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Human Polyclonal PKD1 Primary Antibody für 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 3 Pubmed References
SNX3 (zeige SNX3 Antikörper)-retromer complex regulates the surface expression and function of PC1 (zeige PCSK1 Antikörper) and PC2 (zeige KRT6B Antikörper)
Study identified a novel heterozygous frameshift mutation in PKD1 gene segregating between affected and unaffected individuals suggesting an involvement in polycystic kidney disease (PKD (zeige PRKD1 Antikörper)).
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 (zeige FRS2 Antikörper) as a novel mediator of androgen-induced PKD1 repression.
Hyperactivation of the ERK (zeige EPHB2 Antikörper) pathway may be caused by down-regulation of PC-1 (zeige PCSK1 Antikörper) and PC-2 (zeige KRT6B Antikörper) 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 (zeige PKD2 Antikörper) 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 (zeige ESR1 Antikörper)-positive breast cancer progression via LPA (zeige APOA Antikörper)/PKD-1-CD36 (zeige CD36 Antikörper) signaling-mediated microvascular remodeling
Isolated polycystic liver disease genes define effectors of polycystin-1 function
mechanical load upregulates expression of Runx2 (zeige RUNX2 Antikörper) gene via potentiation of PC1 (zeige PCSK1 Antikörper)-JAK2 (zeige JAK2 Antikörper)/STAT3 (zeige STAT3 Antikörper) signaling axis, culminating to possibly control osteoblastic differentiation and ultimately bone formation.
Gly972Arg of PC-1 (zeige PCSK1 Antikörper) 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 (zeige GNB5 Antikörper))-induced proinflammatory reactions and sepsis, and inhibition of PKD1 activation together with antibiotic treatment in GBS (zeige GNB5 Antikörper)-infected neonates could be an effective way to control GBS (zeige GNB5 Antikörper) diseases.
critical functions of PC1 (zeige PCSK1 PLURAL_@27095@) are regulated by its ability to sense cytosolic calcium levels via binding to calmodulin
cortactin (zeige CTTN Antikörper) binds to E-cadherin (zeige CDH1 Antikörper), and that a posttranslational modification of cortactin (zeige CTTN Antikörper), RhoA (zeige RHOA Antikörper)-induced phosphorylation by protein kinase D1 (PKD1; also known as PRKD1 (zeige PRKD1 Antikörper)) at S298, impairs adherens junction assembly and supports their dissolution.
Galpha12 (zeige GNA12 Antikörper) 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 (zeige HDAC7 Antikörper), where it interacts with forkhead box protein O1 (zeige FOXO1 Antikörper) to suppress endothelial CD36 (zeige CD36 Antikörper) 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 (zeige DGKA Antikörper) 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.
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