing papers in PubMed, 68 citations in OpenAlex.

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  8. Phosphatase Signaling as a Therapeutic Strategy in Schizophrenia.International journal of molecular sciences · 2026
    Review
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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

15 authors at 2 institutions in 2 countries.

Shan WangDepartment of Cognitive Neurosciences, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6525 HR Nijmegen, the Netherlands.
Jon-Ruben van RhijnDepartment of Cognitive Neurosciences, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6525 HR Nijmegen, the Netherlands.
Ibrahim AkkouhDepartment of Medical Genetics, Oslo University Hospital, 0424 Oslo, Norway; NORMENT, Institute of Clinical Medicine, University of Oslo, 0372 Oslo, Norway.
Naoki KogoDepartment of Human Genetics, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6500 HB Nijmegen, the Netherlands; Department of Biophysics, Donders Institute for Brain Cognition and Behaviour, 6525 AJ Nijmegen, the Netherlands.
Nadine MaasDepartment of Cognitive Neurosciences, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6525 HR Nijmegen, the Netherlands.
Anna BleeckDepartment of Cognitive Neurosciences, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6525 HR Nijmegen, the Netherlands.
Irene Santisteban OrtizDepartment of Cognitive Neurosciences, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6525 HR Nijmegen, the Netherlands.
Elly LewerissaDepartment of Human Genetics, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6500 HB Nijmegen, the Netherlands.
Ka Man WuDepartment of Human Genetics, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6500 HB Nijmegen, the Netherlands.
Chantal SchoenmakerDepartment of Human Genetics, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6500 HB Nijmegen, the Netherlands.
Srdjan DjurovicDepartment of Medical Genetics, Oslo University Hospital, 0424 Oslo, Norway; NORMENT, Department of Clinical Science, University of Bergen, 5021 Bergen, Norway.
Hans van BokhovenDepartment of Cognitive Neurosciences, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6525 HR Nijmegen, the Netherlands; Department of Human Genetics, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6500 HB Nijmegen, the Netherlands.
Tjitske KleefstraDepartment of Human Genetics, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6500 HB Nijmegen, the Netherlands.
Nael Nadif KasriDepartment of Cognitive Neurosciences, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6525 HR Nijmegen, the Netherlands; Department of Human Genetics, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6500 HB Nijmegen, the Netherlands.
Dirk SchubertDepartment of Cognitive Neurosciences, Radboudumc, Donders Institute for Brain Cognition and Behaviour, 6525 HR Nijmegen, the Netherlands. Electronic address: d.schubert@donders.ru.nl.
Radboud University Nijmegen · NLOslo University Hospital · NO

Funding

ZonMw 91217055
6 · The paper itself

Abstract

Heterozygous loss-of-function (LoF) mutations in SETD1A, which encodes a subunit of histone H3 lysine 4 methyltransferase, cause a neurodevelopmental syndrome and increase the risk for schizophrenia. Using CRISPR-Cas9, we generate excitatory/inhibitory neuronal networks from human induced pluripotent stem cells with a SETD1A heterozygous LoF mutation (SETD1A

Indexed as

Induced Pluripotent Stem CellsSchizophreniaCyclic AMPCyclic AMP-Dependent Protein KinasesHistone-Lysine N-MethyltransferaseHumansNeuronsCyclic AMPCyclic AMP-Dependent Protein KinasesHistone-Lysine N-MethyltransferaseSetd1A protein, humancAMPCP: NeurosciencehiPSChuman neuronsmicroelectrode arraynetwork activityPKAschizophreniaSETD1A

Identifiers

PMID35508131
PMCPMC7615788
OpenAlexW4229023797

What OpenQuestion holds

Textmetadata
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.