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Human Polyclonal PKD1 Primary Antibody for IF (p), IHC (p) - ABIN678083
Chiou, Sang, Cheng, Ho, Wang, Pan: Peracetylated (-)-epigallocatechin-3-gallate (AcEGCG) potently prevents skin carcinogenesis by suppressing the PKD1-dependent signaling pathway in CD34+ skin stem cells and skin tumors. in Carcinogenesis 2013
Show all 4 Pubmed References
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.
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.
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
The novel pathogenic variants c.3607C> T and c.11354G> C in PKD1 is very interesting since they may represent Italian clusters.
SNX3 (show SNX3 Antibodies)-retromer complex regulates the surface expression and function of PC1 (show PCSK1 Antibodies) and PC2 (show KRT6B Antibodies)
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)).
we report for the first time that PKD1 was tightly regulated by androgen at the transcriptional level in prostate cancer cells and was a novel androgen-repressed gene. Further analysis identified FRS2 (show FRS2 Antibodies) as a novel mediator of androgen-induced PKD1 repression.
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.
A novel mutation of the PKD1 gene has been identified with autosomal dominant polycystic kidney disease in an affected Chinese family.
Annualized median liver growth rates were 1.68, 1.5 and 1.24% for PKD1-T, PKD1-NT and PKD2 (show PKD2 Antibodies) mutations, respectively (P = 0.49), and remained unaffected by the ADPKD genotype when adjusted for age, gender and baseline HtLV.
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.
Mutations in PKD1 is associated with autosomal dominant polycystic kidney disease.
critical functions of PC1 are regulated by its ability to sense cytosolic calcium levels via binding to calmodulin
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.
Galpha12 (show GNA12 Antibodies) is required for the development of kidney cysts induced by Pkd1 mutation in mouse autosomal dominant polycystic kidney disease.
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.
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.
Polycystin 1 was overexpressed in M1 cells, no increase in any of these parameters was detected
detected a marked increase in the localization of beta-catenin (show CTNNB1 Antibodies) in the nucleus of crypt epithelial cells in the ileum of PKD1
PKD1 phosphorylates AMPKalpha2 (show PRKAA2 Antibodies) at Ser485/491, thus diminishing AMPK (show PRKAA1 Antibodies) activity.
This gene encodes a member of the polycystin protein family. The encoded glycoprotein contains a large N-terminal extracellular region, multiple transmembrane domains and a cytoplasmic C-tail. It is an integral membrane protein that functions as a regulator of calcium permeable cation channels and intracellular calcium homoeostasis. It is also involved in cell-cell/matrix interactions and may modulate G-protein-coupled signal-transduction pathways. It plays a role in renal tubular development, and mutations in this gene cause autosomal dominant polycystic kidney disease type 1 (ADPKD1). ADPKD1 is characterized by the growth of fluid-filled cysts that replace normal renal tissue and result in end-stage renal failure. Splice variants encoding different isoforms have been noted for this gene. Also, six pseudogenes, closely linked in a known duplicated region on chromosome 16p, have been described.
autosomal dominant polycystic kidney disease 1 protein
, polycystic kidney disease-associated protein
, polycystin 1
, transient receptor potential cation channel, subfamily P, member 1
, autosomal dominant polycystic kidney disease 1 protein homolog
, polycystic kidney disease 1 homolog; polycystin-1
, polycystic kidney disease 1 (autosomal dominant)
, polycystic kidney disease protein 1