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anti-Rat (Rattus) PIK3C2B Antibodies:
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Human Monoclonal PIK3C2B Primary Antibody for IF, WB - ABIN4948244
Norris, Pombo, Shirley, Blevins, Tablin: Association of Factor V Secretion with Protein Kinase B Signaling in Platelets from Horses with Atypical Equine Thrombasthenia. in Journal of veterinary internal medicine 2016
this study suggests that PIK3C2B might only have a minor role in SQCC oncogenesis
PI3KC2B-silencing inhibits early stages of neuroblastoa tumorigenic growth.
Class II enzyme PI3K-C2beta and the class IB isozyme p110gamma mainly regulate the S1P- and high density lipoprotein (HDL)-dependent endothelial cell (EC) migration and PI3K-C2alpha primarily controls EC survival
Data suggest a novel role for nucleotide-free Ras in cell signaling in which PI3KC2beta stabilizes nucleotide-free Ras and that interaction of Ras and PI3KC2beta mutually inhibit one another.
The results of this study showed that strong association between PIK3C2B gene alternation and high-grade oligodendroglial tumors.
These findings provide a unique mechanism for regulating class II PI3Ks, and identify TRIM27 as a previously undescribed negative regulator of CD4 T cells.
Overexpression of PIK3C2B is associated with esophageal squamous cell carcinoma.
different human small cell lung carcinoma cell lines overexpress distinct subsets of PI3Ks, resulting in differences in signalling cascades activated by stem cell factor; insights into specificity and functional significance of PI3K signalling in cancer
activity of nuclear phosphoinositide 3-kinase C2beta investigated in HL-60 cells induced to differentiate along granulocytic or monocytic lineages
plays a regulatory role in cell motility
identified the 185-kDa protein altered by nitrotyrosylation in platelets from patients with systemic sclerosis as phosphoinositide kinase C2beta (PI 3-K); the activity of PI 3-K increases in nitrotyrosylated platelet lystaes from patients with SSc
Class II phosphoinositide 3-kinase C2beta isnot essential for epidermal differentiation
These findings suggest that PI3KC2beta regulates the migration and survival of human tumor cells by distinct molecular mechanisms.
Epidermal growth factor stimulates the appearance of PI3K-C2beta in nuclei.
Data show that the class II phosphatidylinositol 3 kinase C2beta (PI3K-C2beta) is activated by the T-cell receptor (TCR) and functions upstream of NDPK-B to activate KCa3.1 channel activity.
The protein encoded by this gene belongs to the phosphoinositide 3-kinase (PI3K) family. PI3-kinases play roles in signaling pathways involved in cell proliferation, oncogenic transformation, cell survival, cell migration, and intracellular protein trafficking. This protein contains a lipid kinase catalytic domain as well as a C-terminal C2 domain, a characteristic of class II PI3-kinases. C2 domains act as calcium-dependent phospholipid binding motifs that mediate translocation of proteins to membranes, and may also mediate protein-protein interactions. The PI3-kinase activity of this protein is sensitive to low nanomolar levels of the inhibitor wortmanin. The C2 domain of this protein was shown to bind phospholipids but not Ca2+, which suggests that this enzyme may function in a calcium-independent manner.
nuclear cap binding protein subunit 2
, phosphatidylinositol-4-phosphate 3-kinase C2 domain-containing subunit beta
, phosphoinositide-3-kinase, class 2, beta polypeptide
, PTDINS-3-kinase C2 beta
, phosphatidylinositol 3-kinase C2 domain-containing beta polypeptide
, phosphatidylinositol 4-phosphate 3-kinase C2 domain-containing subunit beta
, phosphoinositide 3-kinase-C2-beta
, ptdIns-3-kinase C2 subunit beta