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抗Human PKD2 抗体:
抗Mouse (Murine) PKD2 抗体:
抗Rat (Rattus) PKD2 抗体:
Human Polyclonal PKD2 Primary Antibody for ELISA, WB - ABIN4346790
Fencl, Janda, Bláhová, Hríbal, Stekrová, Puchmajerová, Seeman: Genotype-phenotype correlation in children with autosomal dominant polycystic kidney disease. in Pediatric nephrology (Berlin, Germany) 2009
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 (显示 PRKD1 抗体), while association of IVS4+62C>T was found insignificant.
the PKD1 (显示 PKD1 抗体)/PKD2 mutation status differed by ethnicity, and the PKD1 (显示 PKD1 抗体)/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 (显示 MLXIP 抗体)-106b-5p or downregulation of PKD2 expression can cause A549/DDP (显示 TIMM8A 抗体) cells to become considerably more sensitive to cisplatin. The results showed that miR (显示 MLXIP 抗体)-106b-5p enhanced the sensitivity of A549/DDP (显示 TIMM8A 抗体) 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 (显示 SNX3 抗体)-retromer complex regulates the surface expression and function of PC1 (显示 PCSK1 抗体) and PC2 (显示 KRT6B 抗体)
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 (显示 EPHB2 抗体) pathway may be caused by down-regulation of PC-1 (显示 PCSK1 抗体) and PC-2 (显示 KRT6B 抗体) 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 (显示 PKD1 抗体)-T, PKD1 (显示 PKD1 抗体)-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 (显示 KRT6B 抗体) Cterm to distinct aspects of PC2 (显示 KRT6B 抗体) 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 (显示 PKHD1 抗体) function in this model.
Pkd2(-/-) mice with homozygous PKD2(tg)-transgene alleles (Pkd2(-/-);PKD2(tg/tg (显示 CACNA1A 抗体))) showed significant further amelioration of the cystic severity compared to that in Pkd2(-/-) mice
Pkd1 (显示 PKD1 抗体) and Pkd2 have coordinate effects on osteoblast differentiation and opposite effects on adipogenesis, suggesting that Pkd1 (显示 PKD1 抗体) and Pkd2 signaling pathways can have independent effects on mesenchymal lineage commitment in bone
novel protein complex composed of Rabep1 (显示 RABEP1 抗体), GGA1 (显示 GGA1 抗体) and Arl3 is responsible for the sorting and targeting of the polycystin 1 (显示 PKD1 抗体) 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 (显示 PCSK1 抗体) trafficking and expression require GPS (显示 NBEAL2 抗体) cleavage and PC2 (显示 CBX4 抗体) 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 (显示 CA2 抗体)+)-dependent signaling pathways that stimulate ET-1 (显示 EDN1 抗体) 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 (显示 AGXT 抗体) 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 (显示 MAPK15 抗体) is a ciliary protein required for PKD-2 localization and male mating behavior in Caenorhabditis elegans
acts as a major calcium-release channel (显示 RYR1 抗体) 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 (显示 STAM 抗体)-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 (显示 PCSK1 抗体) 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 (显示 FUBP1 抗体) Binds the 3' Untranslated Region of PKD2 to inhibit PKD2 translation, regulating zebrafish disease phenotypes associated with PKD2 knockdown
TRPP2 and TRPV4 (显示 TRPV4 抗体) are mechanosensitive channels in the endocardium.Oscillatory flow modulates mechanosensitive klf2a expression through trpv4 (显示 TRPV4 抗体) 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 (显示 TRPV4 抗体) 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 (显示 CAMK2G 抗体) in pronephric cells and cilia, whereas constitutively active CaMK-II (显示 CAMK2G 抗体) restores pronephric duct formation in pkd2 morphants
Proper heart valve formation in zebrafish critically depends on protein kinase D2-histone deacetylase 5 (显示 HDAC5 抗体)-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 (显示 PRKCSH 抗体) functions as a chaperone-like molecule, which prevents endoplasmic reticulum-associated degradation of TRPP2.
atp-2 (显示 ATP2A2 抗体), 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 (显示 CA2 抗体)+) release from intracellular Ca(2 (显示 CA2 抗体)+) 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 (显示 TRPC3 抗体) or TRPC7 (显示 TRPM2 抗体) protein induce enhanced receptor-activated Ca(2 (显示 CA2 抗体)+) 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)