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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
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Our results show that we have successfully generated a patient-specific iPS (显示 SLC27A4 抗体) 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 (显示 PKD2 抗体) mutation status differed by ethnicity, and the PKD1/PKD2 (显示 PKD2 抗体) 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 (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)
Study identified a novel heterozygous frameshift mutation in PKD1 gene segregating between affected and unaffected individuals suggesting an involvement in polycystic kidney disease (PKD (显示 PRKD1 抗体)).
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 (显示 FRS2 抗体) as a novel mediator of androgen-induced PKD1 repression.
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.
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 (显示 PKD2 抗体) mutations, respectively (P = 0.49), and remained unaffected by the ADPKD genotype when adjusted for age, gender and baseline HtLV.
PC1/3 (显示 PCSK1 抗体) deficiency was associated with increased expression of melanocortin receptors and PRCP (prolylcarboxypeptidase (显示 PRCP 抗体), a catabolic enzyme for alpha-melanocyte stimulating hormone (alphaMSH (显示 POMC 抗体))), and reduced adrenocorticotropic hormone secretion. We conclude that the obesity accompanying PCSK1 (显示 PCSK1 抗体) deficiency may not be primarily due to alphaMSH (显示 POMC 抗体) 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 (显示 CTTN 抗体) binds to E-cadherin (显示 CDH1 抗体), and that a posttranslational modification of cortactin (显示 CTTN 抗体), RhoA (显示 RHOA 抗体)-induced phosphorylation by protein kinase D1 (PKD1; also known as PRKD1 (显示 PRKD1 抗体)) at S298, impairs adherens junction assembly and supports their dissolution.
Galpha12 (显示 GNA12 抗体) 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 (显示 CTNNB1 抗体) in the nucleus of crypt epithelial cells in the ileum of PKD1
PKD1 phosphorylates AMPKalpha2 (显示 PRKAA2 抗体) at Ser485/491, thus diminishing AMPK (显示 PRKAA1 抗体) 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