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This noticeable hot spot regions hold higher frequency (50%) of pathogenic / likely pathogenic genetic variants constituting single nucleotide variants than large deletion and insertion that actually represents only 41.08% of coding sequence of PKD2. Statistically significant association for IVS3-22AA genotype was observed with PKD (Montrer PRKD1 Protéines), while association of IVS4+62C>T was found insignificant.
the PKD1 (Montrer PKD1 Protéines)/PKD2 mutation status differed by ethnicity, and the PKD1 (Montrer PKD1 Protéines)/PKD2 genotype may affect the clinical phenotype of autosomal dominant polycystic kidney disease
The novel pathogenic variant in c.637C> T in PKD2 is very interesting since they may represent Italian clusters.
Upregulation of miR (Montrer MLXIP Protéines)-106b-5p or downregulation of PKD2 expression can cause A549/DDP (Montrer TIMM8A Protéines) cells to become considerably more sensitive to cisplatin. The results showed that miR (Montrer MLXIP Protéines)-106b-5p enhanced the sensitivity of A549/DDP (Montrer TIMM8A Protéines) cells to cisplatin by targeting the expression of PKD2.
investigated the interaction network of human PKD2 in the cytosol and in Golgi-enriched subcellular protein fractions
SNX3 (Montrer SNX3 Protéines)-retromer complex regulates the surface expression and function of PC1 (Montrer PCSK1 Protéines) and PC2 (Montrer KRT6B Protéines)
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 (Montrer EPHB2 Protéines) pathway may be caused by down-regulation of PC-1 (Montrer PCSK1 Protéines) and PC-2 (Montrer KRT6B Protéines) 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 (Montrer PKD1 Protéines)-T, PKD1 (Montrer PKD1 Protéines)-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 (Montrer KRT6B Protéines) Cterm to distinct aspects of PC2 (Montrer KRT6B Protéines) functions and regulation.
Pkhd1(Flox67HA) is a valid mouse model of autosomal recessive polycystic kidney disease to track Pkhd1-derived products containing the C-terminus. Significantly, exon 67 containing the nuclear localization signal and the polycystin-2 binding domain is not essential for Fibrocystin function in this model.
Pkd2(-/-) mice with homozygous PKD2(tg)-transgene alleles (Pkd2(-/-);PKD2(tg/tg (Montrer CACNA1A Protéines))) showed significant further amelioration of the cystic severity compared to that in Pkd2(-/-) mice
Pkd1 (Montrer PKD1 Protéines) and Pkd2 have coordinate effects on osteoblast differentiation and opposite effects on adipogenesis, suggesting that Pkd1 (Montrer PKD1 Protéines) and Pkd2 signaling pathways can have independent effects on mesenchymal lineage commitment in bone
novel protein complex composed of Rabep1, GGA1 (Montrer GGA1 Protéines) and Arl3 is responsible for the sorting and targeting of the polycystin 1 (Montrer PKD1 Protéines) 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 (Montrer PCSK1 Protéines) trafficking and expression require GPS cleavage and PC2 (Montrer CBX4 Protéines) interaction, respectively, and provide a framework for functional assays to categorize the effects of missense mutations in polycystins.
In inner medullary collecting duct, flow, via polycystin-2 and P2 receptors, engages Ca(2 (Montrer CA2 Protéines)+)-dependent signaling pathways that stimulate ET-1 (Montrer EDN1 Protéines) synthesis.
Pkd2(+/-) cardiomyocytes shift the beta adrenergic receptor pathway and have altered calcium handling, independent of desensitized calcium-contraction coupling.
Epithelial-specific disruption of Pkd2 disrupts male reproductive tract development.
AGT (Montrer AGXT Protéines) inhibition resulted in significant decreases in kidney size and cyst volume and an improvement in kidney function in mice with targeted mutation in Pkd2.
MAPK-15 (Montrer MAPK15 Protéines) is a ciliary protein required for PKD-2 localization and male mating behavior in Caenorhabditis elegans
acts as a major calcium-release channel (Montrer RYR1 Protéines) in the endoplasmic reticulum in cells where rapid calcium signaling is required, and is essential in those excitable cells for rapid responses to stimuli (polycystin-2)
These data reveal that the STAM (Montrer STAM Protéines)-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 (Montrer PCSK1 Protéines) 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
Results show that Far Upstream Element-Binding Protein 1 (Montrer FUBP1 Protéines) Binds the 3' Untranslated Region of PKD2 to inhibit PKD2 translation, regulating zebrafish disease phenotypes associated with PKD2 knockdown
TRPP2 and TRPV4 (Montrer TRPV4 Protéines) are mechanosensitive channels in the endocardium.Oscillatory flow modulates mechanosensitive klf2a expression through trpv4 (Montrer TRPV4 Protéines) and trpp2 during heart valve development.
Intraciliary calcium oscillations depend on Pkd2 and are left-biased at the left-right organizer in response to ciliary motility.
TRPP2 utilizes TRPV4 (Montrer TRPV4 Protéines) to form a mechano- and thermosensitive molecular sensor in the cilium.[TRPP2]
Isolated pkd2 mutant hearts displayed impaired intracellular calcium cycling and calcium alternans. These results indicate heart failure in the pkd2 mutants.
PKD2 suppression inactivates CaMK-II (Montrer CAMK2G Protéines) in pronephric cells and cilia, whereas constitutively active CaMK-II (Montrer CAMK2G Protéines) restores pronephric duct formation in pkd2 morphants
Proper heart valve formation in zebrafish critically depends on protein kinase D2-histone deacetylase 5 (Montrer HDAC5 Protéines)-Kruppel-like factor signaling.
Pkd1a/b and pkd2 interact to regulate extracellular matrix secretion or assembly, and that altered matrix integrity may be a primary defect underlying autosomal dominant polycystic kidney disease tissue pathologies.
PRKCSH (Montrer PRKCSH Protéines) functions as a chaperone-like molecule, which prevents endoplasmic reticulum-associated degradation of TRPP2.
atp-2 (Montrer ATP2A2 Protéines), lov-1, and pkd2 act in the same molecular pathway.
Data indicate that the TRPP2 protein, a member of the transient receptor potential (TRP) channels protein superfamily, is encoded by the PKD2 gene, and TRPP2 mediates Ca(2 (Montrer CA2 Protéines)+) release from intracellular Ca(2 (Montrer CA2 Protéines)+) stores.
The flow-induced calcium signaling depends on the ciliary polycystin-2 calcium channel.
cloning and characterization of the PKD2 cDNA showing that the full-length gene (3370 bases) is highly expressed in kidney, with minimal expression in the liver
EGF may reduce the threshold of PKD2 activation by mechanical and other stimuli by releasing it from PIP(2)-mediated inhibition.
heteromeric cation channels comprised of the TRPP2 mutant and the TRPC3 (Montrer TRPC3 Protéines) or TRPC7 (Montrer TRPM2 Protéines) protein induce enhanced receptor-activated Ca(2 (Montrer CA2 Protéines)+) influx that may lead to dysregulated cell growth in ADPKD
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.
, autosomal dominant polycystic kidney disease type II protein
, transient receptor potential cation channel, subfamily P, member 2
, polycystic kidney disease 2 protein homolog
, polycystin 2
, polycystic kidney disease 2 homolog
, polycystic kidney disease 2 membrane protein
, cation channel
, polycystic kidney disease 2 (autosomal dominant) L homeolog
, Curly up
, Polycystic kidney disease 2 protein homolog
, Transient receptor potential cation channel subfamily P member 2
, curly up
, transient receptor potential cation channel subfamily P member 2
, polycystic kidney disease 2 (autosomal dominant)