常规说明ab94104 is a 293T cell transfected lysate in which Human PLK1 has been transiently over-expressed using a pCMV-PLK1 plasmid. The lysate is provided in 1X Sample Buffer.
Note: For more detailed about how the transfected lysate was prepared view preparation notes
背景Function: Serine/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 specificity: Placenta and colon.
Similarity: Belongs to the protein kinase superfamily. Ser/Thr protein kinase family. CDC5/Polo subfamily.
Contains 2 POLO box domains.
Contains 1 protein kinase domain.
Developmental stage: Accumulates 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.
PTM: 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.