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anti-Human PKD2 Antikörper:
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Human Polyclonal PKD2 Primary Antibody für IP, WB - ABIN152061
Liu, Evans, Britton, Zachary: The zinc-finger transcription factor, early growth response 3, mediates VEGF-induced angiogenesis. in Oncogene 2008
Show all 8 Pubmed References
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 or PRKD3 genes.
This study discovered and characterized a novel, highly conserved N-terminal domain, comprising 92 amino acids, which mediates dimerization of Protein Kinase D (PKD) isoforms, PKD1, PKD2, and PKD3 monomers.
Studies indicate that the loss of protein kinase D PKD1 is thought to promote invasion and metastasis, while PKD2 and upregulated PKD3 to be positive regulators of proliferation.
the knockdown of PKD2 reduces cell death and promotes polyploidization induced by PMA. PMA/PKD2-mediated necrosis via PARP cleavage involves both SOD1-dependent and -independent pathways.
The results implied that PKD2 silencing might inhibit migration of MCF7/DOX cells without affecting chemoresistance significantly
PRKD2 silencing induces glioma cell senescence via p53-dependent and -independent pathways.
Loss of PKD2 enhanced KC proliferative potential while loss of PKD3 resulted in a progressive proliferation defect, loss of clonogenicity and diminished tissue regenerative ability.
Activation of PKD2 and further increase of PKD3 activity leads to additional phosphorylation and inhibition of endogenous phosphatase slingshot 1L.
Both PKD2 and GOLPH3 play important roles in the progression of human gliomas by promoting cell proliferation.
PKD2 controls secretion of MMP7 and 9 in an isoform-specific manner
PRKD2 mediates BAZF gene expression by VEGF-A stimulation.
PRKD2 is a potential target to interfere with glioblastoma cell migration and invasion, two major determinants contributing to recurrence of glioblastoma after multimodality treatment.
results suggest that PKD2 is involved in the regulation of PP2A activity in activated T cells through phosphorylation of Ser171 of SET
We have identified PKD2 and PKD3, especially PKD3, as novel cell growth regulators in HCC1806 triple-negative breast cancer cells
found that AMAP1 had the ability to bind directly to PRKD2 and hence to make a complex with the cytoplasmic tail of the beta1 subunit
upregulation of PKD2 expression may determine the behavior of gastric tumor cells, which promotes invasive phenotype and could result in general poor prognosis.
Tyrosine phosphorylation of PKD2 is required for IFNalpha-stimulated activation of this kinase as well as for efficient serine phosphorylation and degradation of IFNAR1 and ensuing restriction of the extent of cellular responses to IFNalpha.
PKD2 is a common signaling target downstream of various agonist receptors in platelets and G(q)-mediated signals along with calcium and novel PKC isoforms, in particular, PKCdelta activate PKD2 in platelets.
Expression and kinase activity of PKD2 are required for the ligand-inducible stimulation of IFNAR1 ubiquitination and endocytosis and for accelerated proteolytic turnover of IFNAR1.
PKD2 regulates hypoxia-induced VEGF-A expression/secretion by tumour cells and VEGF-A stimulated blood vessel formation and a essential mediator of tumour cell-endothelial cell communication and a target to inhibit angiogenesis in gastrointestinal cancers
The results indicate that down-regulation of PRKD2 is involved in the pathogenesis of hyperinsulinemia which, in turn, results in insulin resistance and metabolic disorders.
Our studies demonstrate that PKD1/2 is a key regulator of MVB maturation and exosome secretion, and constitutes a mediator of the DGK alpha effect on MVB secretory traffic.
Results reveal that whereas protein kinase D1 and protein kinase D2 are essential for neuronal polarity, there exists a functional redundancy between the two proteins.
PKD2 acted as an amplification checkpoint for antigen-stimulated digital cytokine responses and translated the differential strength of TCR signaling to determine the number of naive CD8(+) T cells that became effector cells.
Protein kinase D2 promotes in vitro osteoclast differentiation and fusion
A bioinformatic screen identified the serine-threonine kinase protein kinase D2 (PRKD2) as a potential effector of GABP in hematopoietic stem cells
Transcriptional profiling reveals the full consequences of PKD2 loss and maps in detail the selective, but critical, function for PKD2 in signalling by alpha/beta mature TCR complexes in peripheral T-cells.
Data demonstrate that, unlike PKD1, PKD2 catalytic activity is dispensable for normal embryogenesis.
PKD2, like PKD, facilitates mitogenesis in 3T3 cells
The protein encoded by this gene belongs to the protein kinase D (PKD) family of serine/threonine protein kinases. This kinase can be activated by phorbol esters as well as by gastrin via the cholecystokinin B receptor (CCKBR) in gastric cancer cells. It can bind to diacylglycerol (DAG) in the trans-Golgi network (TGN) and may regulate basolateral membrane protein exit from TGN. Alternative splicing results in multiple transcript variants encoding different isoforms.
serine/threonine-protein kinase D2
, protein kinase D2
, serine/threonine-protein kinase D2-like