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Human Polyclonal PRKD1 Primary Antibody for IHC (p), WB - ABIN391011
Wu, Solaro: Protein kinase C zeta. A novel regulator of both phosphorylation and de-phosphorylation of cardiac sarcomeric proteins. in The Journal of biological chemistry 2007
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Human Polyclonal PRKD1 Primary Antibody for ELISA, WB - ABIN562395
Sin, Martin, Wills, Currie, Baillie: Small heat shock protein 20 (Hsp20) facilitates nuclear import of protein kinase D 1 (PKD1) during cardiac hypertrophy. in Cell communication and signaling : CCS 2015
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Human Polyclonal PRKD1 Primary Antibody for ICC, IF - ABIN4345848
Weinreb, Piscuoglio, Martelotto, Waggott, Ng, Perez-Ordonez, Harding, Alfaro, Chu, Viale, Fusco, da Cruz Paula, Marchio, Sakr, Lim, Thompson, Chiosea, Seethala, Skalova, Stelow, Fonseca, Assaad, How et al.: Hotspot activating PRKD1 somatic mutations in polymorphous low-grade adenocarcinomas of the salivary glands. ... in Nature genetics 2014
cloning and expression analysis of a protein kinase C gene, PKCmu, and its regulation of the promoter region (PKCmu)
PKD1 (显示 PKD1 抗体) contributes to the regulation of physiological angiogenesis and lymphangiogenesis during zebrafish development and is essential for tumor angiogenesis.
PKD1 (显示 PKD1 抗体) not only regulates the hypoxic glycolytic metabolism of cancer cells via regulation of the expression of HIF-1alpha (显示 HIF1A 抗体) and glycolytic enzymes.
these results describe a novel mechanism governing PRKD1 gene expression in pancreatic ductal adenocarcinoma and provide a functional link between oncogenic KRas, NF-kappaB (显示 NFKB1 抗体) and expression of PRKD1.
p110alpha (显示 PIK3CA 抗体) subunit of PI3K (显示 PIK3CA 抗体) and PKD mediate YAP (显示 YAP1 抗体) activation in response to insulin (显示 INS 抗体) and neurotensin (显示 NTS 抗体) in pancreatic cancer cells. Inhibitors of PI3K (显示 PIK3CA 抗体) or PKD disrupt crosstalk between insulin receptor (显示 INSR 抗体) and GPCR (显示 NMUR1 抗体) signaling systems by blocking YAP (显示 YAP1 抗体)/TEAD-regulated gene expression in pancreatic cancer cells
High PRKD1 expression is associated with drug resistance in breast cancer.
Our findings directly associate the AR/NCOA1 (显示 NCOA1 抗体) complex with PRKD1 regulation and cellular migration and support the concept of therapeutic inhibition of NCOA1 (显示 NCOA1 抗体) in prostate cancer.
None of the Polymorphous low-grade adenocarcinoma (PLGA) lacking PRKD1 somatic mutations or PRKD gene family rearrangements harboured somatic mutations in the kinase domains of the PRKD2 (显示 PKD2 抗体) or PRKD3 (显示 PRKD3 抗体) genes.
A single nucleotide polymorphism located within the fourth intron of PRKD1 (rs57803087) was strongly associated with DPP-4 (显示 DPP4 抗体) inhibitor response in patients with type 2 diabetes
Mutation in PRKD1 gene is associated with congenital heart defects.
Bradykinin stimulates myofibroblast migration through protein kinase D-mediated activation of COX-2 (显示 COX2 抗体) and Hsp27 (显示 HSPB1 抗体).
Lysophosphatidic acid/PKD-1 (显示 PKD1 抗体) signaling leads to nuclear accumulation of histone deacetylase 7 (显示 HDAC7 抗体), where it interacts with forkhead box protein O1 (显示 FOXO1 抗体) to suppress endothelial CD36 (显示 CD36 抗体) transcription and mediates silencing of antiangiogenic switch, resulting in proangiogenic and proarteriogenic reprogramming.
The study demonstrates an essential role for PKD1 (显示 PKD1 抗体) in the beta-cell adaptive secretory response to high-fat feeding in mice.
These findings imply that PKD1 (显示 PKD1 抗体) plays a critical regulatory role in Group B streptococci (GBS (显示 GNB5 抗体))-induced proinflammatory reactions and sepsis, and inhibition of PKD1 (显示 PKD1 抗体) activation together with antibiotic treatment in GBS (显示 GNB5 抗体)-infected neonates could be an effective way to control GBS (显示 GNB5 抗体) diseases.
Our studies demonstrate that PKD1 (显示 PKD1 抗体)/2 is a key regulator of MVB maturation and exosome secretion, and constitutes a mediator of the DGK alpha (显示 DGKA 抗体) effect on MVB secretory traffic.
Our results show that AKAP13 (显示 AKAP13 抗体)-PKD1 (显示 PKD1 抗体) signaling is critical for transcriptional regulation of key contractile, cell death, and metabolic pathways during the development of compensatory hypertrophy in vivo.
PKD1 (显示 PKD1 抗体) acts downstream of TGFalpha and Kras, to mediate formation of ductal structures through activation of the Notch (显示 NOTCH1 抗体) pathway.
Results reveal that whereas protein kinase D1 and protein kinase D2 (显示 PKD2 抗体) 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.
regulatory kinase of eNOS (显示 NOS3 抗体) in endothelial cells whose activity orchestrates mammalian vascular tone
Overexpression of constitutively active PKD1 (显示 PKD1 抗体) in rodent heart results in dilated cardiomyopathy.
AngII activates PKD via a mechanism involving Src family kinases and PKC, to underlie increased aldosterone production.
Data indicate that Ser738/742-to-glutamate (显示 GRIN2A 抗体) protein kinase D mutant increased AngII-induced CREB (显示 CREB1 抗体) protein and activating transcription factor 2 (显示 ATF2 抗体) phosphorylation, and phospho-CREB (显示 CREB1 抗体) binding to the steroidogenic acute regulatory protein (显示 STAR 抗体) promoter.
These results indicate that PKD is downstream of PLD (显示 PLD 抗体) and suggest that PKD is one of the mechanisms through which PLD (显示 PLD 抗体) promotes aldosterone production in response to AngII in adrenal glomerulosa cells.
PKD mediates acute AngII-induced aldosterone secretion.
Protein kinase D-HDAC5 (显示 HDAC5 抗体) pathway plays an important role in VEGF (显示 VEGFA 抗体) regulation of gene transcription and angiogenesis
PRKD1 is a serine/threonine kinase that regulates a variety of cellular functions, including membrane receptor signaling, transport at the Golgi, protection from oxidative stress at the mitochondria, gene transcription, and regulation of cell shape, motility, and adhesion (summary by Eiseler et al., 2009
protein kinase D1
, protein kinase C, mu
, serine/threonine-protein kinase D1-like
, protein kinase C mu type
, protein kinase D
, serine/threonine-protein kinase D1
, protein kinase C mu