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SNX3 (show SNX3 ELISA Kits)-retromer complex regulates the surface expression and function of PC1 (show PCSK1 ELISA Kits) and PC2 (show KRT6B ELISA Kits)
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 ELISA Kits)).
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 ELISA Kits) as a novel mediator of androgen-induced PKD1 repression.
Hyperactivation of the ERK (show EPHB2 ELISA Kits) pathway may be caused by down-regulation of PC-1 (show PCSK1 ELISA Kits) and PC-2 (show KRT6B ELISA Kits) 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 ELISA Kits) mutations, respectively (P = 0.49), and remained unaffected by the ADPKD genotype when adjusted for age, gender and baseline HtLV.
this study shows that diet-induced obesity links to estrogen receptor (show ESR1 ELISA Kits)-positive breast cancer progression via LPA (show APOA ELISA Kits)/PKD-1-CD36 (show CD36 ELISA Kits) signaling-mediated microvascular remodeling
Isolated polycystic liver disease genes define effectors of polycystin-1 function
mechanical load upregulates expression of Runx2 (show RUNX2 ELISA Kits) gene via potentiation of PC1 (show PCSK1 ELISA Kits)-JAK2 (show JAK2 ELISA Kits)/STAT3 (show STAT3 ELISA Kits) signaling axis, culminating to possibly control osteoblastic differentiation and ultimately bone formation.
Gly972Arg of PC-1 (show PCSK1 ELISA Kits) polymorphisms are associated with polycystic ovary syndrome.
Mutations in PKD1 is associated with autosomal dominant polycystic kidney disease.
These findings imply that PKD1 plays a critical regulatory role in Group B streptococci (GBS (show GNB5 ELISA Kits))-induced proinflammatory reactions and sepsis, and inhibition of PKD1 activation together with antibiotic treatment in GBS (show GNB5 ELISA Kits)-infected neonates could be an effective way to control GBS (show GNB5 ELISA Kits) diseases.
critical functions of PC1 (show PCSK1 ELISA Kits) are regulated by its ability to sense cytosolic calcium levels via binding to calmodulin
cortactin (show CTTN ELISA Kits) binds to E-cadherin (show CDH1 ELISA Kits), and that a posttranslational modification of cortactin (show CTTN ELISA Kits), RhoA (show RHOA ELISA Kits)-induced phosphorylation by protein kinase D1 (PKD1; also known as PRKD1 (show PRKD1 ELISA Kits)) at S298, impairs adherens junction assembly and supports their dissolution.
Galpha12 (show GNA12 ELISA Kits) 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.
Lysophosphatidic acid/PKD-1 signaling leads to nuclear accumulation of histone deacetylase 7 (show HDAC7 ELISA Kits), where it interacts with forkhead box protein O1 (show FOXO1 ELISA Kits) to suppress endothelial CD36 (show CD36 ELISA Kits) transcription and mediates silencing of antiangiogenic switch, resulting in proangiogenic and proarteriogenic reprogramming.
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 ELISA Kits) effect on MVB secretory traffic.
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