Ask about this productRelated genes to: CNTNAP3 antibody
- Gene:
- CNTNAP3 NIH gene
- Name:
- contactin associated protein like 3
- Previous symbol:
- -
- Synonyms:
- CASPR3, KIAA1714, FLJ14195, CNTNAP3A
- Chromosome:
- 9p12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-06
- Date modifiied:
- 2017-05-12
Related products to: CNTNAP3 antibody
Related articles to: CNTNAP3 antibody
- Major depressive disorder (MDD), generalized anxiety disorder (GAD), and obsessive-compulsive disorder (OCD) frequently co-occur and share overlapping symptomatology. This in silico study systematically investigated shared transcriptomic signatures and biological pathways using peripheral blood expression data. Differential expression analysis revealed 13 genes commonly dysregulated in at least two disorders, including CNTNAP3, PROK2, S100P, HLA-DPB1, and IRAK3. Correlation patterns uncovered disorder-specific rewiring of gene-gene networks, with polarity shifts and strength alterations particularly involving EIF5A2 and CNTNAP3B in MDD and OCD. Functional enrichment revealed convergence in neurotransmission, synaptic regulation, immune signaling, and metabolic pathways. Five biological pathways, including "defense response to bacterium" (GO-BP), "cytokine signaling in the immune system," "TCR signaling," and "neutrophil degranulation" (Reactome), and "leishmaniasis" (KEGG), were enriched across all three disorders, alongside multiple overlaps in GO-MF and GO-CC domains. Protein-protein interaction mapping revealed ribosomal hub dominance in OCD and immune/inflammatory node centrality in MDD and GAD. A panel of 21 secreted dysregulated genes in MDD, validated for ELISA detection, demonstrated robust classification power (AUC > 0.70). Drug-gene interaction analysis identified four downregulated compounds, carbamazepine, flupirtine, indomethacin, and doxorubicin hydrochloride, shared across all three disorders, suggesting therapeutic repurposing potential. These findings highlight shared immunometabolic dysregulation and nominate blood-based biomarkers and pharmacological targets applicable across psychiatric diagnostic categories. - Source: PubMed
Publication date: 2026/02/27
Salimian Niloufar - Schizophrenia (SCZ) and bipolar disorder (BPD) are highly heritable psychiatric disorders with complex genetic and environmental underpinnings. Allele-specific expression (ASE) has emerged as a critical mechanism linking noncoding genetic variants to disease risk through epigenetic and environmental modulation. Here, whole-genome and transcriptome analyses of monozygotic twin pairs discordant for BPD or SCZ are performed, identifying that noncoding genetic variants drive differential ASE patterns of long noncoding RNAs (lncRNAs) in affected individuals compared to their unaffected co-twins. The rs112651172 (C/G) is identified as a functional ASE variant regulating PAXIP1-AS1 expression via allele-specific transcription factor binding: SMC3 binds the C allele, while CEBPB binds the G allele, resulting in G allele-specific upregulation in patients. Eevated PAXIP1-AS1 expression is consistently observed in SCZ and BPD postmortem brain tissues from PsychENCODE or LIBD datasets. In mice, G allele overexpression in the prefrontal cortex induces anxiety- and depression-like behaviors, social deficits, memory impairments, sensorimotor gating abnormalities, and reduced neuronal excitability. Mechanistically, PAXIP1-AS1 upregualtes CNTNAP3 by sequestering the transcriptional repressor ZGPAT. Knockdown of CNTNAP3 reversed the observed phenotypes. These findings establish rs112651172 as a regulatory variant linking noncoding genetic risk to psychiatric phenotypeshrough ASE-driven lncRNA dysregulation, suggesting new therapeutic targets in SCZ and BPD. - Source: PubMed
Publication date: 2025/09/05
Ni ChaoyingChen HeChen QiaqiLiao YangyangWang YunqianYe LinyanWu XiaohuiNi HongyuJiang TingyunLi ShufenYang QiongXue HongWang ZhongjuYi FengZhao Cunyou - Alcohol use disorder is closely related to genetic and environmental factors. However, the contribution of coding variation to alcohol use disorder susceptibility remains poorly understood. We aimed to identify genetic mutations in alcohol use disorder by whole exon sequencing. We performed whole-exome sequencing in 83 patients with alcohol use disorder and compared it with exome sequences of healthy controls that were collected from the 1000 Genomes Project. GO and KEGG enrichment analysis and protein interaction analysis were performed for the mutated genes in each group. Three online protein function prediction sites were used to predict whether SNPs/InDels cause protein coding changes. Further, we conducted a rare variant exploration. We identified 106 525 SNV and 19 826 InDel gene mutations in alcohol use disorder. In the healthy and alcohol use disorder groups, mutations in CNTNAP3, ZNF683, ALDPH2, CCHCR1, ZNF45 and ESRRA loci were found to be deleterious mutations in all three sites; CNTNAP3, ZNF683, ALDPH2, CCHCR1, ZNF45 and ESRRA may be potential targets for future precision treatment of alcohol use disorders, and further provide new ideas for drug development. - Source: PubMed
Liu LeiZhang BoDong YongLiu Li PingWang Jing YingLiu JunZhou Guang YuKang Chuan YiHu XiaoruiCheng ChangZhao NaLu JiaWang HuaizhiHu JianWang Xiaohong - To investigate the role of achaete-scute complex-like 2 (ASCL2) in stomach adenocarcinoma (STAD), we analyze whether ASCL2 suppression could retard cancer development and further observe the relevance between ASCL2 and inflammation via Toll-like receptor 4 (TLR4) activation in STAD, both in vitro and in vivo. - Source: PubMed
Publication date: 2022/08/25
Zheng EnqiCai ZhunLi WangyongNi ChuandouFang Qian - Major depressive disorder (MDD) is a leading cause of disability worldwide. Adolescence is a crucial period for the occurrence and development of depression. There are essential distinctions between adolescent and adult depression patients, and the etiology of depressive disorder is unclear. The interactions of multiple genes in a co-expression network are likely to be involved in the physiopathology of MDD. In the present study, RNA-Seq data of mRNA were acquired from the peripheral blood of MDD in adolescents and healthy control (HC) subjects. Co-expression modules were constructed via weighted gene co-expression network analysis (WGCNA) to investigate the relationships between the underlying modules and MDD in adolescents. In the combined MDD and HC groups, the dynamic tree cutting method was utilized to assign genes to modules through hierarchical clustering. Moreover, functional enrichment analysis was conducted on those co-expression genes from interested modules. The results showed that eight modules were constructed by WGCNA. The blue module was significantly associated with MDD after multiple comparison adjustment. Several Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways associated with stress and inflammation were identified in this module, including histone methylation, apoptosis, NF-kappa β signaling pathway, and TNF signaling pathway. Five genes related to inflammation, immunity, and the nervous system were identified as hub genes: , , , , and . All of these findings supported that MDD was associated with stress, inflammation, and immune responses, helping us to obtain a better understanding of the internal molecular mechanism and to explore biomarkers for the diagnosis or treatment of depression in adolescents. - Source: PubMed
Publication date: 2022/03/05
Zhao BaoFan QingyueLiu JintongYin AihuaWang PingpingZhang Wenxin