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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 study has identified PKD1 as a frequently downregulated gene in HNSCC, and functionally, under certain cellular context, may play a role in GRP/bombesin-induced oncogenesis in HNSCC.
Data found that MTA1 is a PKD1-interacting substrate, and that PKD1 phosphorylates MTA1, supports its nucleus-to-cytoplasmic redistribution and utilizes its N-terminal and kinase domains to effectively inhibit the levels of MTA1 via polyubiquitin-dependent proteosomal degradation.
Two novel mutations, c.6953_6977del and c.10937T>G (p.Val3646Gly) of the PKD1 gene are associated with the polycystic kidney disease.
this study reports the 3.6-angstrom cryo-electron microscopy structure of truncated human PKD1-PKD2 complex assembled in a 1:3 ratio.
VEGF/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.
The novel frameshift mutations reported by this study are p. Q1997X, P. D73X and p. V336X.
newly identified sites for known mutations will facilitate the early diagnosis and prediction of prognosis in patients with ADPKD
PKD1 cytoplasmic C-terminal tail domain has a crucial role in renal prognosis in autosomal dominant polycystic disease.
PKD 1 mutation is associated with Autosomal dominant polycystic kidney disease.
Our results show that we have successfully generated a patient-specific iPS 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 mutation status differed by ethnicity, and the PKD1/PKD2 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-retromer complex regulates the surface expression and function of PC1 and PC2
Study identified a novel heterozygous frameshift mutation in PKD1 gene segregating between affected and unaffected individuals suggesting an involvement in polycystic kidney disease (PKD).
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 as a novel mediator of androgen-induced PKD1 repression.
novel frameshift mutation c.3903delC, p.A1302Pfs identified to be responsible for renal disease
Hyperactivation of the ERK pathway may be caused by down-regulation of PC-1 and PC-2 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 mutations, respectively (P = 0.49), and remained unaffected by the ADPKD genotype when adjusted for age, gender and baseline HtLV.
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.
PKD1 contributes to the osteoblast differentiation and bone development via elevation of osteoblast markers through activation of STAT3 and p38 MAPK signaling pathways.
PKD1 mediates the PKC effects on KV11.1 and we found that PKD targets S284 in the N-terminus of the channel.
PC1/3 deficiency was associated with increased expression of melanocortin receptors and PRCP (prolylcarboxypeptidase, a catabolic enzyme for alpha-melanocyte stimulating hormone (alphaMSH)), and reduced adrenocorticotropic hormone secretion. We conclude that the obesity accompanying PCSK1 deficiency may not be primarily due to alphaMSH 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 binds to E-cadherin, and that a posttranslational modification of cortactin, RhoA-induced phosphorylation by protein kinase D1 (PKD1; also known as PRKD1) at S298, impairs adherens junction assembly and supports their dissolution.
Galpha12 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 in the nucleus of crypt epithelial cells in the ileum of PKD1
PKD1 phosphorylates AMPKalpha2 at Ser485/491, thus diminishing AMPK activity.
These data potentially explain the severe renal manifestations of the tuberous sclerosis/polycystic kidney disease contiguous gene syndrome and open new perspectives for the use of mTOR inhibitors in PKD.
novel protein complex composed of Rabep1, GGA1 and Arl3 is responsible for the sorting and targeting of the polycystin 1 andpolycystin 2 to the cilium.
Polycystin-1 regulation of the microtubule cytoskeleton impacts on the turnover rates of focal adhesions in migrating cells and we link all these properties to the capability of PC-1 to regulate the activation state of Focal Adhesion Kinase.
Pkd1 and pkd2 are present in primary cilia of radial glia. Ablation of Pkd1 or Pkd2 affected planar cell polarity development in radial glia and epithelial cells.
Pkd1 haploinsufficiency accelerated the development of tubular dilations after nephron reduction, a phenotype that was associated to a further increase of cell proliferation in a model of polycystic kidney disease.
Pkd1 mutation or deletion leads to the activation of Galpha12, which promotes the maturation of ADAM10 that increases the shedding of E-cadherin in kidney epithelial cells.
PC-1 knockout mice manifested decreased cardiac function relative to littermate controls, and alpha1C L-type calcium channel protein levels were significantly lower in PC-1 knockout hearts.
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