Ask about this productRelated genes to: PKP3 antibody
- Gene:
- PKP3 NIH gene
- Name:
- plakophilin 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-14
- Date modifiied:
- 2016-10-05
Related products to: PKP3 antibody
Related articles to: PKP3 antibody
- Estrogen receptor-positive breast cancer progression involves extensive cellular remodeling, yet the contribution of RNA-binding proteins to this process remains incompletely defined. Here, we constructed a single-cell transcriptomic atlas of 198,286 cells from 39 samples spanning normal tissue, primary tumors, and metastatic lesions. We identified stage-specific transcriptional and post-transcriptional reprogramming across different cell types. Several RBPs, including , , and , were progressively upregulated during malignant progression and associated with cytoskeletal remodeling, extracellular matrix interactions, and stress adaptation. Cell-cell communication analyses revealed metastasis-associated signaling programs involving TIMP1-MMP1 and TGFB1-COL7A1/MMP1, which were spatially enriched at tumor margins and invasive fronts. Functional perturbation experiments in ER breast cancer cells showed that TGF-β stimulation enhanced invasive behavior, whereas knockdown of MMP1 or COL7A1 attenuated epithelial-mesenchymal transition (EMT) marker expression and invasion. Together, our study delineates RBP-associated regulatory programs linking cellular state transitions to invasive signaling in ER breast cancer. - Source: PubMed
Publication date: 2026/05/28
Dong MingjieLi XinyuYang SongyuLi ShujuanLiu ZhengzhengPeng ChuoLi RongyaoLiang WeixinLi XiaBai Jing - Psoriasis is a chronic inflammatory skin disease that is characterized by abnormal keratinocyte proliferation and differentiation. This study aimed to explore potential regulatory mechanisms and key genes related to autophagy in the pathogenesis of psoriasis. - Source: PubMed
Publication date: 2026/05/04
Zhou YingChen BingjieChen JunmingFang LingluZhang LitianDou ShuhuiLi FangguHuang JingtongChen Chongyang - The specific role and mechanism of SHP2 in polycystic ovary syndrome (PCOS) remain unclear. This study aimed to evaluate the therapeutic potential of SHP2 and elucidate the signaling pathways through which it modulates granulosa cell fate in PCOS. A PCOS rat model was established via letrozole administration. Rats were divided into three groups ( = 6 each): Sham, Model, and SHP2-overexpressing (SHP2-OE). The SHP2-OE group received lentiviral injection prior to modeling. Ovarian histopathology was assessed using Hematoxylin and Eosin (HE) staining. Serum sex hormones were measured by ELISA. Western blotting was used to detect the protein expression of the IRE1α/XBP1/NLRP3 and ZEB1/PKP3 signaling pathways in granulosa cells after different stimulations. Flow cytometry was used to detect granulosa cell apoptosis. In vivo, SHP2 overexpression significantly ameliorated PCOS-induced ovarian damage, characterized by reduced ovarian weight, fewer cystic follicles, and increased corpora lutea. Hormonally, SHP2-OE decreased levels of estradiol, testosterone, and luteinizing hormone, while increasing follicle-stimulating hormone. Mechanistically, in vitro analysis revealed that testosterone treatment inhibited SHP2 phosphorylation and downregulated PKP3, nuclear E2F1, and CyclinB1. In addition to addition, testosterone activated the IRE1α/XBP1/NLRP3 and ZEB1 pathways, upregulating p-IRE1α, XBP-1s, p-SP1, ZEB1, NLRP3, and GSDMD, thereby promoting granulosa cell apoptosis and pyroptosis. SHP2 alleviates PCOS-related reproductive endocrine abnormalities and ovarian pathological changes by regulating the IRE1α/XBP1/NLRP3 and ZEB1/PKP3 signaling pathways, thereby influencing granulosa cell pyroptosis and proliferation. - Source: PubMed
Publication date: 2026/03/21
Wang DongXueWang JingNaYang BoZhao XinFeng XiaoyeDing QiWu YuanyuanBao LiLi - High-grade serous ovarian cancer (HGSOC) is the second most lethal gynecologic malignancy, often diagnosed at a late stage due to the lack of reliable early detection strategies. Currently, there are no specific diagnostic or prognostic biomarkers for ovarian cancer (OC). Thus, there is a great need for novel validated biomarkers for OC diagnosis. - Source: PubMed
Publication date: 2026/01/27
Vaicekauskaitė IevaJuodakis JuliusKazlauskaitė PaulinaČiurlienė RūtaSmailytė GiedrėLazutka Juozas RimantasSabaliauskaitė Rasa - In epithelia, the desmosome is a cell-cell adhesive junction that anchors keratin filaments, thereby providing tissue integrity and mechanical resistance. Compared with considerable study on the desmosome in stratified epithelia, the mechanism of desmosome assembly and its functional roles remain incompletely understood in single-layered (simple) epithelia. Here we show that not only E-cadherin (E-cad) but also cadherin-6 (Cdh6) participates in recruitment of plakoglobin (Pg) from E-cad-containing cytoplasmic vesicles to cell-cell junctional regions during Ca-induced desmosome formation in simple epithelial MDCK cells. Subsequently, Pg cooperates with its related proteins plakophilin-2 (PKP2) and plakophilin-3 (PKP3), being recruited independently of E-cad/Cdh6, in junctional localization of the desmosomal cadherins desmoglein-2 (Dsg2) and desmocollin-2 (Dsc2) and the keratin-anchoring protein desmoplakin (DP), leading to functional keratin filament network formation. We also demonstrate that DP contributes to establishment of apical-basal cell polarity during cystogenesis in 3D culture of MDCK cells; depletion of DP results in formation of aberrant cysts containing cells with inverted polarity. Furthermore, the morphology of the nucleus in MDCK cells appears to be regulated by proper desmosome assembly and subsequent keratin network formation, because depletion of DP as well as that of E-cad/Cdh6, Pg, or PKP2/3 results in an irregular nuclear shape. - Source: PubMed
Nita TobuhiroHayase JunyaKohda AkiraShiose AkiraSumimoto HidekiKamakura Sachiko