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Human Polyclonal PKD1 Primary Antibody pour 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. dans Carcinogenesis 2013
Show all 4 Pubmed References
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 (Montrer SLC27A4 Anticorps) 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 (Montrer PKD2 Anticorps) mutation status differed by ethnicity, and the PKD1/PKD2 (Montrer PKD2 Anticorps) 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 (Montrer SNX3 Anticorps)-retromer complex regulates the surface expression and function of PC1 (Montrer PCSK1 Anticorps) and PC2 (Montrer KRT6B Anticorps)
Study identified a novel heterozygous frameshift mutation in PKD1 gene segregating between affected and unaffected individuals suggesting an involvement in polycystic kidney disease (PKD (Montrer PRKD1 Anticorps)).
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 (Montrer FRS2 Anticorps) as a novel mediator of androgen-induced PKD1 repression.
Hyperactivation of the ERK (Montrer EPHB2 Anticorps) pathway may be caused by down-regulation of PC-1 (Montrer PCSK1 Anticorps) and PC-2 (Montrer KRT6B Anticorps) in lymphatic malformations, contributing to increased proliferation of lymphatic endothelial cells.
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 (Montrer STAT3 Anticorps) and p38 MAPK (Montrer MAPK14 Anticorps) signaling pathways.
PKD1 mediates the PKC effects on KV11.1 (Montrer KCNV2 Anticorps) and we found that PKD (Montrer PRKD1 Anticorps) targets S284 in the N-terminus of the channel.
PC1/3 (Montrer PCSK1 Anticorps) deficiency was associated with increased expression of melanocortin receptors and PRCP (prolylcarboxypeptidase (Montrer PRCP Anticorps), a catabolic enzyme for alpha-melanocyte stimulating hormone (alphaMSH (Montrer POMC Anticorps))), and reduced adrenocorticotropic hormone secretion. We conclude that the obesity accompanying PCSK1 (Montrer PCSK1 Anticorps) deficiency may not be primarily due to alphaMSH (Montrer POMC Anticorps) 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 (Montrer CTTN Anticorps) binds to E-cadherin (Montrer CDH1 Anticorps), and that a posttranslational modification of cortactin (Montrer CTTN Anticorps), RhoA (Montrer RHOA Anticorps)-induced phosphorylation by protein kinase D1 (PKD1; also known as PRKD1 (Montrer PRKD1 Anticorps)) at S298, impairs adherens junction assembly and supports their dissolution.
Galpha12 (Montrer GNA12 Anticorps) 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.
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