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抗Human PLK1 抗体:
抗Mouse (Murine) PLK1 抗体:
抗Rat (Rattus) PLK1 抗体:
Human Polyclonal PLK1 Primary Antibody for IHC - ABIN966866
Lake, Jelinek: Cell cycle- and terminal differentiation-associated regulation of the mouse mRNA encoding a conserved mitotic protein kinase. in Molecular and cellular biology 1994
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Human Polyclonal PLK1 Primary Antibody for IHC - ABIN966867
Golsteyn, Schultz, Bartek, Ziemiecki, Ried, Nigg: Cell cycle analysis and chromosomal localization of human Plk1, a putative homologue of the mitotic kinases Drosophila polo and Saccharomyces cerevisiae Cdc5. in Journal of cell science 1994
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Human Monoclonal PLK1 Primary Antibody for FACS, IHC - ABIN1098105
Lin, Sun, Wang: Suppression of Polo like kinase 1 (PLK1) by p21(Waf1) mediates the p53-dependent prevention of caspase-independent mitotic death. in Cellular signalling 2011
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Xenopus laevis Polyclonal PLK1 Primary Antibody for WB - ABIN152619
Kumagai, Dunphy: Purification and molecular cloning of Plx1, a Cdc25-regulatory kinase from Xenopus egg extracts. in Science (New York, N.Y.) 1996
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Human Monoclonal PLK1 Primary Antibody for ICC, ELISA - ABIN969580
Lee, Rhee: PLK1 phosphorylation of pericentrin initiates centrosome maturation at the onset of mitosis. in The Journal of cell biology 2011
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Human Polyclonal PLK1 Primary Antibody for ICC, IF - ABIN256400
Seeger-Nukpezah, Liebau, Höpker, Lamkemeyer, Benzing, Golemis, Schermer: The centrosomal kinase Plk1 localizes to the transition zone of primary cilia and induces phosphorylation of nephrocystin-1. in PLoS ONE 2012
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Human Polyclonal PLK1 Primary Antibody for IHC (p), WB - ABIN392446
Negishi, Kumano, Nishida: Polo-like kinase 1 is required for localization of Posterior End Mark protein to the centrosome-attracting body and unequal cleavages in ascidian embryos. in Development, growth & differentiation 2011
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Human Polyclonal PLK1 Primary Antibody for IHC, ELISA - ABIN129581
Adler, Müller, Rached, Dekant, Mally: Modulation of key regulators of mitosis linked to chromosomal instability is an early event in ochratoxin A carcinogenicity. in Carcinogenesis 2009
Human Monoclonal PLK1 Primary Antibody for ICS - ABIN1177154
Peter, Gleixner, Cerny-Reiterer, Herrmann, Winter, Hadzijusufovic, Ferenc, Schuch, Mirkina, Horny, Pickl, Müllauer, Willmann, Valent: Polo-like kinase-1 as a novel target in neoplastic mast cells: demonstration of growth-inhibitory effects of small interfering RNA and the Polo-like kinase-1 targeting drug BI 2536. in Haematologica 2011
Human Monoclonal PLK1 Primary Antibody for ICS - ABIN1177152
Jang, Ma, Terada, Erikson: Phosphorylation of threonine 210 and the role of serine 137 in the regulation of mammalian polo-like kinase. in The Journal of biological chemistry 2002
that SUMOylation is an important regulatory mechanism governing PLK1's mitotic function
The authors show that human Cyclin (显示 PCNA 抗体)-Dependent-Kinases (CDKs) target the RAD9 (显示 RAD9A 抗体) subunit of the 9-1-1 checkpoint clamp (显示 PDZK1 抗体) on Thr292, to modulate DNA damage checkpoint activation. Thr292 phosphorylation on RAD9 (显示 RAD9A 抗体) creates a binding site for Polo-Like-Kinase1 (PLK1), which phosphorylates RAD9 (显示 RAD9A 抗体) on Thr313.
Thus, Cyclin A (显示 CCNA2 抗体)/Cdk1 (显示 CDK1 抗体) phosphorylation primes MYPT1 (显示 PPP1R12A 抗体) for Plk1 binding. These data demonstrate cross-regulation between Cyclin A (显示 CCNA2 抗体)/Cdk1 (显示 CDK1 抗体)-dependent and Plk1-dependent phosphorylation of substrates during mitosis to ensure efficient correction of kinetochore microtubule attachment errors necessary for high mitotic fidelity.
hnRNPK (显示 HNRNPK 抗体) regulates PLK1 expression by competing with the PLK1-targeting miRNAs, miR (显示 MLXIP 抗体)-149-3p and miR (显示 MLXIP 抗体)-193b-5p.
The expression of APC-DeltaC in colon cells reduces the accumulation of mitotic cells upon PLK1 inhibition, accelerates (显示 APC 抗体) mitotic exit and increases the survival of cells with enhanced chromosomal abnormalities.
a vital role of PLK1-dependent phosphorylation of MTHFR (显示 MTHFR 抗体) in replication via histone methylation, and implicate folate metabolism with glioma, is reported.
Polo-like kinase inhibition can sensitize cholangiocarcinoma cells to cisplatin-induced apoptosis with proteasomal Bcl-2 (显示 BCL2 抗体) degradation as an additional pro-apoptotic effect.
Results showed that Polo-like kinase 1 (Plk1) plays an important role in the conversion of cancer stem cells (CSCs) between active and quiescent states.
Authors demonstrated that WDR62 (显示 WDR62 抗体) is a PLK1 substrate that is phosphorylated at Ser (显示 SIGLEC1 抗体) 897, and that this phosphorylation at the spindle poles promotes astral microtubule assembly to stabilize spindle orientation.
findings thus elucidate a critical role for Plk1 in CyclinB1-Cdk1 (显示 CDK1 抗体) activation and mitotic entry and outline how CyclinA2-Cdk (显示 CDK4 抗体), an S-promoting factor, poises cells for commitment to mitosis.
Novel roles for Plk and GSK3 regulation of ADAM13 (显示 ADAM33 抗体) function in cranial neural crest cell migration.
Plx1-mediated degradation of Bora in interphase generates oscillations in Plx1 activity and is essential for development.
Coordinated interplays between Plx1 and Gwl (显示 MASTL 抗体) are required for reactivation of these kinases from the G(2)/M DNA damage checkpoint and efficient checkpoint recovery.
the penultimate CRS (显示 CARS 抗体) serine (Ser (显示 SIGLEC1 抗体) 101) of cyclin b1 (显示 CCNB1 抗体) is a Plx substrate
Results suggest that polo-like kinase (Plx1) could be the missing regulator that prevents maturation-promoting factor autoamplification in stage IV oocytes.
Plx1 cooperates with CaMKII (显示 CAMK2G 抗体) to regulate cyclosome regulators, and is necessary for release of cytostatic factor metaphase arrest and sufficient when overexpressed.
Data show that Plx1 couples tension signals to cellular responses through phosphorylation of the 3F3 (显示 TRIM32 抗体)/2 epitope and targeting structural and checkpoint proteins to kinetochores.
Polo-like kinase Plx1 is an essential factor for calcium ion-induced meiotic exit during cytostatic factor arrest
Polo-like kinase (Plx1) phosphorylates xTRF1 in vitro and the mitotic xTRF1-chromatin association was significantly impaired when Plx1 was immunodepleted from the extracts (Plx1).
Cdk1 (显示 CDK1 抗体) phosphorylation of BubR1 (显示 BUB1B 抗体) controls spindle checkpoint arrest and plk-mediated formation of the 3F3 (显示 TRIM32 抗体)/2 epitope.
These data identify an essential role for HMMR (显示 HMMR 抗体) in the PLK1-dependent regulatory pathway that orients progenitor cell division and supports neural development.
Plk1 inhibition (RNAi, pharmacological compounds) promotes the development of adenomatous polyps in two independent Apc (显示 APC 抗体) (Min/+) mouse models.
integrity is required for PLK1 localization with SUMO-1 (显示 SUMO1 抗体) but not with SUMO-2 (显示 SUMO2 抗体)/3. Inhibition of SUMOylation disrupts proper meiotic bipolar spindle organization and spindle-kinetochore attachment.
CIP2A (显示 KIAA1524 抗体) acts as a scaffold for CEP192-mediated microtubule organizing center assembly by recruiting Plk1 and aurora A (显示 AURKA 抗体) during meiotic maturation in mouse oocytes
Plk1 overexpression may contribute to tumor formation by both inducing chromosomal instability and suppressing the DDR (显示 DDR1 抗体) pathway.
Plk1 is essential for the mammalian embryonic development, and its depletion leads to mitotic alterations and lethality at different stages during mammalian development.
Plk1 regulated angiotensin II-dependent activation of RhoA (显示 RHOA 抗体) and actomyosin dynamics in VSMCs in a mitosis-independent manner. This regulation depended on Plk1 kinase activity. Plk1 haploinsufficiency in mice did not induce obvious cell proliferation defects but did result in arterial structural alterations, which frequently led to aortic rupture and death.
The findings reveal a PLK1-Fbw7 (显示 FBXW7 抗体)-Myc (显示 MYC 抗体) signaling circuit that underlies tumorigenesis and validate PLK1 inhibitors, alone or with Bcl2 (显示 BCL2 抗体) antagonists, as potential effective therapeutics for MYC (显示 MYC 抗体)-overexpressing cancers.
These data implicate the insulin (显示 INS 抗体)-FoxM1 (显示 FOXM1 抗体)/PLK1/CENP-A (显示 CENPA 抗体) pathway-regulated mitotic cell-cycle progression as an essential component in the beta cell adaptation to delay and/or prevent progression to diabetes.
centrosome maturation occurs during interphase in an MLK (显示 MUSK 抗体)-dependent manner, independent of the classic mitotic kinase, Plk1.
Report the 2.3-A crystal structure of the complex of the N-terminal kinase domain (KD) and a C-terminal Polo-box domain (PBD together with a PBD-binding motif of Drosophila melanogaster microtubule-associated protein (显示 FAM82A2 抗体) 205 (Map205(PBM)).
Studies demonstrate that Plk1 is required for embryonic proliferation because its activity is crucial for mitotic integrity.
for the first time that Plk1 can accommodate extended ATP-competitive compounds that project toward the adaptive pocket and help the enzyme order its activation segment
Plk1 plays an essential role during the meiosis I/meiosis II transition in porcine oocytes, and the regulation is associated with Plk1's effects on homologous chromosome segregation in the Anaphase-telophase I stage.
Thus, these results indicated that Plk1 is essential for porcine embryos to complete the first mitotic division. Furthermore, Plk1 regulation was associated with effects on spindle assembly and chromosome arrangement
PLK1 might play a critical role in vascular smooth muscle cell mitosis in hyperplastic intima of the injured vessels.
Data show that Polo-like kinase 1 is activated before M phase promoting factor (MPF (显示 MSLN 抗体)), which is consistent with its role in activating MPF (显示 MSLN 抗体) in mammalian oocytes.
PLK1 inhibition mitigates autophagy in cancer cells both under nutrient starvation and sufficiency, and a role of PLK1 in autophagy is also observed in the invertebrate model organism Caenorhabditis elegans.
These results reveal a crucial and conserved role of phosphorylation of the N terminus of Bora for Plk1 activation and mitotic entry.
Our data further show that PLK-1 is needed for nuclear envelope breakdown during early embryogenesis
PLK-1 substitutes for Mps1 in controlling spindle checkpoint initiation in C. elegans.
NCAPG2 (显示 NCAPG2 抗体) plays an important role in regulating proper chromosome segregation through a functional interaction with PLK1 during mitosis
CDK-1 (显示 CDK1 抗体) activates PLK-1 via SPAT (显示 AGXT 抗体)-1 phosphorylation to promote entry into mitosis.
The result provide key insights into the regulation of homolog pairing and reveal that targeting of plk-1 to the NE by meiotic chromosomes establishes the conserved linkages to cytoskeletal forces needed for homology assessment.
SPAT (显示 AGXT 抗体)-1 and PLK-1 depletion causes impaired polarity with abnormal length of the anterior and posterior PAR (显示 AFG3L2 抗体) domains, and partial plk-1(RNAi) or spat (显示 AGXT 抗体)-1(RNAi), but not air-1(RNAi), can rescue the lethality of a par-2 (显示 F2RL1 抗体) mutant.
Polo kinases, via their polo box domains, bind to and regulate the activity of two key polarity proteins, MEX-5 and MEX (显示 ZSWIM2 抗体)-6.
plk-1 asymmetry contributes to asynchronous cell division in C. elegans embryos.
human homolog catalyzes the phosphorylation of a Golgi reassembly stacking protein (GRASP65); may play a role in Golgi apparatus fragmentation and reorganization during mitosis
, cell cycle regulated protein kinase
, polo (Drosophia)-like kinase
, polo like kinase
, serine/threonine-protein kinase 13
, serine/threonine-protein kinase PLK1
, polo-like kinase homolog
, polo-like protein kinase