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Our studies demonstrate that PKD1 (show PKD1 Proteins)/2 is a key regulator of MVB maturation and exosome secretion, and constitutes a mediator of the DGK alpha (show DGKA Proteins) effect on MVB secretory traffic.
Pkd2(-/-) mice with homozygous PKD2(tg)-transgene alleles (Pkd2(-/-);PKD2(tg/tg (show CACNA1A Proteins))) showed significant further amelioration of the cystic severity compared to that in Pkd2(-/-) mice
Results reveal that whereas protein kinase D1 (show PRKD1 Proteins) and protein kinase D2 are essential for neuronal polarity, there exists a functional redundancy between the two proteins.
Pkd1 (show PKD1 Proteins) and Pkd2 have coordinate effects on osteoblast differentiation and opposite effects on adipogenesis, suggesting that Pkd1 (show PKD1 Proteins) and Pkd2 signaling pathways can have independent effects on mesenchymal lineage commitment in bone
novel protein complex composed of Rabep1, GGA1 (show GGA1 Proteins) and Arl3 is responsible for the sorting and targeting of the polycystin 1 (show PKD1 Proteins) andpolycystin 2 to the cilium.
PKD2 regulates directly and indirectly about 5% of the cytotoxic T-cell phosphoproteome.
The results of this study demonstrate that PC1 (show PCSK1 Proteins) trafficking and expression require GPS cleavage and PC2 (show CBX4 Proteins) interaction, respectively, and provide a framework for functional assays to categorize the effects of missense mutations in polycystins.
PKD2 acted as an amplification checkpoint for antigen-stimulated digital cytokine responses and translated the differential strength of TCR signaling to determine the number of naive CD8 (show CD8A Proteins)(+) T cells that became effector cells.
In inner medullary collecting duct, flow, via polycystin-2 and P2 receptors, engages Ca(2 (show CA2 Proteins)+)-dependent signaling pathways that stimulate ET-1 (show EDN1 Proteins) synthesis.
Pkd2(+/-) cardiomyocytes shift the beta adrenergic receptor pathway and have altered calcium handling, independent of desensitized calcium-contraction coupling.
SNX3 (show SNX3 Proteins)-retromer complex regulates the surface expression and function of PC1 (show PCSK1 Proteins) and PC2 (show KRT6B Proteins)
We aimed to revisit PKD2 prevalence, clinical presentation, mutation spectrum, and prognosis through the Genkyst cohort. Patients with PKD2-related dominant polycystic kidney disease typically present with mild disease
Hyperactivation of the ERK (show EPHB2 Proteins) pathway may be caused by down-regulation of PC-1 (show PCSK1 Proteins) and PC-2 (show KRT6B Proteins) in lymphatic malformations, contributing to increased proliferation of lymphatic endothelial cells.
Annualized median liver growth rates were 1.68, 1.5 and 1.24% for PKD1 (show PKD1 Proteins)-T, PKD1 (show PKD1 Proteins)-NT and PKD2 mutations, respectively (P = 0.49), and remained unaffected by the ADPKD genotype when adjusted for age, gender and baseline HtLV.
Here, we review previous studies that connect the molecular properties of the domains of PC2 (show KRT6B Proteins) Cterm to distinct aspects of PC2 (show KRT6B Proteins) functions and regulation.
Data show that in 82 (87.2%) of the patients, pathogenic mutations were detected in PKD1 (show PKD1 Proteins) (79.0%-92.5%), whereas in 12 (12.8%) patients pathogenic mutations were detected in PKD2 (7.5%-21.0%).
Two cryo-EM structures of distinct channel states of full-length human PC2 (show KRT6B Proteins) in complex with lipids and cations.
The structure of human PC2 (show KRT6B Proteins) in a closed conformation, solved by electron cryomicroscopy at 4.2-A resolution.
SNPs in and near PKD2 showed significant evidence of association in individual samples of black adults (rs17013735, P-value=0.0009) and white adults (rs11938025; P-value=0.0005; rs2725270, P-value=0.003).
Pancreatic cysts were more prevalent in patients with ADPKD with PKD2 mutation than in control subjects or patients with PKD1 (show PKD1 Proteins) mutation.
These data reveal that the STAM (show STAM Proteins)-Hrs complex, which down-regulates ligand-activated growth factor receptors from the cell surface of yeast and mammalian cells, also regulates the localization and signaling of a ciliary PC1 (show PCSK1 Proteins) receptor-TRPP2 complex.
Results demonstrate that somatodendritic and ciliary targeting of PKD-2 requires the transmembrane region of PKD-2 and that the PKD-2 cytosolic termini regulate subcellular distribution and function.
11 mutants found with defects in the ciliary localization (cil) of C. elegans PKD-2, a transient receptor potential polycystin (TRPP) channel
This gene encodes a member of the polycystin protein family. The encoded protein is a multi-pass membrane protein that functions as a calcium permeable cation channel, and is involved in calcium transport and calcium signaling in renal epithelial cells. This protein interacts with polycystin 1, and they may be partners in a common signaling cascade involved in tubular morphogenesis. Mutations in this gene are associated with autosomal dominant polycystic kidney disease type 2.
polycystic kidney disease 2 protein homolog
, polycystin 2
, autosomal dominant polycystic kidney disease type II protein
, transient receptor potential cation channel, subfamily P, member 2
, polycystic kidney disease 2 homolog
, polycystic kidney disease 2 membrane protein
, serine/threonine-protein kinase D2