ID:PLK2_HUMAN DESCRIPTION: RecName: Full=Serine/threonine-protein kinase PLK2; EC=2.7.11.21; AltName: Full=Polo-like kinase 2; Short=PLK-2; Short=hPlk2; AltName: Full=Serine/threonine-protein kinase SNK; Short=hSNK; AltName: Full=Serum-inducible kinase; FUNCTION: Tumor suppressor serine/threonine-protein kinase involved in synaptic plasticity, centriole duplication and G1/S phase transition. Polo-like kinases act by binding and phosphorylating proteins are that already phosphorylated on a specific motif recognized by the POLO box domains. Phosphorylates CENPJ, NPM1, RAPGEF2, RASGRF1, SNCA, SIPA1L1 and SYNGAP1. Plays a key role in synaptic plasticity and memory by regulating the Ras and Rap protein signaling: required for overactivity-dependent spine remodeling by phosphorylating the Ras activator RASGRF1 and the Rap inhibitor SIPA1L1 leading to their degradation by the proteasome. Conversely, phosphorylates the Rap activator RAPGEF2 and the Ras inhibitor SYNGAP1, promoting their activity. Also regulates synaptic plasticity independently of kinase activity, via its interaction with NSF that disrupts the interaction between NSF and the GRIA2 subunit of AMPARs, leading to a rapid rundown of AMPAR-mediated current that occludes long term depression. Required for procentriole formation and centriole duplication by phosphorylating CENPJ and NPM1, respectively. Its induction by p53/TP53 suggests that it may participate in the mitotic checkpoint following stress. CATALYTIC ACTIVITY: ATP + a protein = ADP + a phosphoprotein. ENZYME REGULATION: Activated by phosphorylation of Thr-239. Once activated, activity is stimulated by binding target proteins (By similarity). SUBUNIT: Interacts with NSF; causing NSF dissociation from GRIA2. Interacts with CIB1 (By similarity). SUBCELLULAR LOCATION: Cytoplasm, cytoskeleton, centrosome, centriole. Cell projection, dendrite (By similarity). Note=Localizes to centrosomes during early G1 phase where it only associates to the mother centriole and then distributes equally to both mother and daughter centrioles at the onset of S phase. TISSUE SPECIFICITY: Expressed at higher level in the fetal lung, kidney, spleen and heart. INDUCTION: Directly regulated by p53/TP53. Negatively regulated by miR-126. DOMAIN: The POLO box domains act as phosphopeptide-binding module that recongnize and bind serine-[phosphothreonine/phosphoserine]- (proline/X) motifs. PLK2 recognizes and binds docking proteins that are already phosphorylated on these motifs, and then phosphorylates them (By similarity). PTM: Catalytic activity is enhanced by phosphorylation of Thr-239 (By similarity). MISCELLANEOUS: There are indications that PLK2 might act as a tumor suppressor: PLK2 is significantly down-regulated in a wide range of acute myeloid leukemias (AMLs) and B-cell lymphomas due to aberrant cytosine methylation in the CpG island located at the 5' of the PLK2 gene (PubMed:16160013, PubMed:21340720). Moreover, miR-126, a microRNA that negatively regulates PLK2 is up-regulated in AMLs, suggesting that PLK2 down-regulation by miR-126 could also contribute to leukemogenesis (PubMed:18832181). SIMILARITY: Belongs to the protein kinase superfamily. Ser/Thr protein kinase family. CDC5/Polo subfamily. SIMILARITY: Contains 2 POLO box domains. SIMILARITY: Contains 1 protein kinase domain.
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on Q9NYY3
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.
Biological Process: GO:0000082 G1/S transition of mitotic cell cycle GO:0000278 mitotic cell cycle GO:0006468 protein phosphorylation GO:0006977 DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest GO:0007052 mitotic spindle organization GO:0007093 mitotic cell cycle checkpoint GO:0007265 Ras protein signal transduction GO:0007613 memory GO:0010508 positive regulation of autophagy GO:0016310 phosphorylation GO:0016525 negative regulation of angiogenesis GO:0018105 peptidyl-serine phosphorylation GO:0032092 positive regulation of protein binding GO:0032436 positive regulation of proteasomal ubiquitin-dependent protein catabolic process GO:0032486 Rap protein signal transduction GO:0043066 negative regulation of apoptotic process GO:0043123 positive regulation of I-kappaB kinase/NF-kappaB signaling GO:0045732 positive regulation of protein catabolic process GO:0046599 regulation of centriole replication GO:0048167 regulation of synaptic plasticity GO:0060291 long-term synaptic potentiation GO:0060292 long term synaptic depression GO:0061000 negative regulation of dendritic spine development GO:0071866 negative regulation of apoptotic process in bone marrow GO:0090050 positive regulation of cell migration involved in sprouting angiogenesis GO:2000773 negative regulation of cellular senescence
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Sequence and Links to Tools and Databases 
Common Gene Haplotype Alleles 
