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Knockout (KO) or knockdown of caspase-8 (zeige CASP8 ELISA Kits), CD95 (zeige FAS ELISA Kits) or FADD (zeige FADD ELISA Kits) prevents activation of Plk3 upon CD95 (zeige FAS ELISA Kits) stimulation, suggesting a requirement of a functional death-inducing signaling complex for Plk3 activation.
study revealed an interesting mutual regulation between Plk3 and SIAH2 (zeige SIAH2 ELISA Kits) 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 (zeige ARSA ELISA Kits) could be an oncogene (zeige RAB1A ELISA Kits) for gastric cancer partly through suppressing P21 (zeige CDKN1A ELISA Kits), PLK3, and DDIT3 (zeige DDIT3 ELISA Kits) expression.
Plk3 is involved in the inhibition of cell proliferation and tumorigenesis, which may occur via interactions with p21 (zeige CDKN1A ELISA Kits).
PLK3 predominantly is expressed in Cholangiocarcinomas (CCA (zeige FBN2 ELISA Kits)) 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 (zeige H2AFX ELISA Kits).
Plk3 binds to CtIP (zeige RBBP8 ELISA Kits) phosphorylated at S327 via its Polo (zeige PLK1 ELISA Kits) box domains, which is necessary for robust damage-induced CtIP (zeige RBBP8 ELISA Kits) phosphorylation at S327 and subsequent CtIP (zeige RBBP8 ELISA Kits) phosphorylation at T847.
have identified and validated as in vitro PLK2 (zeige PLK2 ELISA Kits) and PLK3 substrates HSP90 (zeige HSP90 ELISA Kits), GRP-94 (zeige HSP90B1 ELISA Kits), beta-tubulin (zeige TUBB ELISA Kits), calumenin (zeige CALU ELISA Kits), and 14-3-3 epsilon (zeige YWHAE ELISA Kits)
Polo-Like Kinase 3 Appears Dispensable for Normal Retinal Development Despite Robust Embryonic Expression
Calcium- and integrin-binding protein 1 (zeige CIB1 ELISA Kits) is involved in regulating endomitosis, perhaps through its interaction with Plk3
Plk3 functions as an essential component of the hypoxia regulatory pathway by direct phosphorylation of HIF-1alpha (zeige HIF1A ELISA Kits)
Plk3 as a new player in the regulation of the PI3K/PDK1/Akt signaling axis by phosphorylation and stabilization of PTEN.
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 (zeige PLK1 ELISA Kits)-box domain or a Plk3-KD mutant, suppressed the nuclear accumulation of HIF-1 alpha (zeige HIF1A ELISA Kits) induced by nickel or cobalt ions
The specificity of TTP (zeige ZFP36 ELISA Kits) 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