EC Number |
General Information |
Reference |
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2.7.11.21 | evolution |
the enzyme is a member of the polo-like kinase family. Among the five members, PLK2 is the more closely related to PLK1. The overall structure of the PLK2 PBD is similar to that of the PLK1 PBD, which is composed by two polo boxes each contain b6a structures that form a 12-stranded b sandwich domain. The edge of the interface between the two polo boxes forms the phosphorylated Ser-pSer/pThr motifs binding cleft. On the hand, the peripheral regions around the core binding cleft of the PLK2 PBD is distinct from that of the PLK1 PBD, which might confer the substrate specificity of the PBDs of the polo-like kinase family. Comparison of PLK1 and PL2 substrate binding and structure, detailed overview |
739992 |
2.7.11.21 | evolution |
the polo-box domain, PBD, is unique to the five-member family of polo-like kinases, found in only Plk1, Plk2, Plk3 and Plk5. Plk4 does not have a PBD, as it has only a single polo box. Unlike the other family members, Plk5 does not contain a kinase domain |
740315 |
2.7.11.21 | evolution |
the serine/threonine kinase Polo-like kinase 1 (Plk1) is a member of the Polo-like kinases family |
739963, 740152 |
2.7.11.21 | malfunction |
53BP1 is excluded from the chromatin in mitotic cells and did not colocalize with gH2AX in mitotic cells after damage through irradiation. Inhibition of Plk1 by BI2536 inhibitor arrests cells in mitosis and increases the mobility of 53BP. The removal of pS1618-53BP1 modification correlates to disappearance of pS10-histone H3 as well as degradation of cyclin B and Plk1 during mitotic exit |
740271 |
2.7.11.21 | malfunction |
a failure in Plk1 regulation of the timing of CENP-Q dissociation from kinetochores leads to chromosome missegregation. Inhibition of Plk1 activity greatly diminishes hyperphosphorylates, slow-migrating PBIP1 (but not the moderately phosphorylated PBIP1 forms because of the presence of Plk1-independent phosphorylation) and appears to eliminate slow-migrating CENP-Q forms |
740745 |
2.7.11.21 | malfunction |
combination treatment with PLK1 and Bcl2 pharmacological inhibitors specifically induces synergistic cell death, partly because of PLK1 inhibitor-mediated depletion of Myc and Mcl1 expression |
741007 |
2.7.11.21 | malfunction |
complete inhibition of polo kinase 1 can prevent mitotic entry for hours in a vast majority of TERT-RPE1, HeLa or RKO cells, even without prior activation of the DNA damage checkpoint |
762085 |
2.7.11.21 | malfunction |
depletion of PLK1 leads to a delay of cell cycle recovery, and apoptosis |
728226 |
2.7.11.21 | malfunction |
enzyme downregulation in metastatic prostate cancer cells enhances epithelial characteristics and inhibits cell motility |
760980 |
2.7.11.21 | malfunction |
heterozygosity of Plk4 does not lead to polyploidization and centrosome amplification |
728273 |