Browse our anti-PKD2 (PKD2) Antibodies

Human Polycystic Kidney Disease 2 (Autosomal Dominant) (PKD2) interaction partners

1. 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 (show PRKD1 Antibodies), while association of IVS4+62C>T was found insignificant.

2. the PKD1 (show PKD1 Antibodies)/PKD2 mutation status differed by ethnicity, and the PKD1 (show PKD1 Antibodies)/PKD2 genotype may affect the clinical phenotype of autosomal dominant polycystic kidney disease

3. The novel pathogenic variant in c.637C> T in PKD2 is very interesting since they may represent Italian clusters.

4. Upregulation of miR (show MLXIP Antibodies)-106b-5p or downregulation of PKD2 expression can cause A549/DDP (show TIMM8A Antibodies) cells to become considerably more sensitive to cisplatin. The results showed that miR (show MLXIP Antibodies)-106b-5p enhanced the sensitivity of A549/DDP (show TIMM8A Antibodies) cells to cisplatin by targeting the expression of PKD2.

5. investigated the interaction network of human PKD2 in the cytosol and in Golgi-enriched subcellular protein fractions

6. SNX3 (show SNX3 Antibodies)-retromer complex regulates the surface expression and function of PC1 (show PCSK1 Antibodies) and PC2 (show KRT6B Antibodies)

7. 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

8. Hyperactivation of the ERK (show EPHB2 Antibodies) pathway may be caused by down-regulation of PC-1 (show PCSK1 Antibodies) and PC-2 (show KRT6B Antibodies) in lymphatic malformations, contributing to increased proliferation of lymphatic endothelial cells.

9. Annualized median liver growth rates were 1.68, 1.5 and 1.24% for PKD1 (show PKD1 Antibodies)-T, PKD1 (show PKD1 Antibodies)-NT and PKD2 mutations, respectively (P = 0.49), and remained unaffected by the ADPKD genotype when adjusted for age, gender and baseline HtLV.

10. Here, we review previous studies that connect the molecular properties of the domains of PC2 (show KRT6B Antibodies) Cterm to distinct aspects of PC2 (show KRT6B Antibodies) functions and regulation.

Mouse (Murine) Polycystic Kidney Disease 2 (Autosomal Dominant) (PKD2) interaction partners

1. 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 (show PKHD1 Antibodies) function in this model.

2. Pkd2(-/-) mice with homozygous PKD2(tg)-transgene alleles (Pkd2(-/-);PKD2(tg/tg (show CACNA1A Antibodies))) showed significant further amelioration of the cystic severity compared to that in Pkd2(-/-) mice

3. Pkd1 (show PKD1 Antibodies) and Pkd2 have coordinate effects on osteoblast differentiation and opposite effects on adipogenesis, suggesting that Pkd1 (show PKD1 Antibodies) and Pkd2 signaling pathways can have independent effects on mesenchymal lineage commitment in bone

4. novel protein complex composed of Rabep1 (show RABEP1 Antibodies), GGA1 (show GGA1 Antibodies) and Arl3 is responsible for the sorting and targeting of the polycystin 1 (show PKD1 Antibodies) andpolycystin 2 to the cilium.

5. PKD2 regulates directly and indirectly about 5% of the cytotoxic T-cell phosphoproteome.

6. The results of this study demonstrate that PC1 (show PCSK1 Antibodies) trafficking and expression require GPS (show NBEAL2 Antibodies) cleavage and PC2 (show CBX4 Antibodies) interaction, respectively, and provide a framework for functional assays to categorize the effects of missense mutations in polycystins.

7. In inner medullary collecting duct, flow, via polycystin-2 and P2 receptors, engages Ca(2 (show CA2 Antibodies)+)-dependent signaling pathways that stimulate ET-1 (show EDN1 Antibodies) synthesis.

8. Pkd2(+/-) cardiomyocytes shift the beta adrenergic receptor pathway and have altered calcium handling, independent of desensitized calcium-contraction coupling.

9. Epithelial-specific disruption of Pkd2 disrupts male reproductive tract development.

10. AGT (show AGXT Antibodies) inhibition resulted in significant decreases in kidney size and cyst volume and an improvement in kidney function in mice with targeted mutation in Pkd2.

Caenorhabditis elegans (C. elegans) Polycystic Kidney Disease 2 (Autosomal Dominant) (PKD2) interaction partners

1. MAPK-15 (show MAPK15 Antibodies) is a ciliary protein required for PKD-2 localization and male mating behavior in Caenorhabditis elegans

2. acts as a major calcium-release channel (show RYR1 Antibodies) 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)

3. These data reveal that the STAM (show STAM Antibodies)-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 Antibodies) receptor-TRPP2 complex.

4. 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.

5. 11 mutants found with defects in the ciliary localization (cil) of C. elegans PKD-2, a transient receptor potential polycystin (TRPP) channel

Zebrafish Polycystic Kidney Disease 2 (Autosomal Dominant) (PKD2) interaction partners

1. Results show that Far Upstream Element-Binding Protein 1 (show FUBP1 Antibodies) Binds the 3' Untranslated Region of PKD2 to inhibit PKD2 translation, regulating zebrafish disease phenotypes associated with PKD2 knockdown

2. TRPP2 and TRPV4 (show TRPV4 Antibodies) are mechanosensitive channels in the endocardium.Oscillatory flow modulates mechanosensitive klf2a expression through trpv4 (show TRPV4 Antibodies) and trpp2 during heart valve development.

3. Intraciliary calcium oscillations depend on Pkd2 and are left-biased at the left-right organizer in response to ciliary motility.

4. TRPP2 utilizes TRPV4 (show TRPV4 Antibodies) to form a mechano- and thermosensitive molecular sensor in the cilium.[TRPP2]

5. Isolated pkd2 mutant hearts displayed impaired intracellular calcium cycling and calcium alternans. These results indicate heart failure in the pkd2 mutants.

6. PKD2 suppression inactivates CaMK-II (show CAMK2G Antibodies) in pronephric cells and cilia, whereas constitutively active CaMK-II (show CAMK2G Antibodies) restores pronephric duct formation in pkd2 morphants

7. Proper heart valve formation in zebrafish critically depends on protein kinase D2-histone deacetylase 5 (show HDAC5 Antibodies)-Kruppel-like factor signaling.

8. 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.

9. PRKCSH (show PRKCSH Antibodies) functions as a chaperone-like molecule, which prevents endoplasmic reticulum-associated degradation of TRPP2.

10. atp-2 (show ATP2A2 Antibodies), lov-1, and pkd2 act in the same molecular pathway.

Guinea Pig Polycystic Kidney Disease 2 (Autosomal Dominant) (PKD2) interaction partners

1. 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 (show CA2 Antibodies)+) release from intracellular Ca(2 (show CA2 Antibodies)+) stores.

Pig (Porcine) Polycystic Kidney Disease 2 (Autosomal Dominant) (PKD2) interaction partners

1. The flow-induced calcium signaling depends on the ciliary polycystin-2 calcium channel.

2. 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

3. EGF may reduce the threshold of PKD2 activation by mechanical and other stimuli by releasing it from PIP(2)-mediated inhibition.

4. heteromeric cation channels comprised of the TRPP2 mutant and the TRPC3 (show TRPC3 Antibodies) or TRPC7 (show TRPM2 Antibodies) protein induce enhanced receptor-activated Ca(2 (show CA2 Antibodies)+) influx that may lead to dysregulated cell growth in ADPKD