Browse our anti-Polycystic Kidney Disease 1 (Autosomal Dominant) (PKD1) Antibodies

Human Polycystic Kidney Disease 1 (Autosomal Dominant) (PKD1) interaction partners

1. this study reports the 3.6-angstrom cryo-electron microscopy structure of truncated human PKD1-PKD2 (show PKD2 Antibodies) complex assembled in a 1:3 ratio.

2. VEGF (show VEGFA Antibodies)/PKD-1 signaling axis increases angiogenic and arteriogenic gene expression. These studies suggest that the axis may regulate arteriolar differentiation through changing microvascular endothelial cells gene expression.

3. PKD1 cytoplasmic C-terminal tail domain has a crucial role in renal prognosis in autosomal dominant polycystic disease.

4. PKD 1 mutation is associated with Autosomal dominant polycystic kidney disease.

5. Our results show that we have successfully generated a patient-specific iPS (show SLC27A4 Antibodies) cell line with a mutation in PKD1 for study of renal disease pathophysiology.

6. These data reveal a novel function for PKD1 as a regulator of focal adhesion dynamics and by identifying PIP5Klgamma as a novel PKD1 substrate provide mechanistic insight into this process.

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

8. The novel pathogenic variants c.3607C> T and c.11354G> C in PKD1 is very interesting since they may represent Italian clusters.

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

10. Study identified a novel heterozygous frameshift mutation in PKD1 gene segregating between affected and unaffected individuals suggesting an involvement in polycystic kidney disease (PKD (show PRKD1 Antibodies)).

Mouse (Murine) Polycystic Kidney Disease 1 (Autosomal Dominant) (PKD1) interaction partners

1. Results indicate that PKD1 inactivation underlies excitotoxicity-induced neuronal death and suggest that PKD1 inactivation may be critical for the accumulation of oxidation-induced neuronal damage during aging and in neurodegenerative disorders.

2. PKD1 contributes to the osteoblast differentiation and bone development via elevation of osteoblast markers through activation of STAT3 (show STAT3 Antibodies) and p38 MAPK (show MAPK14 Antibodies) signaling pathways.

3. PKD1 mediates the PKC effects on KV11.1 (show KCNV2 Antibodies) and we found that PKD (show PRKD1 Antibodies) targets S284 in the N-terminus of the channel.

4. PC1/3 (show PCSK1 Antibodies) deficiency was associated with increased expression of melanocortin receptors and PRCP (prolylcarboxypeptidase (show PRCP Antibodies), a catabolic enzyme for alpha-melanocyte stimulating hormone (alphaMSH (show POMC Antibodies))), and reduced adrenocorticotropic hormone secretion. We conclude that the obesity accompanying PCSK1 (show PCSK1 Antibodies) deficiency may not be primarily due to alphaMSH (show POMC Antibodies) deficiency.

5. Mutations in PKD1 is associated with autosomal dominant polycystic kidney disease.

6. critical functions of PC1 are regulated by its ability to sense cytosolic calcium levels via binding to calmodulin

7. cortactin (show CTTN Antibodies) binds to E-cadherin (show CDH1 Antibodies), and that a posttranslational modification of cortactin (show CTTN Antibodies), RhoA (show RHOA Antibodies)-induced phosphorylation by protein kinase D1 (PKD1; also known as PRKD1 (show PRKD1 Antibodies)) at S298, impairs adherens junction assembly and supports their dissolution.

8. Galpha12 (show GNA12 Antibodies) is required for the development of kidney cysts induced by Pkd1 mutation in mouse autosomal dominant polycystic kidney disease.

9. PAK-mediated phosphorylation of PKD1 at Ser203 triggers its membrane dissociation and subsequent entry into the nucleus, thereby regulating the phosphorylation of PKD1 nuclear targets, including class IIa histone deacetylases.

10. kd1 mutant mice have transcriptional profiles consistent with changes in lipid metabolism and distinct metabolite and complex lipid profiles in kidneys. .. cells lacking Pkd1 have an intrinsic fatty acid oxidation defect and that manipulation of lipid content of mouse chow modifies cystic disease.