Ask about this productRelated genes to: PCDH17 Blocking Peptide
- Gene:
- PCDH17 NIH gene
- Name:
- protocadherin 17
- Previous symbol:
- -
- Synonyms:
- PCDH68, PCH68
- Chromosome:
- 13q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-12-19
- Date modifiied:
- 2015-08-26
Related products to: PCDH17 Blocking Peptide
Related articles to: PCDH17 Blocking Peptide
- Olfactory dysfunction is a debilitating condition with no established treatment. This study evaluated the efficacy of intranasal (i.n.) NAD administration in restoring olfactory function. Cultured human olfactory stem cells (hOSCs) were treated with NAD and assessed by immunofluorescence staining, PCR, and western blot analyses. In vivo, mice with ZnSO-induced anosmia were treated with i.n. NAD, intraperitoneal dexamethasone, or PBS and evaluated by histological analysis, behavioral tests, bulk RNA-sequencing (RNA-seq), and in situ hybridization. NAD promoted hOSC differentiation into olfactory sensory neurons (OSNs), evidenced by increased stem cell (SOX2 and nestin) and OSN markers (Tuj1 and OMP) expression, and upregulated neuronal differentiation-related genes (SOX2, NESTIN, NEUROD1, NEUROG1, and OMP). In vivo, the NAD group showed significant olfactory function improvement and marked olfactory epithelium repair. Bulk RNA-seq of the olfactory turbinate tissue identified 113 differentially expressed genes (cluster T1) upregulated in control and NAD groups. The Gene Ontology (GO) term "modulation of chemical synaptic transmission" was associated with cluster T1, and 25 genes implicated in this GO were upregulated in the NAD group. Integration with publicly available single-cell RNA-seq data identified six neuronal marker genes - ABHD2, DLGAP2, FOXO3, HIPK2, KCNMA1, and PCDH17 - upregulated by NAD. Protein expression of DLGAP2 and PCDH17 was higher in differentiated hOSCs treated with NAD. In situ hybridization confirmed that Dlgap2, Foxo3, and Pcdh17 expression was restored in anosmic mice treated with i.n. NAD. The potential therapeutic efficacy of i.n. NAD administration was demonstrated by showing regeneration of OSNs in hOSCs and restoring olfactory function in an anosmia mouse model. - Source: PubMed
Publication date: 2026/07/01
Yoo Shin HyukJang Jung YeonBae Jun-SangVentura ReizaKim Eun HeeKim A YoungMo Ji-HunPark JaewooKang KyuhoYun YeogyunLee Jun HeeKim Yong-JaeLee Dong-JoonKim Ji Heui - The evolutionary expansion of the primate prefrontal cortex (PFC) presents a profound biological enigma: how does this region achieve a highly ordered, modular architecture in the absence of direct dense sensory templates that govern primary sensory areas? In this review, we synthesize classical neuroanatomical frameworks with recent advances in spatial transcriptomics and connectomics to delineate a model of intrinsic elaboration. We propose that PFC modularity emerges from a developmental program facilitated by expansion of the outer subventricular zone (OSVZ) and the legacy of whole-genome duplication (2R-WGD). Central to this proposal is a "Dual-Control Model" of circuit assembly, inferred by integrating anatomical tracer data with spatial and spatiotemporal transcriptomic datasets. This framework suggests that long-range connectivity is established through pre-target axon bundling (fasciculation), governed by a high-dimensional navigation code (e.g., ephrin/Eph, PCDH11X, PCDH17, ROBO2), while these bundles are anchored onto vertical columnar scaffolds through synaptic docking mechanisms (e.g., CBLN2, cadherins). By contrasting the PFC with the map-driven visual system, point-driven olfactory system, and layer-driven hippocampus, we argue that PFC uniqueness lies not in novel genes but in a combinatorial logic of a shared molecular toolkit, which can be understood as intrinsic elaboration. This framework may facilitate the emergence of a cognitive scaffold under relatively weak external sensory constraints. These molecular systems are considered to operate in concert with activity-dependent developmental refinement rather than independently of neural activity. - Source: PubMed
Publication date: 2026/06/02
Yamamori TetsuoWatakabe AkiyaSkibbe Henrik - Ewing sarcoma (ES) is an aggressive bone tumor in children and adolescents, and metastatic dissemination remains the major cause of treatment failure. Protocadherin 17 (PCDH17), a member of the cadherin superfamily, has been reported to exert context-dependent roles in solid tumors, but its significance in ES is unclear. Here, we analyzed Gene Expression Omnibus (GEO) datasets to evaluate PCDH17 expression, its association with overall survival and event-free survival, and the enrichment of biological pathways related to PCDH17 levels, and further examined PCDH17 expression in ES cell lines. The biological functions of PCDH17 were investigated using short hairpin RNA-mediated knockdown in A673 and RD-ES cells, followed by Cell counting kit-8 (CCK-8), colony formation, wound healing and transwell invasion assay, as well as western blotting (WB) and immunofluorescence (IF). PCDH17 was markedly upregulated in ES tissues and cell lines compared with normal counterparts, and high expression correlated with shorter survival. Gene set enrichment analysis (GSEA) indicated that high PCDH17 expression is associated with transcriptional programs driving cell cycle progression and oncogenic growth. Functionally, silencing PCDH17 significantly impairs proliferation, colony formation, migration and invasion of ES cells, and attenuates mesenchymal marker expression as well as associated morphological features. Collectively, our data indicate that PCDH17 is upregulated in ES and associated with worse survival, and that PCDH17 depletion suppresses malignant phenotypes in vitro. Together, these results nominate PCDH17 as a candidate prognostic biomarker and potential therapeutic target, which merits further validation. - Source: PubMed
Publication date: 2026/04/28
Zhou LeiZhang QianYu ShangjiangJiang RunyiWu AnshunJiang DongjieZhou ZihuanWei WeiHe ShaohuiWei Haifeng - To understand how neural circuits are assembled, it is essential to identify and characterize the axonal guidance cues and receptors that determine the axonal trajectories and connections between neurons. We performed single-cell RNA sequencing of olfactory sensory neurons from zebrafish to identify candidate axonal guidance-related genes that are differentially expressed according to sensory axon target location in the olfactory bulb. Among the candidates we identified were several members of the non-clustered delta-protocadherin family of adhesion molecules. We found that two members of the delta1-protocadherin family, pcdh7b and pcdh11, are most highly expressed in sensory neurons that project to a specific identifiable neuropil in the early olfactory bulb called the DZ protoglomerulus. Knocking down either one of these protocadherins impairs the ability of sensory axons to terminate within the DZ protoglomerulus. Knockdown does not affect the ability of other sensory axons from terminating normally in a separate neuropil called the CZ protoglomerulus. In contrast, two members of the delta2-protocadherin family, pcdh10b and pcdh17, are most highly expressed in sensory neurons that project to the CZ protoglomerulus. Knocking down pcdh10b induces ectopic terminations of CZ projecting sensory axons. Knocking down pcdh17 induces substantial ectopic axonal trajectories and impairs CZ projecting sensory axons from finding and terminating in the CZ protoglomerulus. Knockdowns of either pcdh10b or pcdh17 do not affect DZ projecting sensory axons. We conclude that delta1-protocadherins help DZ projecting sensory axons enter and remain within the DZ protoglomerulus, while delta2-protocadherins help CZ projecting sensory axons navigate to the CZ protoglomerulus. - Source: PubMed
Publication date: 2026/04/01
Barnes Daniel TCrenshaw Ezekiel M DCurran Matthew JHerr Jessica BDevereaux Emily SSeligman Carly DRaper Jonathan A - Sex differences, in terms of prevalence, symptoms and disease progression, are established in the etiology of complex neurodegenerative diseases, including amyotrophic lateral sclerosis, Parkinson's disease and Alzheimer's disease, but the underlying biology driving these differences remains poorly understood. There is emerging evidence, through genetic and functional analyses, affirming the role of the immune system in such diseases, but a thorough assessment of sex differences linking the immune system and neurodegenerative diseases is understudied. Here, we applied a robust causal inference approach, two-sample Mendelian randomization, to evaluate the causal effect of immune-related protein levels on three neurodegenerative diseases with large-scale sex-stratified genome-wide association data available: amyotrophic lateral sclerosis (females = 10,895 cases, 57,062 controls; males = 15,547 cases, 50,145 controls), Parkinson's disease (females = 7,947 cases, 90,662 controls; males = 13,020 cases, 89,660 controls) and Alzheimer's disease (females = 18,822 cases, 281,415 controls; males = 17,293 cases, 213,339 controls). As exposures, we focused on 932 immune system-related proteins with significant protein cis-quantitative trait loci (FDR cutoff < 0.01) from a large sex-combined plasma protein dataset (N = 33,477), for which corresponding genes were included in the Immunology Database and Analysis Portal gene list. We tested for a causal relationship between genetically predicted levels of each of these proteins and each neurodegenerative disease in sex-stratified and sex-combined data, followed by colocalization and estimation of sex-differential effects. We additionally performed exploratory analyses using sex-combined CSF protein cis-quantitative trait loci (N = 971) as exposures. We observed evidence for a sex-differential causal relationship between FCGR2A and Parkinson's disease, and between CD2AP, MAMDC2, PCDH17 or CSF3 and Alzheimer's disease. We validated significant results using two independent protein cis-quantitative trait loci datasets for those plasma proteins available. After performing sensitivity analyses, we validated the potential causal relationships of OMG on Parkinson's disease and of GRN, SERPINF2 and TREM2 on Alzheimer's disease. Mendelian randomization with CSF protein cis-quantitative trait loci showed a potential causal effect of ADGRE2, GPNMB and COLEC11 on Parkinson's disease and of CD33 on Alzheimer's disease, without evidence of sex-differential effects. Finally, we substantiated our findings of protein-disease pairs using triangulation, specifically reporting independent supporting evidence from the literature and drug-related databases. Overall, our results point to potential causal effects of genetically predicted levels of immune system-related plasma and CSF proteins in Alzheimer's disease and Parkinson's disease, some of which may be considered as potential candidates for drug development. - Source: PubMed
Publication date: 2025/12/24
Lona-Durazo FridaByrne Ross PPilon Marc-OlivierGreicius Michael DDubé Marie-PierreBelloy Michael EMcLaughlin Russell LGagliano Taliun Sarah A