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PKP3 overexpression increases the stability of other desmosomal proteins independently of the increase in DSC2 levels and regulates desmosome formation and stability by a multimodal mechanism affecting transcription, protein stability and cell border localization of desmosomal proteins.
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Children with low 25-hydroxyvitamin D and TMEM16J rs7111432-AA or PKP3 rs10902158-GG polymorphisms were at increased risk for tuberculosis or death.
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Data suggest juxtamembrane regions/domains of desmocollin-2 (DSC2), plakophilin 2 (PKP2), and plakophilin 3 (PKP3) are involved in desmosome formation in epithelial cells; DSC2 participates in desmosome formation in absence of desmoglein 2 (DSG2).
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The results suggest that MMP7 over-expression may be one of the mechanisms by which PKP3 loss leads to increased cell invasion and tumor formation.
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reactive oxygen species (ROS) trigger the c-Src kinase-mediated tyrosine (Tyr)-195 phosphorylation of PKP3.
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These findings reveal Pkp3 as a coordinator of desmosome and adherens junction assembly and maturation through its functional association with Rap1.
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cytoplasmic PKP1/3 are components of mRNA ribonucleoprotein particles and act as posttranscriptional regulators of gene expression.
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Pemphigus vulgaris autoimmune globulin induces Src-dependent tyrosine-phosphorylation of PKP3 and its detachment from DSG3.
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The study describes a new protein variant of the human PKP3 gene, namely PKP3b, which differs from the published PKP3a only at the amino-terminus by the splicing in of the newly identified exon 1b.
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stratifin plays a role in regulating plakophilin-3 incorporation into the desmosomal plaque by forming a plakophilin-3 stratifin complex in the cytosol and thereby affecting desmosome dynamics in squamous epithelial cells.
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In breast cancer, compared with normal tissue, PKP1 and PKP2 expressions were indifferent (P > 0.05), but PKP3 expression was significantly increased
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Plakophilin3 loss leads to an increase in PRL3 levels promoting K8 dephosphorylation, which is required for transformation and metastasis.
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These results demonstrate a strong association of single-nucleotide polymorphisms in the PKP3-SIGIRR-TMEM16J gene region and tuberculosis in discovery and validation cohorts.
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plakoglobin and E-cadherin recruit plakophilin3 to the cell border to initiate desmosome formation
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loss of PKP3 expression during gastric adenocarcinoma progression may indicate an invasive phenotype.
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both loss of PKP1 and up-regulation of PKP3 expression are biologically important events in prostate cancer and are associated with a more aggressive phenotype
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PKP3 mRNA can be used as a marker of subclinical disease in gastrointestinal cancer and thus holds potential clinical relevance as a predictor for disease outcome
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PKP3, whose desmosomal expression and protein interactions are broader than those of PKP1 and -2, is a unique multiprotein binding element in many epithelial desmosomes.
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Cytoplasmic PKP3 is constitutively associated with RNA-binding proteins and indicate an involvement in processes of translation and RNA metabolism.
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The transcriptional repression of PKP3 by ZEB1 contributes to ZEB1-mediated disintegration of intercellular adhesion and epithelial to mesenchymal transition.
