Autism-associated SHANK3 haploinsufficiency causes I h channelopathy in human neurons
Open accessAbstract
Faulty channels, not faulty synapses: SHANK3 is a widely expressed scaffolding protein that is enriched in postsynaptic specializations. In mutant mice, SHANK3 mutations cause autism-like behavioral changes and exhibit alterations in synaptic transmission. Yi et al. produced human neurons lacking SHANK3 but not other genes that are also involved in the autism-like disease Phelan-McDermid syndrome. Instead of affecting synapses, SHANK3 mutations primarily caused a channelopathy, with the major phenotype consisting of a specific impairment of HCN channels. Chronic impairment of membrane currents through channelopathy could account for the phenotypes observed in Phelan-McDermid neurons, such as alterations in cognitive functions and the predisposition to epilepsy. Science , this issue p. 10.1126/science.aaf2669
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In mice, both congenital knockout and haploinsufficiency of Shank3 lead to diminished social interest in others and are associated with disruption of cortical and subcortical circuits thought to be involved in ASD and its ontogenesis.
“In mice, both congenital knockout and haploinsufficiency of Shank3 leads to diminished social interest in others and is associated with the disruption of cortical and subcortical circuits thought to be involved in ASD 22–26 and its ontogenesis 22,25,27,28.”
From Reduced sociability and social agency encoding in adult Shank3-mutant mice are restored through gene re-expression in real time (2021) · cites this paper as [22]
Consistent with prior reports, HET mice generally do not display anxiety-related behavior.
“Therefore, consistent with prior reports 22,33, the HET mice generally do not display anxiety-related behavior.”
From Reduced sociability and social agency encoding in adult Shank3-mutant mice are restored through gene re-expression in real time (2021) · cites this paper as [22]
The HET mice therefore displayed diminished sociability.
“The HET mice therefore displayed diminished sociability 22,33.”
From Reduced sociability and social agency encoding in adult Shank3-mutant mice are restored through gene re-expression in real time (2021) · cites this paper as [22]
Heterozygous constructs were used to mimic the physiological expression of Shank3 and because, unlike animals with homozygous mutations, they generally do not exhibit motoric dysfunction, anxiety or self-injurious behavior that could potentially confound social testing.
“In our study, we used heterozygous constructs to mimic the physiological expression of Shank3 and because, unlike animals with homozygous mutations, they generally do not exhibit motoric dysfunction, anxiety or self-injurious behavior that could potentially confound social testing 22,33.”
From Reduced sociability and social agency encoding in adult Shank3-mutant mice are restored through gene re-expression in real time (2021) · cites this paper as [22]
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- Authors
- Yi, F., Danko, T., Botelho, S. C., Patzke, C., Pak, C., Wernig, M., & Südhof, T. C.
- Affiliations
- Stanford Medicine (US)
- Department of Molecular and Cellular Physiology, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305, USA.
- Howard Hughes Medical Institute (US)
- Corresponding author
- Yi, Fei
- Südhof, Thomas C.
- Venue
- Science
- Published
- 2016-05-06
- Volume
- 352
- Issue
- 6286
- Pages
- aaf2669-aaf2669
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC4901875
- OpenAlex
- W2292973084
- Cited by
- 313
- References
- 60
- Citations by year
- 2026: 14 · 2025: 21 · 2024: 35 · 2023: 27 · 2022: 32 · 2021: 26 · 2020: 44 · 2019: 35 · 2018: 34 · 2017: 34 · 2016: 10
- FWCI
- 30.43
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (MH092931, NS077906, U19MH104172)
- Vetenskapsradet, Sweden
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- SHANK3, haploinsufficiency, autism spectrum disorder, Phelan-McDermid syndrome, hyperpolarization-activated cation channels, HCN channels, human neurons, postsynaptic scaffolding, synaptic connectivity, neuronal morphology, heterozygous mutation
- MeSH terms
- Autism Spectrum Disorder, Action Potentials, Animals, Cells, Cultured, Chromosome Deletion, Chromosomes, Human, Pair 22, Genetic Engineering, Humans, Microfilament Proteins, Nerve Tissue Proteins, Synaptic Transmission, Neurons, Synapses, Mutagenesis, Gene Deletion, Mice, Knockout, Genetic Predisposition to Disease, Chromosome Disorders, Mice, Channelopathies, Embryonic Stem Cells, Haploinsufficiency, Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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