Associated Papers
Increased NMDARs in neurons and glutamine synthetase in astrocytes underlying autistic-like behaviors of Gabrb1-/- mice.
Wang J et al.
Iscience, 2023
37599823 (PubMed )
Supplement: mmc2.zip › Supplemental_tables › Supplemental_table_3.xlsx › Table_S3
Novel Homozygous TTI2 Variant Causing Autosomal Recessive Syndromic Intellectual Disability and Primary Microcephaly from Pakistan: A Case Report (Exome Report).
Qarnain Z et al.
Case Reports in Genetics, 2022
Whole-exome sequencing identifies homozygous mutation in TTI2 in a child with primary microcephaly: a case report.
Picher-Martel V et al.
Bmc Neurology, 2020
Pathological priming causes developmental gene network heterochronicity in autistic subject-derived neurons.
Schafer ST et al.
Nature Neuroscience, 2019
30617258 (PubMed )
Supplement: NIHMS1512664-supplement-Sup_Table_5.xlsx › whole_genelist_SAFARI
Novel Compound Heterozygous Mutations in TTI2 Cause Syndromic Intellectual Disability in a Chinese Family.
Wang R et al.
Frontiers in Genetics, 2019
Allele-specific expression in a family quartet with autism reveals mono-to-biallelic switch and novel transcriptional processes of autism susceptibility genes.
Lin CY et al.
Scientific Reports, 2018
29523860 (PubMed )
Supplement: 41598_2018_22753_MOESM11_ESM.xlsx › Table_S10
A Syndromic Intellectual Disability Disorder Caused by Variants in TELO2, a Gene Encoding a Component of the TTT Complex.
You J et al.
American Journal of Human Genetics, 2016
Mutation in TTI2 reveals a role for triple T complex in human brain development.
Langouët M et al.
Human Mutation, 2013
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