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Symbol PLK1 contributors: mct - updated : 08-10-2017
HGNC name polo-like kinase 1 (Drosophila)
HGNC id 9077
Location 16p12.2      Physical location : 23.690.200 - 23.701.688
Synonym name
  • cell cycle regulated protein kinase
  • serine/threonine-protein kinase 13
  • polo-like kinase (Drosophila)
  • Synonym symbol(s) PLK, STPK13, PLK-1, MGC26269, MGC5363
    TYPE functioning gene
    STRUCTURE 11.49 kb     10 Exon(s)
    regulatory sequence Promoter
    Binding site   transcription factor
    text structure
  • TP53 and P21 are negative regulators of PLK1 transcription
  • RB proteins repress PLK1 transcription
  • MAPPING cloned Y linked N status confirmed
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    10 - 2204 68 603 - 2009 19400994
    Type ubiquitous
       expressed in (based on citations)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    Digestiveliver   highly
    Lymphoid/Immunelymph node   highly
    Reproductivefemale systemuteruscervix highly
    Skin/Tegumentskin   highly
    cell lineage
    cell lines
    at STAGE
    physiological period pregnancy
    cell cycle     cell cycle, checkpoint, G2M
    Text placenta
  • N-terminal catalytic and kinase domain
  • zinc finger protein, Krüppel related
  • an autoregulator non catalytic C terminal region
  • two POLO-box domains (PBDs), recognizing similar phosphoserine/threonine motifs, associating with two different domains of MAVS, and which mediates protein interactions
  • C-terminal regulatory domain with two polo-box domains
    interspecies homolog to rattus Plk1 (94. 20 pc)
    homolog to murine Plk1 (94.03 pc)
    intraspecies homolog to ERV3 related sequence Hplk (see TSG7C)
    FAMILY serine/threonine kinase family
    CATEGORY transcription factor
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,cytoskeleton,microtubule,mitotic spindle
  • at the centrosome during interphase
  • localize to the spindle midzone at anaphase I and telophase I
  • with PLEKHG6 colocalize at the spindle pole and central spindle during mitosis and cytokinesis
  • localizes to centrosomes and kinetochores in almost all stages of mitosis, and it also accumulates at the spindle midzone and the midbody at the onset of anaphase
  • localization of PLK1 to kinetochores required the involvement of BIRC5
  • PLK1 colocalizes with NPHP1 to the transition zone of primary cilia in epithelial cells
  • localizes to centrosomes from late G2 to metaphase, and loss of PLK1 function often induces spindle pole fragmentation and multipolar spindle formation
  • FRY and PLK1 dynamically change their subcellular localization during the cell cycle, they colocalize to centrosomes in early mitosis
  • CLIP1 colocalizes with Polo-like kinase 1 (PLK1) at kinetochores during early mitosis
  • NCAPG2 colocalizes with PLK1 at prometaphase kinetochores
  • RNF2 co&
  • 8209;localized with PLK1 at mitotic chromosomes in the prometaphase and metaphase
    basic FUNCTION
  • may be promoting genome stability by regulating DNA replication under stressful conditions
  • plays several roles in mitosis, and has been suggested to have a role in tumorigenesis
  • involved in a variety of mitotic events, including G2/M transition, centrosome maturation and separation, mitotic spindle formation, chromosome segregation, and cytokinesis
  • required for cell cycle progression not only in mitosis but also for DNA synthesis, maintenance of DNA integrity, and prevention of cell death
  • potent regulator of M phase
  • PLK1 controls centrosome maturation by phosphorylating centrosomal proteins, including NEDD1 and pericentrin
  • modulates TOPORS activity in suppressing TP53 function and have a tumorigenic potential
  • regulator of IFN induction and provide the basis for the development of inhibitors preventing the PLK1/MAVS association to sustain innate immunity
  • ERCC6L and PLK1 kinase coordinately maintain chromosome architecture during prometaphase
  • with BIRC5 are important mediators of cell survival that are required for chromosome alignment, cytokinesis, and protection from apoptosis
  • involved in phosphorylation of DCTN1 which is essential for nuclear envelope breakdown during prophase
  • kinase that is responsible for M phase-specific phosphorylation of centrobin
  • enhances centrobin activity for proper spindle formation during mitosis
  • its phosphorylation is required for centrobin function in spindle assembly during mitosis
  • PLK1 phosphorylation of DCTN1 at least partially promotes its dissociation from microtubules at late G2 and the released DCTN1 would go to nuclear enveloppe to initiate nuclear envelope breakdown
  • required for completion of nuclear envelope breakdown at late prophase
  • mitotic kinase that plays an essential role in centrosome regulation and mitotic spindle assembly
  • involved in many cell-cycle-related events, such as bipolar spindle formation and sister chromatid segregation
  • phosphorylates CLIP1 at early mitosis and maximum CLIP1 phosphorylation by CSNK2A1 likely occurs at middle/late mitosis
  • mitotic kinase governing multiple events in mitosis, and is also localized to the kinetochores as well as the centrosome
  • novel regulator of KIF2C in mammalian cells
  • responsible of direct inhibition of the PDZ ligand underlying the GORASP1 self-interaction
  • plays a pivotal role during M-phase progression
  • recruits itself to centromeres by phosphorylating and binding to a centromere scaffold, MLF1IP
  • in G2 phase, can trigger centrosome separation independently of CDK1
  • role of KIF11, PLK1 and the NIMA-family kinases NEK7 and NEK9 in the control of centrosome separation and normal mitotic progression
  • regulates CDC25B-dependent mitosis entry
  • its activity is required for the nuclear translocation of CDC25B at the G2-M transition and for its subsequent activation
  • PLK1-mediated phosphorylation of RIOK2 regulates metaphase-anaphase transition during mitotic progression
  • potential novel role of PLK1 in facilitating DNA replication under conditions of stress to maintain genomic integrity
  • critical for the initiation of centrosome maturation
  • phosphorylates the essential RAD51 recombinase at serine 14 (S14) during the cell cycle and in response to DNA damage
  • role in linking DNA damage recognition with HR repair and suggest a molecular mechanism for cancer development associated with elevated activity of PLK1
  • TCOF1 and PLK1 are critically required for proper cortical neurogenesis, which has important implications in the regulation of mammalian brain size and the pathogenesis of congenital neurodevelopmental disorders such as microcephaly
  • PLK1 regulates both the localization and activity of KIF2B during mitosis to promote the correction of k-MT attachment errors to ensure mitotic fidelity
  • is a novel transition zone signaling protein, suggesting a function of PLK1 in cilia dynamics
  • plays a crucial role in mitotic spindle pole integrity
  • because PLK1 is also involved in MT-kinetochore attachment, the defect in FRY-mediated PLK1 activation in early mitosis may also contribute to the chromosome misalignment induced by FRY depletion
  • phosphorylates SUGT1 at the kinetochores to promote timely kinetochore-microtubule attachment
  • PLK1 dynamics at kinetochores control two critical mitotic processes: initially establishing correct kinetochore-microtubule attachments and subsequently silencing the spindle checkpoint
  • controlled PLK1 activity is required for gradual biochemical and structural maturation of the centrioles and timely appendage assembly
  • activity of CDK1 and PLK1 allows spatiotemporally controlled suppression of TP53BP1 function during mitosis
  • induces maturation and distancing of the daughter centriole, allowing reduplication of the mother centriole even if the original daughter centriole is still orthogonal to it
  • plays pivotal roles in mitosis, cytokinesis and DNA damage response in eukaryotic cells
  • during the G2 to M phase transition, a portion of mitotic regulator PLK1 localizes to the kinetochores and regulates the initiation of kinetochore-microtubule attachments for proper chromosome alignment
    a component
  • PLK1 forms a ternary complex with MLF1IP and CENPQ
  • ERCC6L-PLK1 complex plays a critical role in maintaining prometaphase chromosome architecture
  • CDKN1A/NFYA/PLK1 axis critical for maintaining the checkpoint function of TP53 to prevent mitotic death in the DNA damage-induced response
    small molecule
  • PLK1 likely maintains the integrity of the spindle poles by phosphorylating KIZ
  • interacting directly with ERCC6L (recruits PLK1 to chromosome arms and disruption of this interaction abolishes PLK1 localization on chromosome arms)
  • PLK1 controls AURKA localization and function by regulating cellular levels of BORA
  • BORA/AURKA-dependent phosphorylation is a prerequisite for PLK1 to promote mitotic entry after a checkpoint-dependent arrest
  • KIF2A is regulated positively by PLK1 and negatively by Aurora A
  • SEPT9 is a putative binding partner of PLK1, which has been shown to act as a regulator of cytokinesis
  • binds and directly phosphorylates the RACGAP subunit of centralspindlin (also known as RACGAP1) at the midzone
  • PLK1 associates with TUBG1 in mitosis and PLK1 activity contributes to phosphorylation of TUBG1
  • interacting with BIRC5 during mitosis and PLK1 phosphorylates survivin at serine 20, which is essential for accurate chromosome alignment and cell proliferation but is dispensable for its anti-apoptotic activity in cancer cells
  • DCTN1 interacts with PLK1 through its C-terminal polo-box domain, which was proposed as the motif for association with its substrates
  • MAP9 and PLK1 co-localize and interact at spindle poles during mitosis and this interaction requires specifically the PBD of PLK1
  • CLIP1 is a potential PLK1 target (interacts with PLK1 through its N-terminus)
  • PLK1 binds the GORASP1 C-terminal domain under mitotic conditions
  • PLK1 activity negatively regulates CEP55 to ensure orderly abscission factor recruitment and ensures that this occurs only once cell contraction has completed
  • interacts with the MLF1IP-CENPQ complex and regulates its dissociation from mitotic kinetochores
  • RNF8 is downregulated in many cancer cells and inversely correlated with PLK1
  • PLK1 interacts with the DExH/D RNA helicase, DDX39B
  • via the formation of the NEDD1-PLK1 complex and subsequent HAUS8 phosphorylation, PLK11 regulates spindle MT-based MT nucleation to accomplish normal bipolar spindle formation and mitotic progression
  • PLK1 controls the NEK2-PPP1CC antagonism in centrosome disjunction
  • one of ATXN10 binding partners
  • RIOK2 interacts with the N-terminal domain of PLK1
  • ORC2 is a PLK1 substrate and PLK1 phosphorylates ORC2 at Ser188
  • CEP55 associates with and is phosphorylated by PLK1 during mitosis (tight regulation of CEP55 protein levels by TP53 is mediated by PLK1 phosphorylation)
  • PLK1-mediated phosphorylation of pericentriolar matrix initiates centrosome maturation by organizing the spindle pole-specific PCM lattice
  • OPTN is associated with a myosin phosphatase complex (MP), which antagonizes the mitotic function of PLK1
  • TEX14 is recruited to kinetochores (KTs) by PLK1 in a CDK1-dependent manner during early mitosis
  • TCOF1 and PLK1 are novel regulators of spindle fidelity, mitotic progression, and proliferation in the maintenance and localization of neural progenitor cells
  • PLK1 directly phosphorylates KIF2B at threonine 125 (T125) and serine 204 (S204), and these two sites differentially regulate KIF2B function
  • negatively regulates PRC1 to prevent premature midzone formation before cytokinesis (PMIDF:
  • FRY binds to PLK1 and AURKA and promotes AURKA-mediated PLK1 activation
  • PLK1, phosphorylates central element proteins SYCP1 and TEX12, and PLK-mediated phosphorylation of central element proteins is required for meiotic prophase exit
  • SUGT1, a cochaperone for HSP90AA1, 1s a novel PLK1 substrate during mitosis
  • EIF4EBP1, beyond its role in translation regulation, can function as a regulator of mitosis via interacting with PLK1, and possibly plays a role in genomic stability maintaining
  • during mitosis the kinetochore (KT)-microtubule (MT)-associated protein CLASP2 is progressively and distinctively phosphorylated by CDK1 and PLK1 kinases, concomitant with the establishment of KT-MT attachments
  • PLK1 and BUB1B cooperate to stabilize kinetochore-microtubule interactions by regulating PP2A-B56alpha-mediated dephosphorylation of AURKB substrates at the kinetochore-microtubule interface
  • PLK1 phosphorylates MISP, thus stabilizing cortical and astral microtubule attachments required for proper mitotic spindle positioning
  • CIP2A is required for mitotic progression by regulating the polo-like kinase PLK1
  • recruitment of PLK1 to centrosomes by FOPNL may act as a signal to license efficient progression of S-phase
  • BRCA1 downregulates the kinase activity of PLK1 by modulating the dynamic interactions of AURKA, BORA, and PLK1
  • STMN1 regulates mitotic entry, partially via MTs, to control localization and activation of both AURKA and PLK1
  • BRCA2, a key RAD51 binding partner, coordinates the activity of the central cell-cycle drivers CDKs and PLK1 to promote RAD51-mediated genome stability control
  • PLK1 regulates KIF2C potentially by regulating its degradation and hence controlling its turnover in mitosis
  • NCAPG2 directly interacts with the polo-box domain (PBD) of PLK1 via its highly conserved C-terminal region
  • CENPQ targets PLK1 to kinetochores and is also required for the recruitment of CENPE to kinetochores
  • BRCA1 and BRIP1 cooperatively promote interstrand crosslinker induced centrosome amplification through the activation of PLK1
  • mitotic phosphorylation of TP53BP1 by PLK1 and CDK1 that impairs the ability of TP53BP1 to bind the ubiquitinated H2A and to properly localize to the sites of DNA damage
  • is the responsible kinase for phosphorylation of IRS2 on two serine residues
  • NAXE functions as a negative regulator to block phosphorylation of NIN mediated by AURKA and PLK1
  • RSF1 directly binds PLK1
  • USP16 deubiquitinates PLK1, resulting in an enhanced interaction with kinetochore-localized proteins such as BUB1B, and thereby retains PLK1 on the kinetochores to promote proper chromosome alignment in early mitosis
  • USP16 promotes the localization and maintenance of PLK1 on the kinetochores for proper chromosome alignment
  • TOPBP1 physically binds PLK1 and promotes PLK1 kinase-mediated phosphorylation of RAD51 at serine 14, a modification required for RAD51 recruitment to chromatin
  • interaction between KMT2E and PLK1 in the cytosol that is crucial for sustaining spindle bipolarity during mitosis
  • PPP1R12A localization to kinetochores depends on CCNA1/CDK1 activity and PPP1R12A destabilizes kinetochore microtubule (k-MT) attachments by negatively regulating PLK1 at kinetochores
  • PLK1 kinase activity was required for ubiquitin&
  • 8209;dependent degradation of RNF2
  • TPX2 promotes the proliferation and migration of human Ovarian cancer cells by regulating PLK1 expression
  • ripoptosome-mediated regulation of PLK1 contributes to faithful chromosome segregation during mitosis
  • PLK1 is recruited into mitotic ripoptosomes, where PLK1's activity is controlled via RIPK1-dependent recruitment and CASP8-mediated cleavage
  • cell & other
    activated by phosphorylation of a conserved threonine residue (Thr 210) in the T-loop of the PLK1 kinase domain
    AURKA (initial activation of PLK1 is a primary function of aurora A)
    repressed by hamartin
    Other regulated by the POLO-box domain implicated in phospho-dependent substrate targeting necessary for proper mitotic progression
    inactivated in response to DNA damage
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --over  
    in primary colorectal cancers and associated with p53 accumulation
    tumoral     --over  
    in infantile hepatoblastomas with poorer outcome
    tumoral       gain of function
    in esophageal cancer
    tumoral     --over  
    in bladder cancer (confers tumor progression advantages to urothelial cancer cells, although other factors are also involved)
    induces DNA instability, which may be mediated by the accumulation of FBXO5, an inhibitor of APC/C, and geminin, an inhibitor of pre-prereplicative complex formation
    increase MAVS activity, while its overexpression inhibited MAVS
    tumoral     --over  
    associated with shortened event-free survival and was an independent prognostic factor for non-Hodgkin lymphoma
    tumoral     --over  
    of PLK1 and KIF2C activities seen in cancer cells may account for a mechanism underlying the pathogenesis of genomic instability
    Variant & Polymorphism
    Candidate gene
    Therapy target
    with TP63, may be a candidate as a molecuar target of liver tumor treatments
    new therapeutic target for non-Hodgkin lymphoma
    attractive target for the development of anticancer agents due to its importance in regulating cell-cycle progression
    for therapeutic of hepatoblastoma, and esophageal cancer