Overview

  • Product nameAnti-PLK1 antibody
    See all PLK1 primary antibodies
  • Description
    Rabbit polyclonal to PLK1
  • Tested applicationsWBmore details
  • Species reactivity
    Reacts with: Mouse, Human
    Predicted to work with: Rat, Dog, Pig, Xenopus laevis, Caenorhabditis elegans, Monkey, Zebrafish
  • Immunogen

    Synthetic peptide:

    ELHKRRKALTEPEA

    , corresponding to internal sequence amino acids 140-153 of Human PLK1

  • Positive control
    • Human HCT-116 or mouse NIH 3T3 cell line.

Properties

Applications

Our Abpromise guarantee covers the use of ab47073 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
WB 1/1000 - 1/2000. Detects a band of approximately 67 kDa (predicted molecular weight: 68 kDa).

Target

  • FunctionSerine/threonine-protein kinase that performs several important functions throughout M phase of the cell cycle, including the regulation of centrosome maturation and spindle assembly, the removal of cohesins from chromosome arms, the inactivation of APC/C inhibitors, and the regulation of mitotic exit and cytokinesis. Required for recovery after DNA damage checkpoint and entry into mitosis. Required for kinetochore localization of BUB1B. Phosphorylates SGOL1. Required for spindle pole localization of isoform 3 of SGOL1 and plays a role in regulating its centriole cohesion function. Phosphorylates BORA, and thereby promotes the degradation of BORA. Contributes to the regulation of AURKA function. Regulates TP53 stability through phosphorylation of TOPORS.
  • Tissue specificityPlacenta and colon.
  • Sequence similaritiesBelongs to the protein kinase superfamily. Ser/Thr protein kinase family. CDC5/Polo subfamily.
    Contains 2 POLO box domains.
    Contains 1 protein kinase domain.
  • Developmental stageAccumulates to a maximum during the G2 and M phases, declines to a nearly undetectable level following mitosis and throughout G1 phase, and then begins to accumulate again during S phase.
  • Post-translational
    modifications
    Catalytic activity is enhanced by phosphorylation of Thr-210. Phosphorylation at Thr-210 is first detected on centrosomes in the G2 phase of the cell cycle, peaks in prometaphase and gradually disappears from centrosomes during anaphase.
    Autophosphorylation and phosphorylation of Ser-137 may not be significant for the activation of PLK1 during mitosis, but may enhance catalytic activity during recovery after DNA damage checkpoint.
    Ubiquitinated by the anaphase promoting complex/cyclosome (APC/C) in anaphase and following DNA damage, leading to its degradation by the proteasome. Ubiquitination is mediated via its interaction with FZR1/CDH1. Ubiquitination and subsequent degradation prevents entry into mitosis and is essential to maintain an efficient G2 DNA damage checkpoint.
  • Cellular localizationNucleus. Chromosome > centromere > kinetochore. Cytoplasm > cytoskeleton > centrosome. During early stages of mitosis, the phosphorylated form is detected on centrosomes and kinetochores. Localizes to the outer kinetochore. Presence of SGOL1 and interaction with the phosphorylated form of BUB1 is required for the kinetochore localization.
  • Information by UniProt
  • Database links
  • Alternative names
    • Cell cycle regulated protein kinase antibody
    • PLK 1 antibody
    • PLK antibody
    • PLK-1 antibody
    • plk1 antibody
    • PLK1_HUMAN antibody
    • polio like kinase antibody
    • Polo like kinase 1 antibody
    • Polo-like kinase 1 antibody
    • Serine/threonine protein kinase antibody
    • Serine/threonine protein kinase 13 antibody
    • Serine/threonine protein kinase PLK1 antibody
    • Serine/threonine-protein kinase 13 antibody
    • Serine/threonine-protein kinase PLK1 antibody
    • STPK 13 antibody
    • STPK13 antibody
    see all

Anti-PLK1 antibody images

References for Anti-PLK1 antibody (ab47073)

ab47073 has not yet been referenced specifically in any publications.

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