Ask about this productRelated genes to: PRICKLE3 antibody
- Gene:
- PRICKLE3 NIH gene
- Name:
- prickle planar cell polarity protein 3
- Previous symbol:
- LMO6
- Synonyms:
- -
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-21
- Date modifiied:
- 2016-01-15
Related products to: PRICKLE3 antibody
Related articles to: PRICKLE3 antibody
- Oligoasthenoteratozoospermia (OAT) is a prevalent phenotype among infertile males, yet its underlying genetic etiology remains largely undefined. In this study, we found Spem2 deficiency did not affect the development of spermatogenic cells or the eventual generation of elongated spermatids within the testis, but affected the normal formation of residual bodies during the late stage of spermiation, which led to incomplete cytoplasmic removal of spermatids, abnormal sperm release and caused OAT. Affected sperm exhibited severely bent heads, cytoplasmic remnants encasing the head, and multiple sperm gathered. We further found SPEM2 may be involved in maintaining spermiation and cell polarity through interactions with cell polar molecules VANGL2, PRICKLE3 and DVL3. In vitro experiments showed that the transmembrane region of SPEM2 was its key functional domain and the binding domain for interactions between SPEM2 and VANGL2. Importantly, Spem2-deficient sperm enabled successful fertilization via ICSI. Three novel SPEM2 heterozygous pathogenic variants were identified in four OAT patients by the whole-exome sequencing. Our findings revealed key roles of SPEM2 in spermiation, explored the potential pathogenesis of male infertility caused by SPEM2 deficiency, and provided essential information for genetic and reproductive counseling for such patients. - Source: PubMed
Publication date: 2026/04/24
Li YongLu WenqingMeng LanlanTan ChenXu CaolingWang TiantianYuan YuweiYang RuiXie ChunboWang WeiliTu ChaofengHe Wen-BinLu Guang-XiuLin GeHu LiangZhang Qian-JunDu JuanBao JianqiangTan Yue-Qiu - The PRICKLE proteins (PRICKLE1-PRICKLE4) play essential roles in the WNT/planar cell polarity (WNT/PCP) pathway in vertebrates. This signaling system governs cell polarity, tissue architecture, and coordinated cell movements, yet the specific roles and molecular mechanisms of individual PRICKLE members within this pathway are poorly understood. Here, we identify PRICKLE3 as a previously unrecognized, central regulator of WNT/PCP signaling in human cells, Xenopus laevis and zebrafish (Danio rerio) embryos. Using enhanced proximity biotinylation (miniTurboID) combined with mass spectrometry, we found PRICKLE3 enriched at the plasma membrane, where it associates with core WNT/PCP proteins, including VANGL1 and VANGL2. Through immunoblotting, live imaging and functional assays, we further demonstrated that PRICKLE3 selectively enhances VANGL1/2 stability by protecting them from Casein kinase 1ε (CK1ε)-mediated phosphorylation. Mechanistically, PRICKLE3 modulates an interaction network involving VANGL1/2, CK1ε, and the ubiquitin ligase RNF43, thereby increasing VANGL stabilization and accumulation at the plasma membrane. These effects were unique to PRICKLE3, as PRICKLE1 showed no comparable activity. Together, our findings reveal a PRICKLE3-specific mechanism that couples CK1ε inhibition with RNF43 suppression to stabilize VANGL complexes. We also provide a comprehensive interactome and molecular tools to support further functional dissection of the PRICKLE family in development and disease. - Source: PubMed
Publication date: 2025/12/27
Radaszkiewicz Katarzyna ARadaszkiewicz Tomasz WKolářová PavlaPaclíková PetraGömöryová KristínaNovotná ŠárkaMaia Lorena AgostiniČíhalová TerezaLe YaoBárta TomášHanáková KateřinaHýsková AnnaTripsianes KonstantinosZdráhal ZbyněkWinkler ChristophHarnoš Jakub - Prickle planar cell polarity protein 3 (PRICKLE3) is involved in tumor malignant progression. However, little information is available regarding its detailed mechanism in non-small cell lung cancer (NSCLC). The clinicopathological significance of PRICKLE3 in NSCLC specimens was assessed. PRICKLE3-overexpression and PRICKLE3-knockout NSCLC cells were generated in vivo and in vitro. The interaction among PRICKLE3, ubiquitin-specific peptidase 9, X-chromosome (USP9X) and dishevelled2 (DVL2) in NSCLC cells was identified. We found that PRICKLE3 overexpression was correlated with advanced TNM stage, lymphatic metastasis, and poor prognosis in NSCLC patients. PRICKLE3 knockdown inhibited the viability, colony formation, and invasiveness in A549 and H1299 cells, and its overexpression promoted the viability, colony formation, and invasiveness in HBE, H460, and LK2 cells. PRICKLE3 promoted NSCLC growth in vivo. PRICKLE3-DVL2 interaction enhanced the β-catenin phosphorylation at serine 675 for β-catenin nuclear translocation. Furthermore, PRICKLE3 interacted with USP9X to inhibit the DVL2 ubiquitination for the DVL2 stability and the activation of canonical WNT signaling. Overall, we demonstrate a novel signal transduction pathway where PRICKLE3 interacts with USP9X and DVL2 to enhance the DVL2 deubiquitination mediated by USP9X for stabilizing DVL2 expression and activate the canonical WNT signaling for promoting the NSCLC progression. - Source: PubMed
Publication date: 2025/09/19
Yang MengdiLu YudieZheng JingrongZhao XinranWu GuangpingWang EnhuaZhao Huanyu - Amelogenesis imperfecta (AI) encompasses a group of conditions characterized by abnormalities in the development or function of tooth enamel. Clinical manifestations include different forms and degrees of enamel frailty, associated with sensitivity, tooth fractures, stains, abnormal tooth morphology, missing teeth, etc. AI is genetically heterogeneous, with over 70 genes associated with autosomal dominant, autosomal recessive, X-linked, and oligogenic inheritance. - Source: PubMed
Publication date: 2025/09/01
Lanza Célia Regina MoreiraRodrigues Artur MeloMascarenhas Iasmin Fonseca TolentinoSouza Talita Roberta Ferreira deReis Matheus OliveiraAvelar Felipe MorandoCarvalho Maria Raquel SantosAzevedo Vasco Ariston Carvalho deBarh Debmalya - Chemoresistance constitutes a prevalent factor that significantly impacts thesurvival of patients undergoing treatment for smal-cell lung cancer (SCLC). Chemotherapy resistance in SCLC patients is generally classified as primary or acquired resistance, each governedby distinct mechanisms that remain inadequately researched. - Source: PubMed
Publication date: 2024/06/18
Yang FangFan JinhuaYang RunxiangCun Yupeng