Affinage

PLK3

Serine/threonine-protein kinase PLK3 · UniProt Q9H4B4

Length
646 aa
Mass
71.6 kDa
Annotated
2026-06-10
100 papers in source corpus 27 papers cited in narrative 27 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PLK3 (PRK/FNK) is a polo-family serine/threonine kinase that functions as a multi-substrate effector coupling genotoxic, oxidative, hypoxic, and death-receptor stress signals to cell-cycle checkpoints and apoptosis (PMID:8702627, PMID:12242661). Its catalytic activity is rapidly induced by DNA damage in an ATM-dependent manner and by reactive oxygen species, and is enhanced by mitotic-specific and stress-induced phosphorylation (PMID:9677325, PMID:11551930, PMID:12242661, PMID:12548019). Within the DNA-damage checkpoint PLK3 phosphorylates Cdc25C on S191/S216 to control its nuclear accumulation and entry into mitosis, phosphorylates p53 on S20 to stabilize it and drive p21 induction and apoptosis, and primes Chk2 at S62/S73 to facilitate downstream ATM-mediated Chk2 activation and G2/M arrest (PMID:10557092, PMID:11551930, PMID:14968113, PMID:16481012); Chk2 itself acts upstream of PLK3 in this circuit (PMID:12548019). PLK3 has broad acidophilic substrate specificity and additional targets that extend its reach beyond the checkpoint: it phosphorylates HIF-1α to promote its proteasomal degradation under hypoxia, phosphorylates PTEN at T366/S370 to stabilize it and suppress Akt signaling, phosphorylates topoisomerase IIα at T1342, inhibits p73, and phosphorylates caspase-8 at T273 downstream of the CD95 DISC to amplify extrinsic apoptosis (PMID:18062778, PMID:19490146, PMID:20889502, PMID:20940307, PMID:22828320, PMID:27325299). Its tandem polo-box domain targets the enzyme to centrosomes, spindle poles, and the midbody and is itself sufficient to drive mitotic arrest and apoptosis (PMID:16478733), and via this domain PLK3 also acts downstream of MEK1 to phosphorylate VRK1 at S342 and drive Golgi fragmentation (PMID:19103756). PLK3 is negatively controlled by PP6, which constitutively dephosphorylates its T-loop T219, and by SETDB1-mediated lysine methylation that suppresses its activity toward HIF-1α (PMID:32575753, PMID:38520019). Genetic models establish PLK3 as a determinant of tumor biology and tissue homeostasis, including a requirement for PLK3-mediated p53-S20 phosphorylation in gain-of-function mutant p53 oncogenesis (PMID:33514736) and a miR-24/PLK3/cyclin E1 axis controlling cell-cycle entry in regenerating tissue (PMID:34107258).

Mechanistic history

Synthesis pass · year-by-year structured walk · 27 steps
  1. 1996 High

    Established PLK3 as a polo-family serine/threonine kinase whose expression is acutely driven by extracellular growth and cytokine signals, framing it as a stimulus-responsive kinase.

    Evidence cDNA cloning, in vitro kinase assay on recombinant protein, and serum/cytokine induction in hematopoietic cells

    PMID:8702627

    Open questions at the time
    • Physiological substrates unidentified at this stage
    • Casein used as generic substrate, not a real target
    • Regulation of kinase activity unknown
  2. 1997 High

    Defined a conserved mitotic regulatory role by showing PLK3 phosphorylates Cdc25C, peaks in S/G2, and functionally substitutes for yeast CDC5.

    Evidence In vitro kinase assay, Xenopus oocyte maturation, yeast cdc5 complementation, cell-cycle fractionation

    PMID:9353331

    Open questions at the time
    • Specific Cdc25C phosphosites not yet mapped
    • How PLK3 activity is timed to the cell cycle unresolved
  3. 1998 Medium

    Demonstrated that PLK3 activity is controlled by phosphorylation, linking mitotic-specific modification to increased catalytic output.

    Evidence Mobility-shift analysis, phosphatase reversal of immunoprecipitate kinase activity, cell-cycle synchronization

    PMID:9677325

    Open questions at the time
    • Activating phosphosite and responsible kinase not identified
    • Single lab
  4. 1999 High

    Pinned down Cdc25C serine 216 as a direct PLK3 site and showed physical PLK3-Cdc25C association, connecting PLK3 to the checkpoint phosphosite shared with Chk1/Chk2.

    Evidence Purified recombinant kinase assay, K52R kinase-dead mutant, co-IP, affinity chromatography, phosphopeptide mapping

    PMID:10557092

    Open questions at the time
    • In vivo consequence of S216 phosphorylation on checkpoint not directly tested
    • Relationship to Chk1/Chk2 targeting of the same site unresolved
  5. 1999 Medium

    Identified the C-terminal polo-box domain as a protein-interaction module (binding CIB) and showed stimulus-driven neuronal induction and dendritic targeting, expanding PLK3 beyond cell cycle.

    Evidence Two-hybrid screen, co-IP, co-localization, LTP stimulation paradigms

    PMID:10523297

    Open questions at the time
    • Functional consequence of CIB binding unknown
    • Neuronal substrate not defined
  6. 2000 Medium

    Linked PLK3 to cytokinesis and apoptosis through midbody/cortex localization, and showed the C-terminal domain rather than catalytic activity drives the apoptotic phenotype.

    Evidence Overexpression, EGFP live imaging, TUNEL, Bcl-2 epistasis, domain mutants

    PMID:11156373

    Open questions at the time
    • Overexpression may not reflect endogenous function
    • Mechanism by which the C-terminal domain triggers apoptosis unresolved
  7. 2001 High

    Placed PLK3 in the ATM-dependent DNA-damage response as a direct p53 S20 kinase that stabilizes p53 and enforces growth suppression.

    Evidence Co-IP, GST pull-down, in vitro kinase assay, phosphospecific blotting, ATM-dependence, K52R mutant, p21/proliferation readouts

    PMID:11551930

    Open questions at the time
    • Direct ATM target on PLK3 not mapped
    • Quantitative contribution to p53 stabilization versus other kinases unresolved
  8. 2002 High

    Resolved the regulatory architecture of PLK3 activation by distinguishing ATM-dependent (DNA damage) from ATM-independent (spindle disruption) phosphorylation and identifying Chk2 and p53 as substrates within high-molecular-weight complexes.

    Evidence Sizing-column fractionation, IP kinase assays, in vitro phosphorylation, ATM epistasis, tubulin co-elution

    PMID:12242661

    Open questions at the time
    • Composition of the >600 kDa complexes not defined
    • Direct activating phosphosite still unmapped
  9. 2002 Medium

    Showed reciprocal regulation with Chk2, placing Chk2 upstream as an activator of PLK3 during the oxidative/DNA-damage response.

    Evidence ROS treatment, in vitro kinase assay with immunoprecipitated Chk2 stimulating recombinant PLK3, co-IP, ectopic Chk2 expression

    PMID:12548019

    Open questions at the time
    • Whether Chk2 activates PLK3 directly or via complex assembly unclear
    • Single lab
  10. 2004 High

    Established the functional output of PLK3-Cdc25C phosphorylation by mapping S191/S198 and showing phosphorylation controls Cdc25C nuclear accumulation and Cdc2-Y15 status.

    Evidence In vitro kinase assay, phosphomimetic/phospho-null Cdc25C mutants, immunofluorescence, Cdc2-Y15 blotting, siRNA rescue

    PMID:14968113

    Open questions at the time
    • Endogenous timing of PLK3 action on Cdc25C during checkpoint recovery not addressed
  11. 2006 High

    Positioned PLK3 upstream of ATM-mediated Chk2 activation by showing PLK3 phosphorylation of Chk2 S73 primes T68 phosphorylation and is required for G2/M checkpoint maintenance.

    Evidence In vitro kinase assay, S73A mutant, rescue, ATM epistasis, IP kinase assay, G2/M checkpoint assay, recombinant PLK3 rescue in Chk2-deficient cells

    PMID:16481012

    Open questions at the time
    • Order of PLK3 vs ATM action in vivo not fully time-resolved
    • How PLK3 itself becomes activated upstream of Chk2 unresolved
  12. 2006 Medium

    Defined the tandem polo-box domain as both the localization determinant (centrosome/spindle pole/midbody) and a sufficient driver of mitotic arrest and apoptosis.

    Evidence Domain construct expression, immunofluorescence in HeLa/U2OS, cell-cycle and apoptosis assays

    PMID:16478733

    Open questions at the time
    • Phosphopeptide ligands recognized by the PBD in vivo not identified
    • Overexpression-based phenotypes
  13. 2008 High

    Extended PLK3 signaling to Golgi dynamics by identifying VRK1-S342 as a substrate and placing PLK3 between MEK1 and VRK1 in the Golgi fragmentation pathway.

    Evidence Reciprocal co-IP, pull-down, co-localization, in vitro kinase assay, S342 mutagenesis, siRNA, MEK1 inhibitor epistasis

    PMID:19103756

    Open questions at the time
    • Physiological trigger for MEK1-PLK3-VRK1 Golgi pathway unclear
    • How PLK3 is recruited to Golgi not defined
  14. 2008 Medium

    Defined PLK3 acidophilic substrate specificity by mapping topoisomerase IIα T1342 and showing the +2/+4 acidic determinants distinguish PLK3 from PLK1.

    Evidence In vitro kinase assay with synthetic peptides, co-IP, phosphospecific blotting, overexpression

    PMID:18062778

    Open questions at the time
    • Cellular consequence of T1342 phosphorylation on topoisomerase IIα function not established
  15. 2009 Medium

    Showed PLK3 negatively regulates the p53-family member p73 by phosphorylation, reducing its stability and pro-apoptotic transcriptional activity.

    Evidence Co-IP, GST pull-down, in vitro kinase assay, luciferase reporter, kinase-dead mutant, siRNA, flow cytometry

    PMID:19490146

    Open questions at the time
    • Phosphosite on p73 not mapped
    • Reconciliation with PLK3 pro-apoptotic roles elsewhere unresolved
  16. 2010 High

    Connected PLK3 to hypoxia by showing it phosphorylates HIF-1α to promote its degradation, with genetic null cells accumulating HIF-1α.

    Evidence IP/pull-down, recombinant kinase assay, mass spectrometry sites, half-life analysis, PLK3-null MEFs

    PMID:20889502

    Open questions at the time
    • Mechanism linking phosphorylation to proteasomal targeting not detailed
    • Later KO study found no HIF-1α phenotype, indicating context dependence
  17. 2010 High

    Identified PLK3 as a positive regulator of PTEN stability via T366/S370 phosphorylation, linking it to suppression of PI3K/Akt signaling.

    Evidence In vitro kinase assay, mass spectrometry, phosphospecific blotting, PLK3-null MEFs, MG132 rescue, Akt/GSK3β assays

    PMID:20940307

    Open questions at the time
    • E3 ligase/proteasomal machinery acting on unphosphorylated PTEN not identified
  18. 2012 Medium

    Generalized the PLK3 acidophilic consensus by identifying additional in vitro substrates (HSP90, GRP-94, β-tubulin, calumenin, 14-3-3ε) and mapping their phosphosites.

    Evidence Cell-lysate kinase assay, 2D gel, mass spectrometry phosphosite mapping

    PMID:22828320

    Open questions at the time
    • In vivo relevance of these substrates not tested
    • Lysate assay may capture indirect phosphorylation
  19. 2013 Medium

    Characterized Rho-binding specificity of PRK3 HR1 domains, defining a RhoB-selective interaction module.

    Evidence Quantitative binding affinity measurements and thermal stability assays with HR1a/HR1b constructs

    PMID:24128008

    Open questions at the time
    • Functional consequence of Rho binding for PLK3 signaling unaddressed
    • Note: this finding may reflect a distinct PRK protein family and is not integrated with the kinase activity literature
  20. 2016 High

    Placed PLK3 within extrinsic apoptosis as a DISC-dependent caspase-8 T273 kinase that amplifies CD95-induced cell death.

    Evidence Co-IP, CRISPR/Cas9 KO, kinase activity assay, T273A rescue, CD95/FADD/caspase-8 KO epistasis

    PMID:27325299

    Open questions at the time
    • How DISC formation activates PLK3 catalytically not resolved
  21. 2016 Medium

    Demonstrated cell-type-specific hypoxic outcomes governed by PLK3 transcriptional control, dictating apoptosis versus differentiation in corneal epithelium.

    Evidence Plk3-/- mouse corneas, TUNEL, cell-cycle analysis, p63/keratin 12 and c-Jun phosphorylation readouts

    PMID:27281822

    Open questions at the time
    • Transcriptional regulators suppressing Plk3 in limbal stem cells not identified
    • Direct substrate driving c-Jun phosphorylation unclear
  22. 2020 Medium

    Revised the PLK3 activation model by identifying PP6 as a T-loop (T219) phosphatase and showing, unlike PLK1, T219 phosphorylation does not boost activity; CRISPR KO failed to reproduce several reported stress phenotypes.

    Evidence CRISPR KO in RPE cells, mass spectrometry (PP6), IP, recombinant kinase assay, T219 phosphospecific blotting, RNAi

    PMID:32575753

    Open questions at the time
    • Discrepancy with earlier HIF-1α/DNA-damage phenotypes unresolved
    • True T-loop activation mechanism of PLK3 still undefined
  23. 2021 Medium

    Established PLK3-mediated p53-S20 phosphorylation as mechanistically required for gain-of-function mutant p53 oncogenesis in vivo.

    Evidence PLK3 KO mouse, conditional LSL p53-R172H/K-Ras-G12D alleles, p53-S20 phosphospecific blotting, transactivation and tumor growth assays

    PMID:33514736

    Open questions at the time
    • How the same S20 phosphorylation supports both tumor suppression and GOF oncogenesis context-dependently unresolved
  24. 2021 Medium

    Defined a miR-24/PLK3/cyclin E1 axis controlling cell-cycle entry and tissue regeneration in hair follicle progenitors.

    Evidence miR-24 conditional gain/loss of function, target validation, CCNE1 measurement, in vivo hair regeneration assay

    PMID:34107258

    Open questions at the time
    • Direct PLK3 substrate linking to CCNE1 induction not identified
  25. 2023 Medium

    Showed PLK3 phosphorylates influenza nucleoprotein at S482 to regulate NP oligomerization, polymerase activity, and viral growth, identifying a host-kinase role in viral replication.

    Evidence Co-IP, in vitro phosphorylation, S482 mutagenesis, polymerase and viral growth assays

    PMID:37874309

    Open questions at the time
    • Whether PLK3 is recruited to viral ribonucleoprotein in infected cells not shown
  26. 2023 Low

    Proposed TUBA1A as a cytoplasmic inhibitor of PLK3 that gates APC/C and Foxm1-driven mitotic transition in glioblastoma.

    Evidence Co-IP, TUBA1A knockdown, PLK3 activation assays, APC/C assays, xenograft growth

    PMID:37873730

    Open questions at the time
    • Mechanism of PLK3 activation/inhibition by TUBA1A poorly defined
    • Single lab, Co-IP without reciprocal validation
  27. 2024 Medium

    Identified SETDB1-mediated lysine methylation (K106/K200), scaffolded by lncRNA LINC00115, as a post-translational brake on PLK3 activity toward HIF-1α in drug-resistant breast cancer stem-like cells.

    Evidence RNA pull-down/RIP, mass spectrometry, CRISPR KO, methylation-specific and HIF-1α stability assays

    PMID:38520019

    Open questions at the time
    • How methylation mechanistically impairs catalysis not defined
    • Complex multi-component system, single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • The true physiological activation mechanism of PLK3 and the reconciliation of conflicting stress-response phenotypes across genetic models remain unresolved.
  • Activating upstream kinase/event for endogenous PLK3 unmapped given that T219 phosphorylation does not enhance activity
  • Discrepancy between PLK3-null MEF phenotypes and CRISPR KO negative results for HIF-1α/DNA damage unexplained
  • Structural basis of polo-box-mediated substrate/localization targeting not determined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 10 GO:0016740 transferase activity 4 GO:0008092 cytoskeletal protein binding 2 GO:0140097 catalytic activity, acting on DNA 1
Localization
GO:0005829 cytosol 2 GO:0005794 Golgi apparatus 1 GO:0005815 microtubule organizing center 1 GO:0005856 cytoskeleton 1
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-8953897 Cellular responses to stimuli 4 R-HSA-5357801 Programmed Cell Death 3 R-HSA-73894 DNA Repair 3 R-HSA-162582 Signal Transduction 2
Partners
CASP8CDC25CCHEK2HIF1APPP6CPTENTP53VRK1
Complex memberships
PP6 phosphatase complex

Evidence

Reading pass · 27 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 PRK/PLK3 encodes a protein serine/threonine kinase with an N-terminal catalytic domain homologous to polo-family kinases (CDC5, Drosophila polo, PLK1) and a C-terminal regulatory domain; recombinant protein strongly phosphorylates casein but not histone H1 in vitro; expression is induced by serum and cytokines (IL-3, thrombopoietin) in hematopoietic cells without requiring new protein synthesis. cDNA cloning, in vitro kinase assay with recombinant protein, Northern blotting, serum/cytokine stimulation experiments The Journal of biological chemistry High 8702627
1997 Human PRK/PLK3 phosphorylates Cdc25C in vitro, peaks in kinase activity during late S and G2 phases, potentiates progesterone-induced meiotic maturation of Xenopus oocytes when overexpressed, delays oocyte maturation with antisense transcripts, and rescues the temperature-sensitive CDC5 mutant in S. cerevisiae, establishing a conserved mitotic regulatory role. In vitro kinase assay with recombinant baculovirus-expressed protein, Xenopus oocyte maturation assay, yeast complementation of cdc5 mutant, cell-cycle fractionation The Journal of biological chemistry High 9353331
1998 Fnk/PLK3 protein is present in quiescent cells, increases in abundance from G1 to mitosis, undergoes mitotic-specific phosphorylation that causes a mobility shift and correlates with increased kinase activity; dephosphorylation by phosphatase treatment of mitotic immunoprecipitates reduces this activity, demonstrating phosphorylation-dependent kinase activation. SDS-PAGE mobility shift analysis, phosphatase treatment, immunoprecipitation kinase assay, cell-cycle synchronization The Biochemical journal Medium 9677325
1999 Purified recombinant Prk/PLK3 directly phosphorylates Cdc25C in vitro on serine 216 (the major site also targeted by Chk1/Chk2); kinase-defective PrkK52R mutant cannot phosphorylate Cdc25C; Prk and Cdc25C physically interact by co-immunoprecipitation and affinity chromatography; when co-infected with Prk baculovirus, Cdc25C acquires autophosphorylating kinase activity dependent on catalytically active Prk. In vitro kinase assay with purified recombinant baculovirus proteins, co-immunoprecipitation, affinity chromatography, phosphopeptide mapping, active-site mutant (K52R) Oncogene High 10557092
1999 Fnk/PLK3 interacts specifically with CIB (Ca2+- and integrin-binding protein) via a conserved C-terminal polo-box domain; Fnk and Snk mRNA levels are dramatically induced in neurons by stimuli that produce long-term potentiation; induced Fnk protein is targeted to dendrites of activated neurons. Two-hybrid screen, co-immunoprecipitation, co-localization in mammalian cells, LTP stimulation paradigms, subcellular fractionation/localization The EMBO journal Medium 10523297
2000 Overexpression of PLK3 in mammalian cells induces chromatin condensation, apoptosis, and incomplete cytokinesis; EGFP-Plk3 localizes to the cellular cortex and cell midbody during mitotic exit, consistent with a cytokinesis role; Bcl-2 co-expression cannot block the apoptotic phenotype; the C-terminal domain (but not catalytic activity) is required for apoptosis induction. Transfection/overexpression, EGFP live-cell imaging, TUNEL assay, Bcl-2 co-expression epistasis, deletion/domain mutant analysis Cancer research Medium 11156373
2001 Plk3 physically interacts with p53, and this interaction is enhanced upon DNA damage; recombinant Plk3 phosphorylates a GST-p53 fusion in vitro on serine 20; expression of kinase-defective Plk3(K52R) reduces p53-S20 phosphorylation, decreases p21 levels, and increases cell proliferation; Plk3 kinase activity is rapidly induced by DNA damage in an ATM-dependent manner, while Plk1 activity is reduced; kinase-active Plk3 overexpression induces apoptosis. Co-immunoprecipitation, GST pull-down, in vitro kinase assay with recombinant proteins, immunoblotting with phosphospecific antibodies, ATM-dependent activation assay, kinase-dead mutant expression The Journal of biological chemistry High 11551930
2002 Plk3 becomes phosphorylated following DNA damage (ATM-dependent) or mitotic spindle disruption (ATM-independent); phosphorylation enhances kinase activity; Plk3 physically associates with Chk2 and p53 and phosphorylates both as substrates; phosphorylated Plk3 also co-elutes with unpolymerized tubulin; Plk3 exists in multiple high-molecular-weight complexes (150–>600 kDa) whose composition changes upon phosphorylation. Sizing column fractionation, immunoprecipitation kinase assay, in vitro phosphorylation with recombinant proteins, ATM inhibition/genetic dependence, tubulin co-elution Oncogene High 12242661
2002 Plk3 is rapidly activated by reactive oxygen species in normal diploid fibroblasts (WI-38), correlating with increased p53 levels; Plk3 physically interacts with Chk2 (enhanced by DNA damage); Chk2 immunoprecipitated from Plk3-expressing (T47D) cells stimulates the in vitro kinase activity of recombinant Plk3 more than Chk2 from Plk3-deficient (Daudi) cells; ectopic Chk2 expression activates cellular Plk3, placing Chk2 upstream of Plk3 in the DNA damage response. In vitro kinase assay with purified recombinant Plk3, co-immunoprecipitation, ectopic Chk2 expression, ROS treatment Cell cycle (Georgetown, Tex.) Medium 12548019
2004 Plk3 phosphorylates Cdc25C primarily on S191 and secondarily on S198 in vitro; a phosphomimetic S191D mutant accumulates in the nucleus while S191A facilitates nuclear exclusion; Plk3-WT overexpression drives Cdc25C nuclear accumulation and decreases Cdc2 Y15 phosphorylation; kinase-dead Plk3 overexpression fails to relocalize Cdc25C; the effect is reversed by Plk3 siRNA co-expression. In vitro kinase assay, transfection of phosphomimetic/phospho-null Cdc25C mutants, subcellular localization by immunofluorescence, immunoblotting for Cdc2-Y15, siRNA rescue Oncogene High 14968113
2006 Plk3 phosphorylates Chk2 at S62 and S73 in vitro; S73 phosphorylation by Plk3 facilitates subsequent ATM-dependent phosphorylation of Chk2 on T68 in response to DNA damage; Chk2-S73A mutant fails to associate with large complexes in vivo, has reduced kinase activity toward Cdc25C, is inefficiently phosphorylated at T68 by ATM, and cannot maintain G2/M checkpoint (Cdc2-Y15 hypophosphorylated); in Chk2-deficient Daudi cells, Chk2 kinase activity toward Cdc25C is weak and is restored dose-dependently by adding recombinant Plk3. In vitro kinase assay, site-directed mutagenesis (S73A), transfection/rescue, ATM epistasis, immunoprecipitation kinase assay, G2/M checkpoint assay Mutation research High 16481012
2006 The Polo box domain (PBD) of Plk3, requiring both polo boxes, is sufficient for centrosome, spindle pole, and midbody localization; overexpression of the PBD (but not the kinase domain) causes mitotic arrest, cytokinesis defects, and apoptosis; Plk3 PBD is more potent than Plk1 PBD in suppressing proliferation. Ectopic expression of domain constructs, immunofluorescence localization in HeLa and U2OS cells, cell-cycle analysis, apoptosis assay The Journal of biological chemistry Medium 16478733
2008 Plk3 interacts with VRK1 (forming a stable complex detected by reciprocal immunoprecipitation and pull-down); VRK1 co-localizes with Plk3 at the Golgi apparatus; Plk3 phosphorylates the C-terminal region of VRK1 specifically at Ser342; VRK1-S342 substitution mutants are catalytically active but block Golgi fragmentation; Plk3 functions downstream of MEK1 and upstream of VRK1 in the Golgi fragmentation pathway; kinase-dead Plk3, VRK1 siRNA, or the MEK1 inhibitor PD98059 all inhibit MEK1/Plk3-induced Golgi fragmentation. Reciprocal co-immunoprecipitation, pull-down, immunofluorescence co-localization, in vitro kinase assay, site-directed mutagenesis (S342), siRNA knockdown, epistasis with MEK1 inhibitor and kinase-dead constructs Molecular and cellular biology High 19103756
2008 Plk3 phosphorylates topoisomerase IIα at Thr1342 in vitro using a synthetic peptide and recombinant protein; Thr1342 is not recognized by Plk1; acidic residues at positions +2 and +4 relative to the phosphosite are positive determinants for Plk3 but not Plk1 specificity; Plk3 overexpression induces Thr1342 phosphorylation in cellular topoisomerase IIα; Plk3 and topoisomerase IIα physically interact in cells. In vitro kinase assay with synthetic peptides, co-immunoprecipitation in cells, immunoblotting with phosphospecific antibody, overexpression The Biochemical journal Medium 18062778
2009 Plk3 physically interacts with p73 (by co-immunoprecipitation and GST pull-down); Plk3 phosphorylates the N-terminal portion of p73 in vitro; Plk3 inhibits p73-mediated transcriptional activity and pro-apoptotic function; kinase-deficient Plk3 fails to inhibit p73, demonstrating kinase-activity dependence; Plk3 reduces p73 protein stability; Plk3 knockdown increases p73 stability and promotes cisplatin-induced apoptosis. Co-immunoprecipitation, GST pull-down, in vitro kinase assay, luciferase reporter assay, RT-PCR, kinase-dead mutant, siRNA knockdown, flow cytometry (apoptosis) Genes to cells : devoted to molecular & cellular mechanisms Medium 19490146
2010 Plk3 physically interacts with HIF-1α under hypoxia (by immunoprecipitation and pull-down); purified recombinant Plk3, but not a kinase-defective mutant, phosphorylates HIF-1α in vitro causing a major mobility shift; mass spectrometry identified two serine residues as Plk3 phosphorylation sites; phosphomutant HIF-1α has a much longer half-life than wild-type, demonstrating Plk3 promotes HIF-1α degradation; PLK3-null MEFs contain elevated HIF-1α under hypoxia. Immunoprecipitation, pull-down, in vitro kinase assay with purified recombinant Plk3, mass spectrometry, cycloheximide chase/pulse-chase, PLK3-null MEFs The Journal of biological chemistry High 20889502
2010 Plk3 phosphorylates PTEN in vitro at Thr366 and Ser370 (identified by mass spectrometry and confirmed by phosphospecific antibody); kinase-defective Plk3 mutant cannot phosphorylate PTEN; PLK3-null MEFs have reduced PTEN levels and increased Akt1 activation; Plk3-targeting PTEN mutants are expressed at reduced levels associated with enhanced PDK1 activity; the reduced PTEN in PLK3-null MEFs is stabilized by the proteasome inhibitor MG132, demonstrating Plk3 phosphorylation stabilizes PTEN. In vitro kinase assay, mass spectrometry, phosphospecific immunoblotting, PLK3-null MEFs, kinase-dead mutant, MG132 proteasome inhibitor treatment, Akt/GSK3β activation assays The Journal of biological chemistry High 20940307
2012 In vitro PLK3 phosphorylates HSP90, GRP-94, β-tubulin, calumenin, and 14-3-3 epsilon in cell lysate kinase assays; phosphosites in these substrates were mapped by mass spectrometry and used to define PLK3 substrate consensus determinants as acidophilic (requiring acidic residues surrounding the target Ser/Thr). Cell lysate kinase assay, 2D gel electrophoresis, mass spectrometry substrate identification and phosphosite mapping Biochimica et biophysica acta Medium 22828320
2013 PRK3 HR1a and HR1b domains bind RhoA, RhoB, and RhoC with different affinities; PRK3 HR1b domain uniquely mediates a RhoB-specific interaction requiring both the C-terminus of RhoB and the HR1b domain; RhoB binds all PRK isoforms with higher affinity than RhoA or RhoC; the PRK2/PRK3 HR1 domains generally bind Rho proteins less tightly than PRK1. Quantitative binding affinity measurements (surface plasmon resonance or equivalent), thermal stability assays, domain constructs encompassing HR1a and HR1b Biochemistry Medium 24128008
2016 PLK3 is identified as a new interaction partner of the death receptor CD95; PLK3 enzymatic activity increases upon CD95 ligand stimulation; knockout of caspase-8, CD95, or FADD prevents PLK3 activation, establishing requirement for a functional DISC; PLK3 phosphorylates caspase-8 at Thr273, stimulating its pro-apoptotic function; non-phosphorylatable caspase-8-T273A mutant or PLK3 CRISPR/Cas9 knockout reduces caspase-8 processing after CD95 stimulation. Co-immunoprecipitation, CRISPR/Cas9 knockout, kinase activity assay, site-directed mutagenesis (T273A rescue experiment), genetic epistasis (CD95/FADD/caspase-8 KO) Cell research High 27325299
2016 Hypoxic stress activates Plk3 signaling and c-Jun/AP-1 in corneal epithelial cells leading to apoptosis, but suppresses Plk3 activity at the transcription level in limbal stem cells (HLS), resulting in differentiation instead of apoptosis; hypoxia-induced c-Jun phosphorylation is not observed in HLS cells because Plk3 is suppressed; Plk3-deficient (Plk3-/-) mouse corneas show altered limbal stem cell differentiation and center epithelial apoptosis patterns confirming pathway dependence. Plk3-/- mouse model, DNA fragmentation, TUNEL assay, cell cycle analysis, p63/keratin 12 expression, c-Jun phosphorylation, gene expression analysis The Journal of biological chemistry Medium 27281822
2020 PLK3 interacts with the PP6 (protein phosphatase 6) complex via its polo box domain; PLK3 is phosphorylated at Thr219 in its T-loop; PP6 constantly dephosphorylates Thr219; unlike PLK1, phosphorylation of PLK3-Thr219 does not upregulate enzymatic activity, indicating distinct activation mechanisms between PLK1 and PLK3; CRISPR/Cas9-generated PLK3 knockout cells do not show impaired HIF-1α stabilization under hypoxia, p-c-Jun under osmotic stress, or DNA damage response dynamics. CRISPR/Cas9 knockout in RPE cells, mass spectrometry (PP6 as interactor), immunoprecipitation, in vitro kinase assay with purified EGFP-PLK3, phosphospecific immunoblotting (T219), RNAi knockdown Cells Medium 32575753
2021 PLK3 phosphorylates GOF mutant p53 at serine 20; PLK3 knockout attenuates S20 phosphorylation and reduces transactivation and oncogenicity by GOF p53; GOF p53 TAD mutations (L25Q/W26S) that reduce S20 phosphorylation lose tumorigenicity; these data place PLK3-mediated S20 phosphorylation as mechanistically required for GOF p53-driven oncogenesis. PLK3 knockout mouse model, conditional knock-in alleles (LSL p53-R172H, K-Ras-G12D), phosphospecific immunoblotting for p53-S20, transactivation assays, tumor growth analysis Nature communications Medium 33514736
2023 PLK3 interacts with viral nucleoprotein (NP) of swine influenza H1N1; PLK3 overexpression increases NP phosphorylation and oligomerization; PLK3 phosphorylates NP at serine 482 (S482), and S482 phosphorylation regulates NP oligomerization, viral polymerase activity, and viral growth. Co-immunoprecipitation, in vitro phosphorylation assay, site-directed mutagenesis (S482), viral polymerase activity assay, viral growth assay Emerging microbes & infections Medium 37874309
2024 SETDB1 methylates PLK3 at K106 and K200 (scaffolded by the lncRNA LINC00115); PLK3 methylation decreases PLK3 phosphorylation of HIF1α and increases HIF1α stability in drug-resistant breast cancer stem-like cells; this establishes SETDB1-mediated lysine methylation as a post-translational modification that suppresses PLK3 kinase activity toward HIF1α. RNA pull-down, RNA immunoprecipitation, mass spectrometry, CRISPR/Cas9 knockout, methylation-specific assays, HIF1α stability assays Molecular cancer Medium 38520019
2021 miR-24 directly targets Plk3 mRNA in hair follicle progenitors; miR-24 upregulation blunts growth responsiveness and retards hair regeneration, while its ablation leads to hyper-sensitized growth responsiveness and precocious hair regeneration; reduced Plk3 downstream of miR-24 leads to decreased CCNE1 (cyclin E1) expression, limiting cell-cycle entry. miR-24 conditional overexpression and ablation in skin epithelium, target validation (miR-24 → Plk3), cell-cycle analysis, CCNE1 expression measurement, in vivo hair regeneration assay Cell reports Medium 34107258
2023 TUBA1A (tubulin alpha 1a) interacts with PLK3 in the cytoplasm and inhibits its activation; this interaction licenses APC/C activation and Foxm1-mediated metaphase-to-anaphase transition; TUBA1A knockdown causes mitotic arrest and reduces GBM tumor growth in a PLK3-dependent manner. Co-immunoprecipitation, TUBA1A knockdown, PLK3 activation assays, APC/C activity assays, xenograft tumor growth assay FEBS letters Low 37873730

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 Apoptosis, necrosis, proliferation, and myofibroblast generation in the stroma following LASIK and PRK. Experimental eye research 331 12589777
2009 Comparison of sequential vs same-day simultaneous collagen cross-linking and topography-guided PRK for treatment of keratoconus. Journal of refractive surgery (Thorofare, N.J. : 1995) 226 19772257
2007 Collagen cross-linking (CCL) with sequential topography-guided PRK: a temporizing alternative for keratoconus to penetrating keratoplasty. Cornea 213 17667633
2001 Plk3 functionally links DNA damage to cell cycle arrest and apoptosis at least in part via the p53 pathway. The Journal of biological chemistry 181 11551930
1999 The polo-like protein kinases Fnk and Snk associate with a Ca(2+)- and integrin-binding protein and are regulated dynamically with synaptic plasticity. The EMBO journal 176 10523297
2010 Management of corneal ectasia after LASIK with combined, same-day, topography-guided partial transepithelial PRK and collagen cross-linking: the athens protocol. Journal of refractive surgery (Thorofare, N.J. : 1995) 145 21117539
1998 Neutralizing antibody to TGFbeta modulates stromal fibrosis but not regression of photoablative effect following PRK. Current eye research 145 9678420
2000 Modulation of acute inflammation and keratocyte death by suturing, blood, and amniotic membrane in PRK. Investigative ophthalmology & visual science 138 10967044
1996 Prk, a cytokine-inducible human protein serine/threonine kinase whose expression appears to be down-regulated in lung carcinomas. The Journal of biological chemistry 127 8702627
2002 Mammalian Polo-like kinase 3 (Plk3) is a multifunctional protein involved in stress response pathways. Oncogene 119 12242661
2015 Long noncoding RNA HOXA-AS2 promotes gastric cancer proliferation by epigenetically silencing P21/PLK3/DDIT3 expression. Oncotarget 106 26384350
2003 A novel inducible transactivation domain in the androgen receptor: implications for PRK in prostate cancer. The EMBO journal 92 12514133
1997 Human Prk is a conserved protein serine/threonine kinase involved in regulating M phase functions. The Journal of biological chemistry 90 9353331
2013 Plasma rich in growth factors (PRGF-Endoret) stimulates corneal wound healing and reduces haze formation after PRK surgery. Experimental eye research 88 23872360
2015 The role of Plk3 in oncogenesis. Oncogene 86 25915845
2010 Plk3 functions as an essential component of the hypoxia regulatory pathway by direct phosphorylation of HIF-1alpha. The Journal of biological chemistry 83 20889502
2000 Incomplete cytokinesis and induction of apoptosis by overexpression of the mammalian polo-like kinase, Plk3. Cancer research 77 11156373
2002 Genotoxic stress-induced activation of Plk3 is partly mediated by Chk2. Cell cycle (Georgetown, Tex.) 68 12548019
2004 Cdc25C phosphorylation on serine 191 by Plk3 promotes its nuclear translocation. Oncogene 65 14968113
1999 The physical association and phosphorylation of Cdc25C protein phosphatase by Prk. Oncogene 56 10557092
2010 Regulation of PTEN stability and activity by Plk3. The Journal of biological chemistry 55 20940307
2000 Measurement of mRNAs for TGFss and extracellular matrix proteins in corneas of rats after PRK. Investigative ophthalmology & visual science 55 11095603
2008 Plk3 interacts with and specifically phosphorylates VRK1 in Ser342, a downstream target in a pathway that induces Golgi fragmentation. Molecular and cellular biology 52 19103756
2000 PRK, a cell cycle gene localized to 8p21, is downregulated in head and neck cancer. Genes, chromosomes & cancer 52 10679924
2006 Polo box domain of Plk3 functions as a centrosome localization signal, overexpression of which causes mitotic arrest, cytokinesis defects, and apoptosis. The Journal of biological chemistry 51 16478733
2024 LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling. Molecular cancer 49 38520019
1998 Expression and phosphorylation of fibroblast-growth-factor-inducible kinase (Fnk) during cell-cycle progression. The Biochemical journal 49 9677325
2005 The Plk3-Cdc25 circuit. Oncogene 46 15640846
2006 Priming phosphorylation of Chk2 by polo-like kinase 3 (Plk3) mediates its full activation by ATM and a downstream checkpoint in response to DNA damage. Mutation research 45 16481012
2000 Adhesion induced expression of the serine/threonine kinase Fnk in human macrophages. Oncogene 45 11039900
2016 Ultrastructural Changes and Corneal Wound Healing After SMILE and PRK Procedures. Current eye research 38 26863271
2016 Ligand stimulation of CD95 induces activation of Plk3 followed by phosphorylation of caspase-8. Cell research 38 27325299
2003 Role for RhoB and PRK in the suppression of epithelial cell transformation by farnesyltransferase inhibitors. Oncogene 35 12606940
1996 Inflammatory cells, refractive regression, and haze after excimer laser PRK. Journal of refractive surgery (Thorofare, N.J. : 1995) 35 8705713
2014 The U.S. Army Surface Ablation Study: comparison of PRK, MMC-PRK, and LASEK in moderate to high myopia. Journal of refractive surgery (Thorofare, N.J. : 1995) 34 24702577
2020 Biological effects of mitomycin C on late corneal haze stromal fibrosis following PRK. Experimental eye research 32 32905844
2013 Differential binding of RhoA, RhoB, and RhoC to protein kinase C-related kinase (PRK) isoforms PRK1, PRK2, and PRK3: PRKs have the highest affinity for RhoB. Biochemistry 32 24128008
2022 Losartan Inhibition of Myofibroblast Generation and Late Haze (Scarring Fibrosis) After PRK in Rabbits. Journal of refractive surgery (Thorofare, N.J. : 1995) 31 36476304
2012 Investigation on PLK2 and PLK3 substrate recognition. Biochimica et biophysica acta 31 22828320
2008 ROCK and PRK-2 mediate the inhibitory effect of Y-27632 on polyglutamine aggregation. FEBS letters 29 18423405
2006 Corneal ectasia after PRK: clinicopathologic case report. Cornea 29 17068463
2019 Long-Term Stability With the Athens Protocol (Topography-Guided Partial PRK Combined With Cross-Linking) in Pediatric Patients With Keratoconus. Cornea 26 31169612
2011 Identification of an interaction between the TPalpha and TPbeta isoforms of the human thromboxane A2 receptor with protein kinase C-related kinase (PRK) 1: implications for prostate cancer. The Journal of biological chemistry 25 21357687
2021 The oncogenicity of tumor-derived mutant p53 is enhanced by the recruitment of PLK3. Nature communications 24 33514736
2019 Management of progressive keratoconus with partial topography-guided PRK combined with refractive, customized CXL - a novel technique: the enhanced Athens protocol. Clinical ophthalmology (Auckland, N.Z.) 24 31040638
2005 Molecular phylogeny of the palm genus Chamaedorea, based on the low-copy nuclear genes PRK and RPB2. Molecular phylogenetics and evolution 24 16249101
2014 Efficient Engraftment of Human Induced Pluripotent Stem Cell-Derived Hepatocyte-Like Cells in uPA/SCID Mice by Overexpression of FNK, a Bcl-xL Mutant Gene. Cell transplantation 22 24806294
2008 Combination therapy with transductive anti-death FNK protein and FK506 ameliorates brain damage with focal transient ischemia in rat. Journal of neurochemistry 22 18363825
2007 Finding Plk3. Cell cycle (Georgetown, Tex.) 22 17568195
2007 Transduction of anti-cell death protein FNK protects isolated rat hearts from myocardial infarction induced by ischemia/reperfusion. Life sciences 21 17467744
1999 Caenorhabditis elegans contains structural homologs of human prk and plk. DNA sequence : the journal of DNA sequencing and mapping 21 10376213
2005 Zonal necrosis prevented by transduction of the artificial anti-death FNK protein. Cell death and differentiation 20 15692606
2017 Efficacy and Safety Comparison Between Suberoylanilide Hydroxamic Acid and Mitomycin C in Reducing the Risk of Corneal Haze After PRK Treatment In Vivo. Journal of refractive surgery (Thorofare, N.J. : 1995) 19 29227512
2013 Abortive cell cycle events in the brains of scrapie-infected hamsters with remarkable decreases of PLK3/Cdc25C and increases of PLK1/cyclin B1. Molecular neurobiology 19 23625313
2008 Plk3 phosphorylates topoisomerase IIalpha at Thr(1342), a site that is not recognized by Plk1. The Biochemical journal 19 18062778
2007 A protein derived from the fusion of TAT peptide and FNK, a Bcl-x(L) derivative, prevents cochlear hair cell death from aminoglycoside ototoxicity in vivo. Journal of neuroscience research 19 17387707
2006 Endocytic Ark/Prk kinases play a critical role in adriamycin resistance in both yeast and mammalian cells. Cancer research 19 17178891
2014 Protein Kinase C-Related Kinase (PKN/PRK). Potential Key-Role for PKN1 in Protection of Hypoxic Neurons. Current neuropharmacology 18 24851086
2007 Anti-apoptotic PTD-FNK protein suppresses lipopolysaccharide-induced acute lung injury in rats. Experimental and molecular pathology 17 17959170
2007 Prevention of chemotherapy-induced alopecia by the anti-death FNK protein. Life sciences 17 18164732
2002 Cloning and characterisation of PKB and PRK homologs from Hydra and the evolution of the protein kinase family. Development genes and evolution 17 12459919
2016 Effect of Hypoxia-regulated Polo-like Kinase 3 (Plk3) on Human Limbal Stem Cell Differentiation. The Journal of biological chemistry 16 27281822
2016 Overexpression of PLK3 Mediates the Degradation of Abnormal Prion Proteins Dependent on Chaperone-Mediated Autophagy. Molecular neurobiology 16 27344333
2018 The Acidophilic Kinases PLK2 and PLK3: Structure, Substrate Targeting and Inhibition. Current protein & peptide science 15 29366414
2009 Plk3 inhibits pro-apoptotic activity of p73 through physical interaction and phosphorylation. Genes to cells : devoted to molecular & cellular mechanisms 15 19490146
2009 Corneal endothelial cell density after femtosecond thin-flap LASIK and PRK for myopia: a contralateral eye study. Journal of refractive surgery (Thorofare, N.J. : 1995) 15 20000291
2005 The anti-cell death FNK protein protects cells from death induced by freezing and thawing. Biochemical and biophysical research communications 15 15809074
2022 Inhibition of PLK3 Attenuates Tubular Epithelial Cell Apoptosis after Renal Ischemia-Reperfusion Injury by Blocking the ATM/P53-Mediated DNA Damage Response. Oxidative medicine and cellular longevity 14 35783188
2021 miR-24 controls the regenerative competence of hair follicle progenitors by targeting Plk3. Cell reports 14 34107258
2017 Regulation of protein kinase C-related kinase (PRK) signalling by the TPα and TPβ isoforms of the human thromboxane A2 receptor: Implications for thromboxane- and androgen- dependent neoplastic and epigenetic responses in prostate cancer. Biochimica et biophysica acta. Molecular basis of disease 14 28108419
2015 FRET analysis of CP12 structural interplay by GAPDH and PRK. Biochemical and biophysical research communications 13 25666947
2020 Peptidomimetic Polo-Box-Targeted Inhibitors that Engage PLK1 in Tumor Cells and Are Selective against the PLK3 Tumor Suppressor. ChemMedChem 12 32232973
2009 Confocal microscopy of corneal stroma and endothelium after LASIK and PRK. Journal of refractive surgery (Thorofare, N.J. : 1995) 12 19848379
2001 Intron/exon organization and polymorphisms of the PLK3/PRK gene in human lung carcinoma cell lines. Genes, chromosomes & cancer 12 11746980
2023 PLK3 facilitates replication of swine influenza virus by phosphorylating viral NP protein. Emerging microbes & infections 11 37874309
2011 Mild hypothermia enhanced the protective effect of protein therapy with transductive anti-death FNK protein using a rat focal transient cerebral ischemia model. Brain research 11 22099262
2023 Parkin-mediated mitophagy is negatively regulated by FOXO3A, which inhibits Plk3-mediated mitochondrial ROS generation in STZ diabetic stress-treated pancreatic β cells. PloS one 10 37134105
2020 Phosphorylation of PLK3 Is Controlled by Protein Phosphatase 6. Cells 10 32575753
2012 Tools to discriminate between targets of CK2 vs PLK2/PLK3 acidophilic kinases. BioTechniques 10 26307252
2022 Natural COA water inhibits mitochondrial ROS-mediated apoptosis through Plk3 downregulation under STZ diabetic stress in pancreatic β-cell lines. Biochemistry and biophysics reports 9 35300109
2015 Polo-like kinase 3 (PLK3) mediates the clearance of the accumulated PrP mutants transiently expressed in cultured cells and pathogenic PrP(Sc) in prion infected cell line via protein interaction. The international journal of biochemistry & cell biology 9 25724737
2011 Topical application of the antiapoptotic TAT-FNK protein prevents aminoglycoside-induced ototoxicity. Gene therapy 8 22189415
2024 Plk3 Enhances Cisplatin Sensitivity of Nonsmall-Cell Lung Cancer Cells through Inhibition of the PI3K/AKT Pathway via Stabilizing PTEN. ACS omega 7 38434880
2023 TUBA1A licenses APC/C-mediated mitotic progression to drive glioblastoma growth by inhibiting PLK3. FEBS letters 7 37873730
2009 Overexpression of Plk3 causes morphological change and cell growth suppression in Ras pathway-activated cells. Journal of biochemistry 7 19556223
2009 A novel platelet activating factor receptor antagonist reduces cell infiltration and expression of inflammatory mediators in mice exposed to desiccating conditions after PRK. Clinical & developmental immunology 7 20049336
2007 Transduction of the anti-apoptotic PTD-FNK protein improves the efficiency of transplantation of bone marrow mononuclear cells. Journal of molecular and cellular cardiology 7 17229437
2023 PLK3 promotes the proneural-mesenchymal transition in glioblastoma via transcriptional regulation of C5AR1. Molecular biology reports 6 37568042
2012 Improvement of the post-thaw qualities of Okinawan native Agu pig sperm frozen in an extender supplemented with antiapoptotic PTD-FNK protein. Theriogenology 6 22925637
2008 Transduction of anti-cell death protein FNK suppresses graft degeneration after autologous cylindrical osteochondral transplantation. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 6 18955736
2022 PLK3 amplification and tumor immune microenvironment of metastatic tumors are linked to adjuvant treatment outcomes in uterine serous cancer. NAR cancer 5 36177381
2019 Corneal endothelial damage after simultaneous PRK and corneal cross-linking in stable keratoconus. American journal of ophthalmology case reports 4 30815621
2014 Alcohol-assisted debridement in PRK with intraoperative mitomycin C. Optometry and vision science : official publication of the American Academy of Optometry 3 25062131
2024 Comparative Analysis of Corneal Wound Healing: Differential Molecular Responses in Tears Following PRK, FS-LASIK, and SMILE Procedures. Biomedicines 2 39457602
2016 Cytoskeletal architecture and cell motility remain unperturbed in mouse embryonic fibroblasts from Plk3 knockout mice. Experimental biology and medicine (Maywood, N.J.) 2 26843517
2025 PLK3 weakens antioxidant defense and inhibits proliferation of porcine Leydig cells under oxidative stress. Scientific reports 1 39837970
2024 Activating transcription factor 3 (ATF3) and calcitonin gene-related peptide (CGRP) increase in trigeminal ganglion neurons in female rats after photorefractive keratectomy (PRK)-like corneal abrasion. Neurobiology of pain (Cambridge, Mass.) 1 39315304
2006 [Construction of pMSCV recombinant retroviral vector containing polo-like kinase 3(plk3) cDNA and its effects on cell proliferation]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 1 16388739
1993 PRK using an absorbing cell delivery system for correction of myopia from 4 to 26 D in 3251 eyes. Refractive & corneal surgery 1 8499362
2025 PLK3-Activated Mitochondrial Apoptosis Pathway in the Pathogenesis of Sepsis-Associated Acute Kidney Injury. Journal of biochemical and molecular toxicology 0 40874686

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