ArticleNature genetics2016
TSHZ3 deletion causes an autism syndrome and defects in cortical projection neurons.
Article in Nature genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 142 citations in OpenAlex.
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- Derepression of transposable elements in the mouse prefrontal cortex disrupts social behavior.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- High-throughput transcriptomic screening reveals entrectinib as a repositioning opportunity in 19q12 autism spectrum disorder.Scientific reports · 2025Article
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- Schizophrenia risk gene ZNF536 modulates retinoic acid response and neuronal gene networks in SH-SY5Y cells.Frontiers in molecular neuroscience · 2025Article
- Heterozygous variants in the teashirt zinc finger homeobox 3 (TSHZ3) gene in human congenital anomalies of the kidney and urinary tract.European journal of human genetics : EJHG · 2025Article
- The transcriptomic landscape of spinal V1 interneurons reveals a role for En1 in specific elements of motor output.bioRxiv : the preprint server for biology · 2024Article
- Molecular logic for cellular specializations that initiate the auditory parallel processing pathways.bioRxiv : the preprint server for biology · 2024Article
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Authors and funding
29 authors at 13 institutions in 5 countries.
Funding
Abstract
TSHZ3, which encodes a zinc-finger transcription factor, was recently positioned as a hub gene in a module of the genes with the highest expression in the developing human neocortex, but its functions remained unknown. Here we identify TSHZ3 as the critical region for a syndrome associated with heterozygous deletions at 19q12-q13.11, which includes autism spectrum disorder (ASD). In Tshz3-null mice, differentially expressed genes include layer-specific markers of cerebral cortical projection neurons (CPNs), and the human orthologs of these genes are strongly associated with ASD. Furthermore, mice heterozygous for Tshz3 show functional changes at synapses established by CPNs and exhibit core ASD-like behavioral abnormalities. These findings highlight essential roles for Tshz3 in CPN development and function, whose alterations can account for ASD in the newly defined TSHZ3 deletion syndrome.
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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.