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PKD1 encodes a member of the polycystin protein family. Additionally we are shipping Polycystic Kidney Disease 1 (Autosomal Dominant) Kits (4) and Polycystic Kidney Disease 1 (Autosomal Dominant) Proteins (4) and many more products for this protein.
Showing 10 out of 59 products:
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 2 references for ABIN678083
These results suggest that the Ser (show SIGLEC1 Antibodies) at the 4166 site in PC1 (show PCSK1 Antibodies) is crucial in the PC1 (show PCSK1 Antibodies) mediated MEK (show MAP2K1 Antibodies)/ERK (show EPHB2 Antibodies)/myc (show MYC Antibodies) signaling pathway, which might be the key pathophysiological cause of Aortic dissection.
Novel PKD1 mutations in Chinese autosomal dominant polycystic kidney disease patients
The pathogenic mutation in PKD1 linked pedigree was c.8522G>A (p.E2771K) in exon 23. This C to T transition occurs at the CpG dinucleotides which is the known hotspot point for mutations.
Germline mutations in PKD1 gene is associated with autosomal-dominant polycystic kidney disease.
Host cortactin, PKD1 and actin are recruited by Trypanosoma cruzi extracellular amastigotes based on experiments in fixed and live cells by time lapse confocal microscopy.
PCs expression and p53 (show TP53 Antibodies) activation as a regulator of cell proliferation were further evaluated in vivo and in 69 advanced human carotid atherosclerotic plaques.
These results suggest that, at least in some patients, the severity of the cystic disease is inversely correlated with the level of polycystin 1 function.
Overexpression of PKD1 in a prostate cancer cell line model resulted in decreased cell proliferation and epithelial mesenchymal transition.
and MMP9 (show MMP9 Antibodies) expression in PKD1 constitutively-active MD-MB-231 cells and MCF-7 knockdown cells were decreased and increased respectively
A substantial number of PKD1 missense or synonymous mutations characterize pre-mRNA splicing. One missense and 2 synonymous mutations induce significant defects in pre-mRNA splicing.
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
Our studies demonstrate that PKD1/2 is a key regulator of MVB maturation and exosome secretion, and constitutes a mediator of the DGK alpha (show DGKA Antibodies) effect on MVB secretory traffic.
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.
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 (show FRAP1 Antibodies) inhibitors in PKD (show PRKD1 Antibodies).
Our results show that AKAP13 (show AKAP13 Antibodies)-PKD1 signaling is critical for transcriptional regulation of key contractile, cell death, and metabolic pathways during the development of compensatory hypertrophy in vivo.
PKD1 acts downstream of TGFalpha and Kras, to mediate formation of ductal structures through activation of the Notch (show NOTCH1 Antibodies) pathway.
Results reveal that whereas protein kinase D1 (show PRKD1 Antibodies) and protein kinase D2 (show PKD2 Antibodies) are essential for neuronal polarity, there exists a functional redundancy between the two proteins.
PKD controls synaptic plasticity and learning by regulating actin stability in dendritic spines.
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.
polycystic kidney disease 1 (autosomal dominant)
, polycystin 1
, autosomal dominant polycystic kidney disease 1 protein
, polycystic kidney disease-associated protein
, transient receptor potential cation channel, subfamily P, member 1
, polycystic kidney disease protein 1
, autosomal dominant polycystic kidney disease 1 protein homolog
, polycystic kidney disease 1 homolog; polycystin-1
, protein kinase C mu type
, protein kinase C, mu
, protein kinase D
, serine/threonine-protein kinase D1