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Human PLK3 Protein expressed in Wheat germ - ABIN1315440
Chen, Huang, Liu, Xu, Jiang: Design, synthesis, and evaluation of non-ATP-competitive small-molecule Polo-like kinase 1 (Plk1) inhibitors. in Archiv der Pharmazie 2015
Those data indicate that the overexpression of PLK3-mediated degradation of abnormal PrP is largely dependent on chaperone-mediated autophagy pathway.
Data indicate that elevated levels of Polo-like kinase 3 (Plk3)and pT273 caspase-8 are correlated with favorable clinical outcome in patients with anal squamous cell carcinoma (anal SCC) treated with concomitant chemoradiotherapy (CRT).
Knockout (KO) or knockdown of caspase-8, CD95 or FADD prevents activation of Plk3 upon CD95 stimulation, suggesting a requirement of a functional death-inducing signaling complex for Plk3 activation.
study revealed an interesting mutual regulation between Plk3 and SIAH2 and uncovered a regulatory network that functions to fine-tune the cellular hypoxic response.
the differential effects of hypoxic stress on Plk3 activity in Human Limbal Stem and HCE cells. Instead of apoptosis, hypoxic stress suppresses Plk3 activity to protect limbal stem cells from death and to allow the process of Human Limbal Stem cell differentiation.
Data suggest that HOXA-AS2 could be an oncogene for gastric cancer partly through suppressing P21, PLK3, and DDIT3 expression.
Plk3 is involved in the inhibition of cell proliferation and tumorigenesis, which may occur via interactions with p21.
PLK3 predominantly is expressed in Cholangiocarcinomas (CCA) cells and that high PLK3 expression correlates with prolonged overall survival.
The role of Plk3 in oncogenesis: the aberrant expression of Plk3 was found in different types of tumors.
hyperosmotic stress-activated Plk3 elicited gammaH2AX.
Plk3 binds to CtIP phosphorylated at S327 via its Polo box domains, which is necessary for robust damage-induced CtIP phosphorylation at S327 and subsequent CtIP phosphorylation at T847.
have identified and validated as in vitro PLK2 and PLK3 substrates HSP90, GRP-94, beta-tubulin, calumenin, and 14-3-3 epsilon
Here, the authors report phosphorylation of Thr4 by Polo-like kinase 3 in mammalian cells.
Bcl-xL phosphorylation at Ser49 by polo-like kinase 3 during cell cycle progression and checkpoints
Calcium- and integrin-binding protein 1 regulates microtubule organization and centrosome segregation through polo like kinase 3 during cell cycle progression.
hyperosmotic stress can activate the Plk3 signaling pathway that subsequently regulates the AP-1 complex by directly phosphorylating ATF-2 independent from the effects of JNK and p38 activation.
Plk3 functions as an essential component of the hypoxia regulatory pathway by direct phosphorylation of HIF-1alpha
upregulation of CIB1 in cancer cells may inhibit Plk3 activity, leading to abnormal cell cycle regulation in breast cancer cells.
Plk3 as a new player in the regulation of the PI3K/PDK1/Akt signaling axis by phosphorylation and stabilization of PTEN.
The Plk3 overexpression suppressed cellular growth in a long-term colony-forming assay. And overexpression of Plk3 caused long-term growth suppression in Ras-transformed NIH3T3.
Polo-Like Kinase 3 Appears Dispensable for Normal Retinal Development Despite Robust Embryonic Expression
Calcium- and integrin-binding protein 1 is involved in regulating endomitosis, perhaps through its interaction with Plk3
Data demonstrate that FGF-inducible kinase (Fnk) expression levels in transfected cells can be regulated by nuclear-cytoplasmic trafficking, ubiquitination, and proteosome-dependent degradation.
Plk3 localizes to the nucleolus and is involved in regulation of the G1/S phase transition.
Ectopic expression of the Plk3-kinase domain (Plk3-KD), but not its Polo-box domain or a Plk3-KD mutant, suppressed the nuclear accumulation of HIF-1 alpha induced by nickel or cobalt ions
The specificity of TTP for promoting the degradation of Plk3 was demonstrated by the unaltered decay of Plk3 mRNA in cell
Cytokine-inducible kinase is a putative serine/threonine kinase. CNK contains both a catalytic domain and a putative regulatory domain. It may play a role in regulation of cell cycle progression and tumorigenesis.
, serine/threonine-protein kinase PLK3
, FGF-inducible kinase
, polo-like kinase 3
, serine/threonine-protein kinase PLK3-like
, cytokine-inducible serine/threonine-protein kinase
, proliferation-related kinase
, cytokine inducible kinase
, serine-threonine kinase