Affinage

CDC25B

M-phase inducer phosphatase 2 · UniProt P30305

Length
580 aa
Mass
65.0 kDa
Annotated
2026-06-09
100 papers in source corpus 49 papers cited in narrative 46 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/9 claims corpus-supported (89%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CDC25B is a dual-specificity phosphatase that triggers mitotic entry by removing the inhibitory Thr-14/Tyr-15 phosphates from CDK1, acting as the 'starter phosphatase' for the G2/M transition (PMID:8440392, PMID:9683638). Catalysis proceeds through a two-step phospho-cysteine intermediate mechanism, with the protein substrate itself supplying the catalytic acid for leaving-group protonation (PMID:8910325, PMID:10978163). Functionally, CDC25B specifically activates cyclin B1-CDK1 at centrosomes, and its loss causes G2 delay; its catalytic activity is also required for normal centrosomal gamma-tubulin recruitment and centriole/centrosome duplication (PMID:16216921, PMID:18089784, PMID:18235220). Genetic studies establish a non-redundant requirement in female meiosis—Cdc25b-null oocytes arrest in prophase with low MPF and are rescued by Cdc25b mRNA—whereas in somatic cells Cdc25A compensates for combined loss of Cdc25B and Cdc25C (PMID:11912493, PMID:15767688). CDC25B activity, localization, and abundance are tightly controlled: activating phosphorylation by Aurora-A (Ser-353), CK2 (Ser-186/187), and RSK promotes mitotic entry (PMID:15128871, PMID:16082213, PMID:12527891, PMID:23708659), while CHK1 (Ser-230) and the phosphatase Cdc14A impose inhibitory control (PMID:17003105, PMID:20956543). 14-3-3 binding to Ser-323 and cooperating low-affinity sites (Ser-151/230/309) forms an intramolecular bridge that blocks catalytic-site and nuclear-export-sequence access, sequestering CDC25B in the cytoplasm; checkpoint bypass follows disruption of this interaction (PMID:11466620, PMID:12764136, PMID:15173315). Nucleo-cytoplasmic shuttling is governed by defined NES and NLS elements together with PLK1-driven nuclear import, and PKA-mediated Ser-321 phosphorylation maintains 14-3-3-dependent cytoplasmic sequestration to enforce meiotic prophase arrest (PMID:10822367, PMID:15456846, PMID:19185590, PMID:19223768, PMID:19035343). CDC25B is degraded constitutively by SCF-β-TrCP via a non-phosphorylated DDG motif and in a CDK1-cyclin A-dependent proteasomal manner, with stress kinases (JNK/p38 via Ser-101) and MEK1 also driving its destabilization (PMID:15845771, PMID:9407044, PMID:19638579, PMID:19801682). Independently of its phosphatase activity, CDC25B acts as a ligand-dependent coactivator of steroid receptors through direct protein interaction (PMID:11689696). Its expression is further controlled by p53-mediated transcriptional repression, LSD1/H3K4me2 epigenetic repression in oocytes, and METTL3-deposited m6A that enhances YTHDF1-dependent translation (PMID:21242964, PMID:26626423, PMID:35637959, PMID:35287752).

Mechanistic history

Synthesis pass · year-by-year structured walk · 21 steps
  1. 1993 High

    Established what CDC25B does enzymatically by showing it dephosphorylates the inhibitory residues of CDK1, defining it as an activating mitotic phosphatase.

    Evidence In vitro dephosphorylation of CDK1 with purified CDC25B

    PMID:8440392

    Open questions at the time
    • In vitro substrate specificity did not address in vivo timing or compartmentalized action
    • Did not distinguish CDC25B from CDC25A/C roles
  2. 1996 High

    Defined the catalytic mechanism, showing CDC25B uses a phospho-cysteine intermediate typical of dual-specificity phosphatases.

    Evidence Pre-steady-state kinetics with OMFP and recombinant catalytic domain

    PMID:8910325

    Open questions at the time
    • Used small-molecule substrate, not the physiological CDK substrate
    • Did not resolve the source of the catalytic acid
  3. 1998 High

    Demonstrated CDC25B is required for mitotic entry but not DNA replication, framing it as a G2-peaking 'starter phosphatase'.

    Evidence Neutralizing antibody microinjection plus activity assays in synchronized cells

    PMID:9683638

    Open questions at the time
    • Did not localize the relevant pool of CDC25B
    • Mechanism of S-phase activating phosphorylation not identified
  4. 1999 High

    Showed CDC25B drives premature mitosis overriding the unreplicated-DNA checkpoint and is cytoplasmic via cyclin B1-dependent nuclear export, distinguishing it from CDC25C.

    Evidence Time-lapse imaging and GFP-chimera localization in synchronized cells

    PMID:10444066

    Open questions at the time
    • Export machinery and signals not yet mapped
    • Functional consequence of cytoplasmic pool unclear
  5. 2000 High

    Mapped the NLS, NES, and 14-3-3 (Ser-323) requirement controlling regulated nucleo-cytoplasmic shuttling.

    Evidence Deletion/point mutants, leptomycin B, fractionation and immunofluorescence; two-hybrid 14-3-3 binding mapping

    PMID:10713667 PMID:10822367

    Open questions at the time
    • Phosphorylation-independence of 14-3-3 binding was a single-lab claim
    • Did not show how 14-3-3 affects catalysis
  6. 2001 High

    Defined 14-3-3 as a direct activity brake (blocking substrate access) and uncovered a phosphatase-independent coactivator function for steroid receptors.

    Evidence Checkpoint bypass and activity assays with 14-3-3 mutants; GST-pulldown, two-hybrid and reporter assays for receptor coactivation

    PMID:11466620 PMID:11689696

    Open questions at the time
    • Structural basis of catalytic-site occlusion not resolved
    • Physiological relevance of coactivator role to cell-cycle function unclear
  7. 2002 High

    Established CDC25B as the indispensable CDK1 activator for female meiotic resumption.

    Evidence Cdc25b knockout mice with mRNA-injection rescue and MPF assays

    PMID:11912493

    Open questions at the time
    • Somatic redundancy not yet addressed
    • Upstream control in oocytes not defined
  8. 2003 Medium

    Identified opposing post-translational inputs—CK2 (Ser-186/187, activating) and PKB/Akt (Ser-353, cytoplasmic export)—and refined the 14-3-3 intramolecular bridge model (Ser-151/230/323).

    Evidence In vitro kinase assays, mass spectrometry, co-IP, localization and activity assays

    PMID:12527891 PMID:12764136 PMID:14630392

    Open questions at the time
    • Single-lab site assignments
    • Integration of multiple phospho-inputs in vivo not resolved
  9. 2004 High

    Placed CDC25B in centrosomal G2/M signaling through Aurora-A phosphorylation at Ser-353 and refined isoform-selective 14-3-3 control of localization (Ser-309).

    Evidence In vitro kinase assays, RNAi, phospho-antibody microinjection, phosphomimetics, 14-3-3 isoform co-expression

    PMID:15128871 PMID:15173315 PMID:16082213

    Open questions at the time
    • Crosstalk among Ser-353 kinases (Aurora-A vs Akt) not reconciled
    • Centrosomal substrate spectrum undefined
  10. 2005 High

    Defined the destruction and redox control of CDC25B—SCF-β-TrCP via a non-phospho DDG motif, and structural disulfide-based oxidative inactivation—and pinned its centrosomal cyclin B1-CDK1 activation to mitotic onset.

    Evidence Xenopus extract degradation assays; multi-state crystal structures; RNAi with quantitative live imaging and CDK activity assays; pEg3 Ser-169 mapping

    PMID:15807524 PMID:15845771 PMID:15908796 PMID:16216921

    Open questions at the time
    • In vivo relevance of oxidation states uncertain
    • Coupling of degradation to checkpoint signaling incomplete
  11. 2005 High

    Demonstrated somatic redundancy: Cdc25A compensates for combined Cdc25B/Cdc25C loss.

    Evidence Double-knockout mouse genetics with cell-cycle and checkpoint profiling

    PMID:15767688

    Open questions at the time
    • Did not address tissue-specific non-redundant contexts beyond oocytes
  12. 2006 High

    Identified CHK1 (Ser-230) as a constitutive negative regulator of centrosomal CDC25B and placed CDC25B downstream of CHK1 in coordinating chromatin condensation with spindle assembly; mapped stress-kinase sites (MK2, p38).

    Evidence In vitro kinase assays, mass spectrometry, phospho-antibody localization, gain-of-function mutants, CHK1-inhibitor epistasis

    PMID:16861915 PMID:17003105 PMID:17106257

    Open questions at the time
    • How constitutive CHK1 signaling is integrated with activating inputs at centrosomes unclear
    • Functional weight of individual stress-kinase sites not separated
  13. 2007 Medium

    Extended CDC25B function to centrosome biology—asymmetric mother-centrosome localization, centriole duplication, and phosphatase-dependent gamma-tubulin recruitment.

    Evidence Immunofluorescence, siRNA, catalytic-dead and inducible overexpression with gamma-tubulin readouts; FRET biosensors and degradation-motif mapping

    PMID:17599046 PMID:18089784 PMID:18235220

    Open questions at the time
    • Direct centrosomal substrates not identified
    • Single-lab findings for centrosome duplication role
  14. 2008 High

    Defined PKA-mediated Ser-321 phosphorylation as the mechanism sequestering CDC25B in the cytoplasm via 14-3-3 to maintain meiotic prophase arrest.

    Evidence In vitro PKA assay, oocyte microinjection/GVBD, 14-3-3 co-IP, phospho-antibodies

    PMID:19035343 PMID:19223768

    Open questions at the time
    • Relationship between Ser-321 and Ser-323 14-3-3 control not fully resolved
  15. 2009 Medium

    Expanded the regulatory network with activating (RSK, PLK1-driven import) and destabilizing (JNK/p38 via Ser-101, MEK1) inputs and an oncogenic rapamycin→CDC25B(Ser-375)→AKT axis.

    Evidence In vitro kinase assays, mutagenesis, pharmacological/genetic epistasis, phosphoproteomics and rescue assays

    PMID:19185590 PMID:19276368 PMID:19638579 PMID:19801682

    Open questions at the time
    • Single-lab pathway assignments
    • Hierarchy among competing kinase inputs in vivo undefined
  16. 2010 Medium

    Identified Cdc14A as a direct phosphatase that dephosphorylates and inhibits CDC25B to restrain mitotic entry.

    Evidence Co-IP, in vitro dephosphorylation/activity assays, overexpression/knockdown with CDK1-cyclin B1 readout

    PMID:20956543

    Open questions at the time
    • Single-lab finding
    • Specific Cdc14A target residues on CDC25B not mapped
  17. 2012 Medium

    Showed CDC25B controls G2 length and influences neurogenesis in vivo, linking its cell-cycle role to developmental cell-fate decisions.

    Evidence In vivo RNAi in chick spinal cord with phase-length and differentiation readouts; p53 promoter-repression mapping

    PMID:21242964 PMID:22318230

    Open questions at the time
    • Mechanism connecting G2 length to neuronal conversion unclear
    • Single-lab developmental finding
  18. 2013 Medium

    Clarified redox- and signaling-based activity control: SelW reduces the disulfide to release 14-3-3 and activate CDC25B; cAMP/PKA (MC1R) and 14-3-3ε (Ser-321) inhibit it.

    Evidence siRNA epistasis with 14-3-3 binding assays; MC1R/cAMP rescue with S323A; co-IP and GVBD rescue with 14-3-3ε mutants

    PMID:22982242 PMID:23326474 PMID:23908401

    Open questions at the time
    • Physiological redox triggers of SelW action uncertain
    • Single-lab mechanistic claims
  19. 2015 High

    Established epigenetic control of CDC25B levels: LSD1/H3K4me2 represses CDC25B transcription in oocytes, with CDC25B upregulation responsible for precocious CDK1 activation and oocyte failure.

    Evidence Conditional Lsd1 oocyte knockout, H3K4me2 ChIP, CDC25B quantification and rescue

    PMID:26626423

    Open questions at the time
    • Generalizability beyond oocytes not shown
  20. 2019 Medium

    Showed all seven 14-3-3 isoforms interact with CDC25B in oocytes but that single deletion of YWHAH or YWHAE is dispensable for meiotic arrest, indicating functional redundancy among isoforms.

    Evidence Proximity ligation assay, FRET, R18 peptide injection, single-isoform knockouts

    PMID:31640562

    Open questions at the time
    • Combinatorial isoform requirement not determined
    • Per-isoform site preferences in oocytes not resolved
  21. 2022 Medium

    Identified m6A-based translational control of CDC25B, with METTL3 deposition and YTHDF1 reading accelerating its translation to drive G2/M progression.

    Evidence meRIP-qPCR/m6A-seq, METTL3 and YTHDF1 knockdown, ribosome profiling and cell-cycle analysis

    PMID:35287752 PMID:35637959

    Open questions at the time
    • Spatial/temporal coupling of m6A control to mitotic timing unresolved
    • Specific m6A sites on CDC25B mRNA not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the many competing activating, inhibitory, localization, and degradation inputs are quantitatively integrated to produce a switch-like, spatially controlled CDC25B activation at centrosomes remains unresolved.
  • No unified model reconciles the multiple kinases targeting overlapping residues (e.g., Ser-353, Ser-323)
  • Centrosomal substrate(s) beyond CDK1 not identified
  • Tissue-specific essentiality outside oocytes not mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5 GO:0016787 hydrolase activity 2 GO:0140110 transcription regulator activity 1
Localization
GO:0005815 microtubule organizing center 6 GO:0005829 cytosol 5 GO:0005634 nucleus 4
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-1474165 Reproduction 3 R-HSA-8953854 Metabolism of RNA 1
Partners
AURKACDC14ACDK1CDK2CSNK2BYWHABYWHAEYWHAH

Evidence

Reading pass · 46 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 Human CDC25B phosphatase dephosphorylates both Thr-14 and Tyr-15 of CDK1 (p34cdc2) in vitro, but not Thr-161, establishing it as a dual-specificity activating phosphatase for the mitotic kinase. In vitro dephosphorylation assay with purified CDC25B and CDK1 FEBS letters High 8440392
1996 CDC25B catalytic domain uses a two-step phosphoenzyme intermediate mechanism (formation and breakdown of phospho-cysteine intermediate) characteristic of dual-specificity phosphatases; rate constants for enzyme phosphorylation (~26 s⁻¹) and dephosphorylation (~1.5 s⁻¹) were determined by pre-steady-state kinetics. Pre-steady-state kinetic analysis using OMFP substrate with purified recombinant CDC25B catalytic domain The Journal of biological chemistry High 8910325
1997 Alternative splicing of CDC25B produces at least three variants (CDC25B1, B2, B3) that differ in activity; in fission yeast complementation assays CDC25B2 > CDC25B3 > CDC25B1 in mitosis-inducing activity, suggesting splice variation controls cell proliferation. cDNA cloning, genomic sequencing, in vitro phosphatase assay, episomal expression in S. pombe complementation assay Oncogene Medium 9188863
1997 CDC25B is degraded by the proteasome in a manner dependent on phosphorylation by CDK1-cyclin A but not CDK1-cyclin B, identifying CDK1-cyclin A as a writer that targets CDC25B for proteasomal destruction at the G2/M transition. In vitro phosphorylation assays, proteasome inhibitor treatment, in vivo degradation assays The Journal of biological chemistry High 9407044
1998 Ablation of CDC25B function by microinjection of specific antibodies blocks entry into mitosis in Hs68 cells, but does not affect later stages of mitosis or initiation of DNA replication. CDC25B activity peaks during G2, and is activated by phosphorylation during S-phase both in vitro and in vivo, supporting its role as a 'starter phosphatase' for mitosis. Microinjection of neutralizing antibodies, cell cycle synchronization, kinase/phosphatase activity assays Journal of cell science High 9683638
1999 Overexpression of CDC25B, but not CDC25C, causes S-phase and G2-phase cells to enter mitosis prematurely, overriding the unreplicated-DNA checkpoint. CDC25B is cytoplasmic during S and G2 phases due to nuclear export, and this nuclear export is dependent on cyclin B1, establishing a distinct localization and checkpoint behavior compared to CDC25C. Time-lapse fluorescence microscopy, microinjection of expression constructs, cell synchronization, GFP-chimera imaging The Journal of cell biology High 10444066
2000 CDC25B contains a nuclear localization signal (residues 335–354) and a nuclear export sequence (residues 28–40). Interaction with 14-3-3 proteins via Ser-323 is required for cytoplasmic retention; mutation of Ser-323 or treatment with the exportin inhibitor leptomycin B retains CDC25B in the nucleus, demonstrating regulated nucleo-cytoplasmic shuttling. Transfection of HA-tagged deletion/truncation/point-mutant constructs, leptomycin B treatment, subcellular fractionation/immunofluorescence Oncogene High 10822367
2000 CDC25B interacts with 14-3-3 proteins; in two-hybrid assays all three CDC25B splice variants bind 14-3-3η, β, and ζ but poorly bind ε and θ. Interaction requires the integrity of Ser-323 but is independent of phosphorylation, unlike CDC25C, and a high-affinity site for 14-3-3ζ/η is exposed by N-terminal truncation. Two-hybrid assay, in vitro binding assays, phosphorylation/dephosphorylation experiments, deletion constructs Oncogene Medium 10713667
2000 The catalytic acid required for protonation of the leaving group in CDC25B phosphatase activity resides on the protein substrate (CDK2-pTpY/CycA) rather than within the known structure of CDC25B; neither Glu474 nor Glu478, previously proposed, is responsible for the observed pH dependence observed with the natural substrate. pH-dependent kinetic analysis, site-directed mutagenesis, truncation experiments with small-molecule and natural substrates Biochemistry Medium 10978163
2001 14-3-3 binding to Ser-323 of CDC25B directly inhibits its phosphatase activity by blocking substrate (cyclin/CDK) access to the catalytic site; mutation of Ser-323 or removal of the N-terminal regulatory domain strongly activates CDC25B and enables bypass of the G2 checkpoint, providing mechanistic evidence that 14-3-3 controls CDC25B activity. Cell-based overexpression and checkpoint bypass assays, phosphatase activity assays with 14-3-3 binding mutants Oncogene High 11466620
2001 CDC25B acts as a coactivator for steroid receptors (including the androgen receptor and estrogen receptor) in a hormone-dependent manner, independent of its phosphatase catalytic activity. CDC25B directly interacts with steroid receptors (demonstrated by GST-pulldown and mammalian two-hybrid assays) and synergizes with CBP and p300/PCAF coactivators. Transient transfection reporter assays, cell-free assay with chromatin templates, GST-pulldown, mammalian two-hybrid Molecular and cellular biology High 11689696
2002 Cdc25b is essential for resumption of meiosis in female mice; Cdc25b-/- oocytes remain permanently arrested at prophase with low MPF (CDK1/cyclin B) activity. Microinjection of wild-type Cdc25b mRNA restores MPF activation and meiotic resumption, establishing Cdc25b as the indispensable activator of CDK1 for meiotic entry. Gene-targeted knockout mice (Cdc25b-/-), mRNA microinjection rescue, MPF activity assay Nature genetics High 11912493
2002 The kinase pEg3 (PAR-1/MARK family) specifically phosphorylates CDC25B in vitro on Ser-323 and associates with CDC25B in vitro and in vivo; ectopic expression of active pEg3 causes G2 accumulation that is counteracted by CDC25B overexpression, placing pEg3 as an antagonistic regulator of CDC25B at G2/M. In vitro kinase assay, co-immunoprecipitation, ectopic expression in U2OS cells, cell cycle analysis Oncogene Medium 12400006
2003 Protein kinase CK2 phosphorylates CDC25B in vitro on Ser-186 and Ser-187 (identified by mass spectrometry), interacts with CDC25B via the CK2β subunit (residues 1–55 of CK2β binding residues 122–200 of CDC25B), and phosphorylation by CK2 increases CDC25B catalytic activity both in vitro and in vivo. In vitro kinase assay, mass spectrometry, co-immunoprecipitation, phosphatase activity assay in Sf9 and U2OS cells Oncogene High 12527891
2003 14-3-3 acts as an intramolecular bridge in CDC25B: Ser-151 and Ser-230 in the N-terminal domain are functional low-affinity 14-3-3 binding sites that cooperate with the high-affinity Ser-323 site to form a bridge constraining CDC25B structure and blocking catalytic site access and nuclear export sequence access. Mutagenesis of 14-3-3 binding sites, cell-based localization and activity assays, deletion constructs The Journal of biological chemistry Medium 12764136
2003 PKB/Akt phosphorylates CDC25B on Ser-353, resulting in nuclear export-dependent cytoplasmic accumulation; oxidative stress activates PKB/Akt and reproduces this effect on CDC25B phosphorylation and localization. In vitro kinase assay, mutagenesis (S353A), subcellular fractionation and immunofluorescence, oxidative stress treatment Biology of the cell Medium 14630392
2004 Aurora-A kinase phosphorylates CDC25B on Ser-353 both in vitro and in vivo at the centrosome; this phosphorylated form localizes to centrosomes during mitosis, and microinjection of anti-phospho-S353 antibodies causes mitotic delay while a S353 phosphomimetic mutant enhances mitotic entry, demonstrating Aurora-A–CDC25B centrosomal signaling contributes to the G2-M transition. In vitro kinase assay, RNAi knockdown, immunofluorescence, microinjection of phospho-specific antibodies, overexpression of phosphomimetic mutant Journal of cell science High 15128871 16082213
2004 14-3-3β binding to Ser-309 (not Ser-216 or Ser-137) of CDC25B is sufficient to drive CDC25B to the cytoplasm; 14-3-3ε shares this behavior, while 14-3-3σ binds preferentially at Ser-216 but does not alter CDC25B localization, demonstrating isoform-selective 14-3-3 binding controls CDC25B subcellular distribution. Site-directed mutagenesis, co-expression of FLAG-tagged CDC25B with various 14-3-3 isoforms, immunofluorescence Journal of cell science Medium 15173315
2004 Endogenous CDC25B is mainly nuclear but a fraction is cytoplasmic during G2; a nuclear export sequence (NES) at amino acids 54–67 is required for efficient nuclear shuttling (by FLIP assay) and for the mitotic-inducing function of CDC25B; p38 MAPK signaling regulates CDC25B localization in response to stress via the NES and Ser-323. Immunofluorescence with RNAi validation, FRAP/FLIP in live cells, mutagenesis of NES, p38 inhibitor treatment, UV/cycloheximide stress Journal of cell science Medium 15456846
2005 Beta-TrCP recognizes a non-phosphorylated DDG motif (DDGφXD) in CDC25B; this interaction is essential for ubiquitination and proteasomal degradation of CDC25B under normal (non-checkpoint) conditions, establishing SCF-β-TrCP as the E3 ubiquitin ligase that controls constitutive CDC25B turnover. Xenopus egg extract ubiquitination/degradation assays, mutagenesis of DDG motif, in vivo and in vitro binding assays Proceedings of the National Academy of Sciences of the United States of America High 15845771
2005 Crystal structure of oxidized CDC25B reveals an intramolecular disulfide bond formed upon oxidation, with three P-loop conformations: active (apo), intermediate (sulfenic acid), and closed/inactive (disulfide). The closed conformation prevents substrate binding, defining the mechanism of reversible oxidative inactivation of CDC25B. X-ray crystallography time-course; structures of apo, sulfenic, disulfide, sulfinic and sulfonic forms Biochemistry High 15807524
2005 Cdc25B specifically activates cyclin B1-CDK1 at centrosomes; RNAi depletion of Cdc25B causes G2 delay with reduced cyclin B1-CDK1 and cyclin A-CDK2 activities; time-lapse imaging shows Cdc25B has a unique centrosomal role in initiating mitosis distinct from Cdc25A (chromatin condensation). RNAi (siRNA), quantitative immunofluorescence, 3D time-lapse microscopy, CDK activity assays The Journal of cell biology High 16216921
2005 CDC25B is phosphorylated by pEg3 at Ser-169 in vitro (identified by mass spectrometry); this Ser-169-phosphorylated form accumulates during mitosis and localizes to centrosomes in vivo; RNAi knockdown of pEg3 abolishes the centrosomal signal. In vitro kinase assay, mass spectrometry, phospho-specific antibodies, immunofluorescence, RNAi Cell cycle Medium 15908796
2005 Mice lacking both Cdc25B and Cdc25C are viable and born at expected Mendelian ratios; cells from double-knockout mice have normal cell cycles, DNA damage responses, and Cdc25A regulation, indicating that Cdc25A functionally compensates for the combined loss of Cdc25B and Cdc25C in somatic cells. Double-knockout mouse genetics, cell cycle profiling, checkpoint assays Molecular and cellular biology High 15767688
2006 CHK1 phosphorylates CDC25B in vitro on multiple sites including S230 and S563; S230 phosphorylation occurs in vivo during S and G2 phases in the absence of DNA damage; phospho-S230 CDC25B localizes to centrosomes from early S phase; S230A mutation increases CDC25B's mitotic-inducing activity, establishing CHK1 as a constitutive negative regulator of centrosomal CDC25B. In vitro kinase assay, mass spectrometry, phospho-specific antibodies, immunofluorescence, S230A mutagenesis with functional assay Journal of cell science High 17003105
2006 Chk1 inhibition induces a 'paraspindle' phenotype (regular spindle assembly but aberrant chromatin condensation) that is reverted by Cdc25B siRNA knockdown, and is phenocopied by Cdc25B (but not Cdc25A) overexpression; placing Cdc25B downstream of Chk1 in coordinating mitotic chromatin condensation with spindle assembly. Chk1 kinase inhibitor, siRNA knockdown, overexpression epistasis, microscopy of mitotic phenotypes Cell cycle Medium 17106257
2006 MAPKAP kinase-2 (MK2) phosphorylates CDC25B on multiple sites (S169, S323, S353, S375) and p38 SAPK phosphorylates CDC25B on S249, as determined by mass spectrometry and phospho-specific antibodies; S323-phosphorylated CDC25B is detected at centrosomes during a normal cell cycle. In vitro kinase assay, mass spectrometry, phospho-specific antibodies, immunofluorescence Cell cycle Medium 16861915
2007 CDC25B localizes asymmetrically to the mother centrosome from S to G2 phases, along with CHK1, CDK1 and WEE1; siRNA inhibition of CDC25B causes accumulation of G2 cells with only single centrioles in separated centrosomes, indicating a role for CDC25B in centriole duplication. Immunofluorescence, siRNA knockdown, centrosome marker co-staining Cell cycle Medium 18235220
2007 Overexpression of catalytically active (but not phosphatase-inactive) CDC25B at centrosomes causes centrosome overduplication, aberrant microtubule organization, and abnormal gamma-tubulin accumulation; inhibition of CDC25B phosphatase activity reduces interphase microtubule assembly and centrosomal gamma-tubulin localization, establishing CDC25B as part of the pathway controlling gamma-tubulin recruitment and centrosome duplication. Inducible overexpression, phosphatase-inactive mutant, siRNA, immunofluorescence for gamma-tubulin Cancer research Medium 18089784
2007 CDC25B splice variants show differential mitotic stability: degradation of CDC25B after the metaphase-anaphase transition depends on KEN-box and RRKSE motifs located in the alternatively spliced B domain; CDC25B2, lacking the B domain, is stable during mitosis. Intramolecular FRET biosensors reveal major conformational changes in the N-terminal/B-domain region during mitosis. Time-lapse video microscopy, FRET biosensors, mutagenesis of degradation motifs (KEN-box, RRKSE), cyclin B1 co-degradation kinetics Oncogene Medium 17599046
2008 PKA phosphorylates CDC25B at Ser-321 in vitro (not the S321A mutant); in mouse oocytes phospho-Ser321 CDC25B is cytoplasmic and detected in GV-arrested oocytes; S321A mutant enters the nucleus more rapidly and induces GVBD faster than wild-type; S321A also reduces 14-3-3 association, establishing PKA-mediated phosphorylation of Ser-321 as a mechanism for cytoplasmic sequestration of CDC25B to maintain meiotic prophase arrest. In vitro PKA kinase assay, fluorescent-tagged protein microinjection, GVBD assay in mouse oocytes, 14-3-3 co-immunoprecipitation, phospho-specific western blot Cell cycle High 19035343 19223768
2009 PLK1 activity is required for relocalization of CDC25B from the cytoplasm to the nucleus at the G2-M transition; gain- and loss-of-function of PLK1 show that PLK1 stimulates CDC25B-induced mitotic entry both under normal conditions and after DNA damage-induced G2/M arrest. PLK1 inhibitor, gain/loss-of-function by overexpression and siRNA, subcellular localization by immunofluorescence, mitotic entry assay Biochimica et biophysica acta Medium 19185590
2009 MEK1-dependent activation of the MAPK pathway destabilizes CDC25B protein specifically in G2 phase; re-introduction of CDC25B overcomes the MEK1-dependent G2 delay, defining MEK1 as a regulator of G2/M entry through CDC25B protein stability. MEK1 inhibitor (U0126), MEK1 overexpression, G2/M synchronization, CDC25B reintroduction rescue assay The Journal of biological chemistry Medium 19801682
2009 JNK1/2 and p38 MAPK induce CDC25B degradation in response to nongenotoxic stress (anisomycin); mass spectrometry and site-directed mutagenesis identified Ser-101 as the critical JNK/p38 phosphorylation site; S101A mutant CDC25B is refractory to anisomycin-induced degradation and can override anisomycin-induced G2 arrest. In vitro kinase assay, mass spectrometry, S101A mutagenesis, co-transfection, cell cycle analysis Cancer research High 19638579
2009 Rapamycin induces phosphorylation of CDC25B at Ser-375; mutation S375A substantially reduces CDC25B phosphatase activity and inhibits rapamycin-induced AKT activation; CDC25B depletion attenuates rapamycin-induced oncogenic AKT signaling, establishing a rapamycin→CDC25B(pS375)→AKT oncogenic pathway. Phosphoproteomics (mass spectrometry), siRNA screen, site-directed mutagenesis (S375A), AKT phosphorylation assays Cancer research Medium 19276368
2010 Human Cdc14A phosphatase directly binds to and dephosphorylates Cdc25B, inhibiting its catalytic activity; increased Cdc14A levels delay mitotic entry by inhibiting CDK1-cyclin B1 activity through Cdc25B (and Cdc25A), while reduced Cdc14A accelerates mitotic entry, establishing Cdc14A as a direct negative regulator of CDC25B. Co-immunoprecipitation, in vitro dephosphorylation/activity assay, overexpression and knockdown experiments, CDK1-cyclin B1 activity assay The Journal of biological chemistry Medium 20956543
2011 p53 transcriptionally represses CDC25B through a mechanism involving Sp1/Sp3 and NF-Y binding sites on the Cdc25B promoter; chromatin immunoprecipitation shows p53 occupies the Cdc25B promoter and mediates attenuation through these factors, and this repression occurs independently of p21. Promoter deletion/mutation analysis, ChIP, transient transfection reporter assays, p21-/- cell lines Oncogene Medium 21242964
2012 CDC25B expression in neural progenitors of the developing chick spinal cord shortens G2 phase; RNAi knockdown of CDC25B specifically lengthens G2 without affecting S-phase, and reduces conversion of proliferating progenitors to post-mitotic neurons, establishing CDC25B as a regulator of G2 phase length and neurogenesis. In vivo RNAi knockdown in chick spinal cord, cell cycle phase length measurement, neuronal differentiation assays Development Medium 22318230
2012 Selenoprotein W (SelW) promotes recovery from G2 arrest by activating CDC25B; SelW knockdown causes sustained inactivation of CDC25B (maintained 14-3-3 binding) and delayed CDK1 dephosphorylation. SelW activates CDC25B by promoting dissociation of 14-3-3 from CDC25B through reduction of the intramolecular disulfide bond in a redox-dependent manner. siRNA knockdown of SelW, phospho-CDK1/CDC25B western blots, co-immunoprecipitation of CDC25B with 14-3-3, cell cycle analysis Biochimica et biophysica acta Medium 22982242
2013 RSK (ribosomal S6 kinase) phosphorylates CDC25B (and CDC25A) at a conserved motif near the catalytic domain in vitro and in vivo in mitotic cells; phosphorylation at RSK sites increases CDC25B M-phase-inducing activity; RSK inhibition blocks G2/M transition, establishing RSK as an activating kinase for CDC25B. In vitro kinase assay with recombinant RSK and Xenopus egg extracts, site mutagenesis, RSK inhibitor, M-phase inducing assay Oncogene Medium 23708659
2013 MC1R/cAMP signaling delays G2-M progression in melanoma cells by phosphorylation and inhibition of Cdc25B; expression of a Cdc25B S323A phosphorylation-resistant mutant rescues the MC1R-induced G2 delay, placing Cdc25B downstream of cAMP/PKA in the MC1R pathway. MC1R overexpression, cAMP agonist treatment, Cdc25B S323A rescue, cell cycle analysis Proceedings of the National Academy of Sciences of the United States of America Medium 23908401
2013 14-3-3ε specifically binds CDC25B at Ser-321; mutation Ser321Ala abolishes 14-3-3ε binding and cytoplasmic retention of CDC25B in mouse oocytes; co-expression of 14-3-3ε with wild-type CDC25B or a S321D phosphomimetic prevents GVBD, while S321A co-expressed with 14-3-3ε still induces GVBD, confirming Ser-321 is the specific 14-3-3ε binding site maintaining meiotic arrest. Co-immunoprecipitation, GVBD assay by microinjection, immunofluorescence co-localization, mutagenesis PloS one Medium 23326474
2014 Fragment-based screening identified a compound that binds CDC25B at a pocket adjacent to the protein-protein interaction interface with CDK2/Cyclin A (not the active site); NMR data and crystal structure confirm the allosteric binding site; an analogue disrupts CDC25B–CDK2/Cyclin A interaction and inhibits CDK2 dephosphorylation, establishing that allosteric inhibition via the substrate-binding interface is a viable mechanism. NMR fragment screening, X-ray crystallography, co-immunoprecipitation disruption assay, in vitro CDK2 dephosphorylation assay ACS chemical biology High 25423142
2015 LSD1 (a histone H3K4me2 demethylase) in mouse oocytes represses CDC25B transcription epigenetically; conditional deletion of Lsd1 causes upregulation of CDC25B, leading to precocious meiotic resumption, spindle and chromosomal defects, and oocyte failure, with CDC25B upregulation mechanistically responsible for the precocious CDK1 activation. Conditional oocyte-specific Lsd1 knockout, H3K4me2 ChIP, CDC25B mRNA/protein quantification, rescue experiments Nature communications High 26626423
2019 All seven YWHA (14-3-3) isoforms expressed in mouse oocytes interact with CDC25B, demonstrated by in situ proximity ligation assay and FRET microscopy (YWHAH/14-3-3η interaction confirmed by FRET); injection of R18 (a YWHA-blocking peptide) promotes GVBD; however, complete genetic deletion of YWHAH or YWHAE does not alter meiotic arrest, indicating these two isoforms individually are not essential. In situ proximity ligation assay, FRET microscopy, R18 peptide microinjection, oocyte-specific knockout of YWHAH and YWHAE BMC developmental biology Medium 31640562
2022 METTL3 induces m6A modification on CDC25B mRNA in the M phase; this m6A modification accelerates CDC25B mRNA translation via YTHDF1-dependent reading, increasing CDC25B protein and promoting cell cycle G2/M progression. m6A-seq/meRIP-qPCR, YTHDF1 knockdown, METTL3 knockdown/overexpression, ribosome profiling/translation assay, cell cycle analysis International journal of biological sciences Medium 35287752 35637959

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1998 The cdc25B phosphatase is essential for the G2/M phase transition in human cells. Journal of cell science 250 9683638
2004 Phosphorylation of CDC25B by Aurora-A at the centrosome contributes to the G2-M transition. Journal of cell science 225 15128871
2002 Cdc25b phosphatase is required for resumption of meiosis during oocyte maturation. Nature genetics 222 11912493
1997 Overexpression of CDC25A and CDC25B in head and neck cancers. Cancer research 163 9192810
1998 Overexpression of cdc25A and cdc25B is frequent in primary non-small cell lung cancer but is not associated with overexpression of c-myc. Cancer research 157 9751615
2005 Cdc25B cooperates with Cdc25A to induce mitosis but has a unique role in activating cyclin B1-Cdk1 at the centrosome. The Journal of cell biology 155 16216921
1999 Cdc25B and Cdc25C differ markedly in their properties as initiators of mitosis. The Journal of cell biology 145 10444066
2002 Increased hepatic Forkhead Box M1B (FoxM1B) levels in old-aged mice stimulated liver regeneration through diminished p27Kip1 protein levels and increased Cdc25B expression. The Journal of biological chemistry 135 12221098
2001 Identification of differentially expressed genes in esophageal squamous cell carcinoma (ESCC) by cDNA expression array: overexpression of Fra-1, Neogenin, Id-1, and CDC25B genes in ESCC. Clinical cancer research : an official journal of the American Association for Cancer Research 135 11489794
2005 Normal cell cycle and checkpoint responses in mice and cells lacking Cdc25B and Cdc25C protein phosphatases. Molecular and cellular biology 120 15767688
2005 Beta-TrCP recognizes a previously undescribed nonphosphorylated destruction motif in Cdc25A and Cdc25B phosphatases. Proceedings of the National Academy of Sciences of the United States of America 114 15845771
2011 MicroRNA-148a is down-regulated in human pancreatic ductal adenocarcinomas and regulates cell survival by targeting CDC25B. Laboratory investigation; a journal of technical methods and pathology 102 21709669
2009 CDC25B mediates rapamycin-induced oncogenic responses in cancer cells. Cancer research 98 19276368
2005 CDC25B phosphorylation by Aurora-A occurs at the G2/M transition and is inhibited by DNA damage. Cell cycle (Georgetown, Tex.) 98 16082213
2003 Overexpression of Cdc25B, an androgen receptor coactivator, in prostate cancer. Oncogene 97 12569365
2002 Human pEg3 kinase associates with and phosphorylates CDC25B phosphatase: a potential role for pEg3 in cell cycle regulation. Oncogene 94 12400006
2000 Regulation of CDC25B phosphatases subcellular localization. Oncogene 93 10822367
1997 Alternative splicing of the human CDC25B tyrosine phosphatase. Possible implications for growth control? Oncogene 92 9188863
2005 Structural mechanism of oxidative regulation of the phosphatase Cdc25B via an intramolecular disulfide bond. Biochemistry 91 15807524
2000 Specific interaction between 14-3-3 isoforms and the human CDC25B phosphatase. Oncogene 91 10713667
1997 Phosphorylation of human CDC25B phosphatase by CDK1-cyclin A triggers its proteasome-dependent degradation. The Journal of biological chemistry 91 9407044
1993 Dephosphorylation of human p34cdc2 kinase on both Thr-14 and Tyr-15 by human cdc25B phosphatase. FEBS letters 89 8440392
2001 Cdc25B activity is regulated by 14-3-3. Oncogene 87 11466620
2009 Protein kinase A regulates resumption of meiosis by phosphorylation of Cdc25B in mammalian oocytes. Cell cycle (Georgetown, Tex.) 85 19223768
1997 Overexpression of cyclin-dependent kinase-activating CDC25B phosphatase in human gastric carcinomas. Japanese journal of cancer research : Gann 84 9414655
1997 A dual-specificity phosphatase Cdc25B is an unstable protein and triggers p34(cdc2)/cyclin B activation in hamster BHK21 cells arrested with hydroxyurea. The Journal of cell biology 83 9281587
2006 CHK1 phosphorylates CDC25B during the cell cycle in the absence of DNA damage. Journal of cell science 79 17003105
1999 Induction of mammary gland hyperplasia in transgenic mice over-expressing human Cdc25B. Oncogene 78 10467401
2005 Redox regulation of Cdc25B by cell-active quinolinediones. Molecular pharmacology 76 16155209
1996 Kinetic analysis of the catalytic domain of human cdc25B. The Journal of biological chemistry 76 8910325
2003 Protein kinase CK2 regulates CDC25B phosphatase activity. Oncogene 69 12527891
1999 Increased susceptibility to carcinogen-induced mammary tumors in MMTV-Cdc25B transgenic mice. Oncogene 67 10498865
2004 Discovery and characterization of novel small molecule inhibitors of human Cdc25B dual specificity phosphatase. Molecular pharmacology 66 15231869
2001 Synthesis of a tetronic acid library focused on inhibitors of tyrosine and dual-specificity protein phosphatases and its evaluation regarding VHR and cdc25B inhibition. Journal of medicinal chemistry 66 11563920
2004 Expression and functional significance of CDC25B in human pancreatic ductal adenocarcinoma. Oncogene 65 14712212
2003 14-3-3 acts as an intramolecular bridge to regulate cdc25B localization and activity. The Journal of biological chemistry 64 12764136
2005 Halenaquinone and xestoquinone derivatives, inhibitors of Cdc25B phosphatase from a Xestospongia sp. Bioorganic & medicinal chemistry 63 15670907
2000 CDC25B and p53 are independently implicated in radiation sensitivity for human esophageal cancers. Clinical cancer research : an official journal of the American Association for Cancer Research 62 11156245
2001 Clinical significance of CDC25A and CDC25B expression in squamous cell carcinomas of the oesophagus. British journal of cancer 59 11487274
2019 Circular RNA hsa_circRNA_102958 promotes tumorigenesis of colorectal cancer via miR-585/CDC25B axis. Cancer management and research 58 31413634
2017 KCTD12 promotes tumorigenesis by facilitating CDC25B/CDK1/Aurora A-dependent G2/M transition. Oncogene 57 28869606
1999 Multiple splicing variants of cdc25B regulate G2/M progression. Biochemical and biophysical research communications 57 10403798
2006 Modeling of Cdc25B dual specifity protein phosphatase inhibitors: docking of ligands and enzymatic inhibition mechanism. ChemMedChem 55 16892390
2004 Characterisation of Cdc25B localisation and nuclear export during the cell cycle and in response to stress. Journal of cell science 54 15456846
2008 Protein kinase A modulates Cdc25B activity during meiotic resumption of mouse oocytes. Developmental dynamics : an official publication of the American Association of Anatomists 53 19035343
2001 Constitutive Cdc25B tyrosine phosphatase activity in adult brain neurons with M phase-type alterations in Alzheimer's disease. Neuroscience 53 11516829
2000 Dual-specific Cdc25B phosphatase: in search of the catalytic acid. Biochemistry 52 10978163
2004 Binding of 14-3-3beta but not 14-3-3sigma controls the cytoplasmic localization of CDC25B: binding site preferences of 14-3-3 subtypes and the subcellular localization of CDC25B. Journal of cell science 50 15173315
2001 Cdc25B functions as a novel coactivator for the steroid receptors. Molecular and cellular biology 49 11689696
1998 Antisense phosphorothioate oligonucleotides specifically down-regulate cdc25B causing S-phase delay and persistent antiproliferative effects. International journal of cancer 47 9610732
2015 LSD1 is essential for oocyte meiotic progression by regulating CDC25B expression in mice. Nature communications 46 26626423
2007 CDC25B involvement in the centrosome duplication cycle and in microtubule nucleation. Cancer research 46 18089784
2006 Genotoxic-activated G2-M checkpoint exit is dependent on CDC25B phosphatase expression. Molecular cancer therapeutics 46 16818502
2001 Overexpression of CDC25B overrides radiation-induced G2-M arrest and results in increased apoptosis in esophageal cancer cells. Cancer research 46 11306507
2005 CDC25B phosphorylated by pEg3 localizes to the centrosome and the spindle poles at mitosis. Cell cycle (Georgetown, Tex.) 45 15908796
2019 SNHG16 as the miRNA let-7b-5p sponge facilitates the G2/M and epithelial-mesenchymal transition by regulating CDC25B and HMGA2 expression in hepatocellular carcinoma. Journal of cellular biochemistry 43 31696971
2022 METTL3 promotes cell cycle progression via m6A/YTHDF1-dependent regulation of CDC25B translation. International journal of biological sciences 42 35637959
2016 YWHAE silencing induces cell proliferation, invasion and migration through the up-regulation of CDC25B and MYC in gastric cancer cells: new insights about YWHAE role in the tumor development and metastasis process. Oncotarget 42 27863420
2012 Discovery of new inhibitors of Cdc25B dual specificity phosphatases by structure-based virtual screening. Journal of medicinal chemistry 42 22524450
2009 The polo-like kinase 1 regulates CDC25B-dependent mitosis entry. Biochimica et biophysica acta 42 19185590
2006 Chk1-dependent regulation of Cdc25B functions to coordinate mitotic events. Cell cycle (Georgetown, Tex.) 42 17106257
2009 Development of novel thiazolopyrimidines as CDC25B phosphatase inhibitors. ChemMedChem 41 19212959
2010 Overexpression of CDC25B, CDC25C and phospho-CDC25C (Ser216) in vulvar squamous cell carcinomas are associated with malignant features and aggressive cancer phenotypes. BMC cancer 40 20500813
2006 CDC25B phosphorylation by p38 and MK-2. Cell cycle (Georgetown, Tex.) 39 16861915
2000 Cell cycle regulation of the murine cdc25B promoter: essential role for nuclear factor-Y and a proximal repressor element. The Journal of biological chemistry 39 11104768
2022 METTL3 modulates m6A modification of CDC25B and promotes head and neck squamous cell carcinoma malignant progression. Experimental hematology & oncology 38 35287752
2003 PKB/Akt phosphorylates the CDC25B phosphatase and regulates its intracellular localisation. Biology of the cell 38 14630392
2011 Cdc25B is negatively regulated by p53 through Sp1 and NF-Y transcription factors. Oncogene 37 21242964
2007 Induction of Cdc25B regulates cell cycle resumption after genotoxic stress. Cancer research 37 17409445
2013 MicroRNA-141 is downregulated in human renal cell carcinoma and regulates cell survival by targeting CDC25B. OncoTargets and therapy 35 23596351
2009 Cdc25B dual-specificity phosphatase inhibitors identified in a high-throughput screen of the NIH compound library. Assay and drug development technologies 35 19530895
2011 Transcriptional repression of Cdc25B by IER5 inhibits the proliferation of leukemic progenitor cells through NF-YB and p300 in acute myeloid leukemia. PloS one 34 22132193
2001 Heterozygous disruption of the TATA-binding protein gene in DT40 cells causes reduced cdc25B phosphatase expression and delayed mitosis. Molecular and cellular biology 34 11259592
2006 Identification of an unexpected link between the Shh pathway and a G2/M regulator, the phosphatase CDC25B. Developmental biology 33 16564519
2021 LncRNA FAM83A-AS1 promotes ESCC progression by regulating miR-214/CDC25B axis. Journal of Cancer 32 33442418
2019 CDC25B and CDC25C overexpression in nonmelanoma skin cancer suppresses cell death. Molecular carcinogenesis 32 31237025
2009 MAPK pathway activation delays G2/M progression by destabilizing Cdc25B. The Journal of biological chemistry 32 19801682
2000 New Cdc25B tyrosine phosphatase inhibitors, nocardiones A and B, produced by Nocardia sp. TP-A0248: taxonomy, fermentation, isolation, structural elucidation and biological properties. The Journal of antibiotics 32 10866214
2009 Stress-activated mitogen-activated protein kinases c-Jun NH2-terminal kinase and p38 target Cdc25B for degradation. Cancer research 31 19638579
2008 Overexpression of CDC25B and LAMC2 mRNA and protein in esophageal squamous cell carcinomas and premalignant lesions in subjects from a high-risk population in China. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 31 18559558
2014 MHC-restricted phosphopeptides from insulin receptor substrate-2 and CDC25b offer broad-based immunotherapeutic agents for cancer. Cancer research 30 25297629
2013 MC1R and cAMP signaling inhibit cdc25B activity and delay cell cycle progression in melanoma cells. Proceedings of the National Academy of Sciences of the United States of America 30 23908401
2012 The CDC25B phosphatase shortens the G2 phase of neural progenitors and promotes efficient neuron production. Development (Cambridge, England) 30 22318230
2010 Human Cdc14A phosphatase modulates the G2/M transition through Cdc25A and Cdc25B. The Journal of biological chemistry 30 20956543
2008 Cdc25B phosphatase inhibitors in cancer therapy: latest developments, trends and medicinal chemistry perspective. Anti-cancer agents in medicinal chemistry 30 19075567
2014 Inhibition of CDC25B phosphatase through disruption of protein-protein interaction. ACS chemical biology 29 25423142
2004 Expression of cdc25A and cdc25B phosphatase in breast carcinoma. Breast cancer (Tokyo, Japan) 29 15550849
2003 Coordinate expression of Cdc25B and ER-alpha is frequent in low-grade endometrioid endometrial carcinoma but uncommon in high-grade endometrioid and nonendometrioid carcinomas. Cancer research 29 14559803
2002 Expression of cdc25A and cdc25B proteins in thyroid neoplasms. British journal of cancer 29 12085185
2015 MicroRNA-211, a direct negative regulator of CDC25B expression, inhibits triple-negative breast cancer cells' growth and migration. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 28 25680404
2008 Small interfering RNA targeting CDC25B inhibits liver tumor growth in vitro and in vivo. Molecular cancer 28 18269767
2007 Differential mitotic degradation of the CDC25B phosphatase variants. Oncogene 28 17599046
2007 Asymmetric localization of the CDC25B phosphatase to the mother centrosome during interphase. Cell cycle (Georgetown, Tex.) 28 18235220
2013 RSK promotes G2/M transition through activating phosphorylation of Cdc25A and Cdc25B. Oncogene 27 23708659
2012 Selenoprotein W promotes cell cycle recovery from G2 arrest through the activation of CDC25B. Biochimica et biophysica acta 26 22982242
2008 Proteomics-based identification of autoantibody against CDC25B as a novel serum marker in esophageal squamous cell carcinoma. Biochemical and biophysical research communications 26 18722351
2005 p53 negativity, CDC25B positivity, and metallothionein negativity are predictors of a response of esophageal squamous cell carcinoma to chemoradiotherapy. World journal of gastroenterology 26 16237768
2022 CircZNF609 promotes bladder cancer progression and inhibits cisplatin sensitivity via miR-1200/CDC25B pathway. Cell biology and toxicology 25 35567596
2019 YWHA (14-3-3) protein isoforms and their interactions with CDC25B phosphatase in mouse oogenesis and oocyte maturation. BMC developmental biology 25 31640562
2013 The role of 14-3-3ε interaction with phosphorylated Cdc25B at its Ser321 in the release of the mouse oocyte from prophase I arrest. PloS one 25 23326474

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