Affinage

CDK20

Cyclin-dependent kinase 20 · UniProt Q8IZL9

Length
346 aa
Mass
38.7 kDa
Annotated
2026-06-09
43 papers in source corpus 14 papers cited in narrative 14 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CDK20 (CCRK) is a serine/threonine protein kinase that functions as the master upstream activator of a ciliary kinase cascade controlling intraflagellar transport (IFT) turnaround, ciliary length, and Hedgehog signaling (PMID:23743448, PMID:28817564, PMID:41385589). It activates the related kinases ICK/CILK1, MAK, and CDKL5 by phosphorylating their activation loops—a mechanism demonstrated directly for CDKL5, whose activation-loop phosphorylation by CDK20 was mapped by mass spectrometry and controls CDKL5 ciliary localization and flagellar length across Chlamydomonas and mouse (PMID:41385589)—and acts upstream of MAK and ICK in photoreceptor axoneme maintenance and retinal survival (PMID:39293864). At the ciliary tip, CDK20 operates within a complex with BROMI/TBC1D32, FAM149B1, and CFAP20 to govern IFT turnaround; loss of CDK20 causes overaccumulation of IFT proteins at bulged tips, aberrant ciliary enrichment of GPR161 and Smoothened, and excessive tip-derived extracellular vesicles, with rescue requiring both its kinase activity and BROMI-binding competence (PMID:34624068, PMID:35609210). CDK20 is required for proper Hedgehog pathway output, acting at or downstream of Smoothened and upstream of Gli2/Gli3 (PMID:28817564). Beyond cilia, CDK20 drives oncogenic signaling circuits, including an EZH2/NF-κB/IL-6 cascade promoting immunosuppression in hepatocellular carcinoma (PMID:28939663) and a STAT3–AR–mTORC1 feedforward loop (PMID:30523261), competes with NRF2 for KEAP1 binding via an ETGE motif to activate the NRF2 cytoprotective program (PMID:28534518), and stabilizes KU70 to promote NHEJ repair (PMID:40940753). Its previously proposed CDK-activating kinase (CAK) activity toward CDK2 has been experimentally refuted, with CDK7 confirmed as the sole mammalian CAK (PMID:16552187).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2006 High

    Resolved whether CDK20 is a CDK-activating kinase: it has no intrinsic CAK activity and does not phosphorylate the CDK2 T-loop, redirecting the field away from a cell-cycle CAK role.

    Evidence RNAi knockdown with in vitro CAK assay, in vivo T-loop phosphorylation, PARP cleavage and flow cytometry in mammalian cells

    PMID:16552187

    Open questions at the time
    • Did not identify the bona fide substrates or activating partners of CDK20
    • Proliferation/apoptosis phenotype mechanism left undefined
  2. 2010 Medium

    Tested CDK20's role in cell-cycle progression in cancer cells, linking it to CDK2/Rb phosphorylation and cyclin E expression with G1 arrest upon loss.

    Evidence siRNA/shRNA knockdown with phospho-Western (CDK2-pThr160, Rb-pSer795) and cell-cycle analysis in colorectal cancer lines

    PMID:20466538

    Open questions at the time
    • No in vitro kinase reconstitution to confirm direct phosphorylation
    • Apparent tension with the 2006 refutation of CAK activity not reconciled
  3. 2013 High

    Established CDK20 as a regulator of ciliogenesis via the substrate kinase ICK and the related MAK, linking ciliary control to glioblastoma proliferation.

    Evidence RNAi knockdown, immunofluorescence and live-cell imaging of ciliary tip ICK, proliferation assays in NIH3T3 and glioblastoma cells

    PMID:23743448

    Open questions at the time
    • Direct phosphorylation of ICK by CDK20 not biochemically mapped here
    • Mechanism connecting ciliary control to proliferation incompletely defined
  4. 2017 High

    Defined three distinct CDK20 effector arms—Hedgehog/ciliary IFT, KEAP1/NRF2 cytoprotection, and EZH2/NF-κB/IL-6 immunosuppression—broadening its role beyond cilia into oncogenic and redox signaling.

    Evidence Mouse mutant genetics with Hh epistasis and ciliary localization (PLoS Genet); TAP/Co-IP with ETGE-motif competition and NRF2 reporters (Oncogene); CRISPR/transgenic mice with ChIP and immunosuppression assays (Gut)

    PMID:28534518 PMID:28817564 PMID:28939663

    Open questions at the time
    • Whether KEAP1 binding and kinase activity are mechanistically coupled is unresolved
    • Direct kinase substrates within the NF-κB/EZH2 arm not identified
  5. 2018 High

    Mapped a STAT3–AR–mTORC1 feedforward circuit downstream of CDK20 driving metabolic-oncogenic signaling and MDSC recruitment.

    Evidence Lentiviral ablation and transgenic hepatic induction in mice, ChIP for STAT3–AR co-occupancy, phospho-pathway readouts (GSK3β, mTORC1 substrates)

    PMID:30523261

    Open questions at the time
    • Direct kinase target initiating the loop not pinpointed
    • Connection between this circuit and the ciliary kinase function unexplored
  6. 2019 High

    Placed CDK20 (DYF-18) genetically upstream of MAK (DYF-5) and upstream of axonemal microtubule stability, mechanistically linking the cascade to tubulin turnover and cilia length/branching.

    Evidence C. elegans genetics with tubulin and IFT mutant epistasis, live IFT motor imaging, EBP-2 dynamics

    PMID:30955935

    Open questions at the time
    • Biochemical demonstration of DYF-5 activation-loop phosphorylation not shown in this system
    • Generalization to mammalian axonemes inferred, not directly tested
  7. 2021 High

    Showed CDK20 requires both kinase activity and BROMI/TBC1D32 binding to control IFT turnaround at the ciliary tip, situating it upstream of ICK with ICK-like KO phenotypes.

    Evidence CCRK-KO cells with WT vs. kinase-dead and BROMI-binding mutant rescue, IFT/membrane receptor immunofluorescence, extracellular vesicle analysis

    PMID:34624068

    Open questions at the time
    • Whether BROMI is a substrate or a scaffold for substrate presentation unclear
    • Direct phosphorylation event at the tip not biochemically captured
  8. 2022 High

    Defined the multi-protein tip complex (CDK20–BROMI–FAM149B1–CFAP20) acting together upstream of ICK, since KO of each component produced identical ciliary defects.

    Evidence Reciprocal Co-IP defining complex composition, KO cells with BROMI-binding mutant rescue, immunofluorescence

    PMID:35609210

    Open questions at the time
    • Stoichiometry and order of assembly of the complex not resolved
    • Catalytic substrate(s) within the complex not identified
  9. 2024 Medium

    Extended the CDK20–MAK/ICK axis to photoreceptor ciliary maintenance, establishing physiological relevance for retinal survival.

    Evidence Mouse Ccrk conditional KO with retinal degeneration phenotyping, epistasis with Mak/Ick, IFT immunofluorescence

    PMID:39293864

    Open questions at the time
    • Single study
    • Direct activation-loop phosphorylation of MAK/ICK in photoreceptors not biochemically shown
  10. 2025 High

    Provided direct biochemical proof that CDK20 phosphorylates the CDKL5 activation loop to activate it and control its ciliary transport and flagellar length, completing the mechanistic logic of the cascade; also implicated CDK20 in KU70 stabilization and NHEJ.

    Evidence MS phosphorylation mapping and kinase-activation reconstitution in Chlamydomonas with Cdk20-KO rescue in mouse (PLoS Biol); Co-IP, EJ5-GFP NHEJ reporter and AR-luciferase in breast cancer cells (Cells)

    PMID:40940753 PMID:41385589

    Open questions at the time
    • KU70 interaction rests on single Co-IP without reciprocal validation
    • Whether KU70 stabilization requires CDK20 catalytic activity not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CDK20 itself is activated and regulated, and how its ciliary kinase function mechanistically integrates with its oncogenic NRF2/NF-κB/STAT3-AR and DNA-repair roles, remains unresolved.
  • No identified activating cyclin/partner or upstream regulator of CDK20 catalytic activity
  • No structural model linking kinase, ETGE, and BROMI-binding functions
  • Whether oncogenic circuits depend on ciliary cascade substrates is untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 3 GO:0016740 transferase activity 2 GO:0098772 molecular function regulator activity 2
Localization
GO:0005929 cilium 5
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1266738 Developmental Biology 2 R-HSA-168256 Immune System 2 GO:0005929 cilium 1 R-HSA-73894 DNA Repair 1 R-HSA-8953897 Cellular responses to stimuli 1
Partners
BROMI/TBC1D32CDKL5CFAP20FAM149B1ICK/CILK1KEAP1KU70MAK
Complex memberships
CDK20–BROMI(TBC1D32)–FAM149B1–CFAP20 ciliary tip complex

Evidence

Reading pass · 14 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 PNQALRE/CCRK/CDK20 has no intrinsic CDK-activating kinase (CAK) activity as a monomer; it does not phosphorylate Cdk2 T-loop in vitro or in vivo, and its depletion by RNAi does not reduce Cdk2 T-loop phosphorylation or CAK activity of cell extracts. Instead, CDK7 is confirmed as the sole mammalian CAK. CDK20 knockdown impairs cell proliferation and increases apoptosis (sub-G1 DNA content, PARP cleavage) without discrete cell-cycle arrest. RNAi knockdown, in vitro CAK assay, in vivo T-loop phosphorylation measurement, PARP cleavage assay, flow cytometry Cell cycle (Georgetown, Tex.) High 16552187
2013 CCRK/CDK20 and its substrate ICK inhibit ciliogenesis; CCRK depletion causes accumulation of ICK at ciliary tips, altered intraflagellar transport (IFT), and inhibition of cell cycle re-entry. In glioblastoma cells with high CCRK, its depletion restores primary cilia through ICK and the ICK-related kinase MAK, thereby inhibiting glioblastoma cell proliferation. RNAi knockdown, immunofluorescence, live-cell imaging of ciliary tip ICK accumulation, cell proliferation assays in NIH3T3 and glioblastoma cells EMBO reports High 23743448
2017 CCRK/CDK20 activates NF-κB via EZH2 and facilitates NF-κB–EZH2 co-binding to the IL-6 promoter, driving immunosuppressive MDSC expansion in hepatocellular carcinoma. This CCRK→EZH2/NF-κB→IL-6 cascade promotes T-cell suppression. CRISPR/Cas9 Ccrk depletion, liver-specific transgenic mice, ChIP showing NF-κB–EZH2 co-occupancy at IL-6 promoter, flow cytometry, co-culture immunosuppression assays, IL-6 trap rescue Gut High 28939663
2017 CDK20/CCRK binds directly to the ubiquitin ligase adaptor KEAP1 via an evolutionarily conserved ETGE motif on CDK20, competing with NRF2 for KEAP1 binding. This competition enhances NRF2 transcriptional activity, lowers cellular ROS, and confers radiochemoresistance in lung cancer cells. Tandem affinity purification, co-immunoprecipitation, ETGE-motif competition binding assays, CDK20 knockdown with NRF2 reporter assays, ROS measurement, clonogenic survival assays Oncogene High 28534518
2017 CCRK/CDK20 is required for proper Hedgehog (Hh) pathway signaling in mice; Ccrk mutant cells show defective ciliary length regulation, impaired intraflagellar transport, and slowed ciliary enrichment of Smoothened and Gli2. Genetic analyses place CCRK at the level of or downstream of Smoothened and upstream of Gli2/Gli3. Mouse knockout/mutant genetics, epistasis analyses, immunofluorescence of ciliary protein localization, IFT velocity measurements, in vitro Hh signaling assays PLoS genetics High 28817564
2018 CCRK/CDK20 drives a feedforward signaling loop: it induces STAT3–AR promoter co-occupancy to transcriptionally upregulate AR, which in turn activates mTORC1/4E-BP1/S6K/SREBP1 cascades via GSK3β phosphorylation. Additionally, CCRK activates mTORC1-dependent G-csf expression to recruit immunosuppressive PMN-MDSCs. Lentiviral Ccrk ablation in diet-induced obese mice, transgenic hepatic CCRK induction, ChIP for STAT3–AR co-occupancy, phosphorylation assays for GSK3β and mTORC1 substrates, cytokine measurement Nature communications High 30523261
2019 In C. elegans, DYF-18/CCRK and DYF-5/MAK act in a kinase cascade to control cilia branching and length; loss of dyf-18 leads to elongated, unbranched cilia with increased tubulin load, reduced tubulin turnover, and EBP-2 decoration of axonemal microtubules along their lengths. Microtubule-destabilizing tubulin mutations and IFT tubulin-transport mutations suppress cilia elongation in dyf-18 mutants, placing CCRK upstream of MAK and upstream of axonemal microtubule stability. C. elegans genetics (dyf-18 null mutants), epistasis with tubulin and IFT mutants, live-cell IFT motor imaging, EBP-2 dynamics (FRAP/live imaging), fluorescence intensity measurements of tubulin load Current biology : CB High 30955935
2010 CCRK/CDK20 is required for phosphorylation of CDK2 on Thr-160 and Rb on Ser-795 and for expression of cyclin E in colorectal cancer cells; its knockdown causes G1 phase arrest and reduced proliferation. siRNA and shRNA knockdown, Western blotting for CDK2-pThr160 and Rb-pSer795, flow cytometry cell cycle analysis, cell proliferation assays in LoVo and DLD1 cells European journal of cancer (Oxford, England : 1990) Medium 20466538
2021 CCRK/CDK20 interacts with BROMI/TBC1D32 and this interaction is required for regulating IFT turnaround at the ciliary tip; CCRK-KO cells show overaccumulation of IFT proteins at bulged ciliary tips, GPR161 and Smoothened enrichment on the ciliary membrane, and elimination of tip material as extracellular vesicles. Rescue requires both kinase activity and BROMI-binding competence of CCRK, and phenotypes resemble ICK-KO, placing CCRK upstream of ICK. CCRK-knockout cell generation, exogenous rescue with wild-type vs. kinase-dead and BROMI-binding mutants, immunofluorescence of IFT proteins and ciliary membrane receptors, extracellular vesicle analysis PloS one High 34624068
2022 CCRK/CDK20 interacts with BROMI/TBC1D32, FAM149B1/JBTS36, and CFAP20 to regulate IFT turnaround at the ciliary tip. BROMI mutants defective in CCRK binding cannot rescue BROMI-KO ciliary defects; CCRK-KO, BROMI-KO, and FAM149B1-KO cells show identical phenotypes including cilia elongation and IFT/ICK tip accumulation, indicating these proteins function together upstream of ICK. Co-immunoprecipitation (CCRK–BROMI, CCRK–FAM149B1, BROMI–FAM149B1, BROMI–CFAP20), KO cell generation, rescue with BROMI binding mutants, immunofluorescence Molecular biology of the cell High 35609210
2024 CCRK kinase is an upstream activator of both MAK and ICK in retinal photoreceptor cells; the CCRK–MAK/ICK axis constitutes an IFT regulator essential for photoreceptor ciliary axoneme maintenance and retinal survival. Mouse Ccrk conditional knockout, retinal degeneration phenotyping, genetic epistasis with Mak and Ick mutants, IFT protein localization by immunofluorescence Life science alliance Medium 39293864
2025 CDK20/LF2 phosphorylates the activation loop of CDKL5 (Chlamydomonas LF5), activating it; this phosphorylation controls CDKL5 ciliary localization, downregulates its IFT-mediated transport as flagella reach steady state, and influences flagellar length. Mouse Cdk20 is required for proper Cdkl5 localization within cilia, and Cdkl5 loss elongates cilia in a CDK20-dependent manner. Live-cell imaging, immunofluorescence, biochemical assays, mass spectrometry phosphorylation mapping, Chlamydomonas and mouse Cdk20-KO genetic analysis, reconstitution of kinase activation PLoS biology High 41385589
2025 CCRK/CDK20 interacts with KU70, modulates its protein stability, and thereby enhances non-homologous end joining (NHEJ) DNA repair activity downstream of the AR–CCRK axis in breast cancer cells. Co-immunoprecipitation (CCRK–KU70), EJ5-GFP NHEJ reporter assay, CCRK knockdown/overexpression, ARE-luciferase AR activity assay, cell viability and comet assays Cells Medium 40940753
2011 In C. elegans, the CDK/CCRK/LF2p-related kinase DYF-18 is required for proper intraflagellar transport function and ciliogenesis; dyf-18 mutants display dye-filling defects indicative of IFT disruption in ciliated sensory neurons. C. elegans mutant analysis (dye-filling assay), transcriptional GFP reporters for expression in ciliated sensory neurons, genetic epistasis with DAF-19 RFX targets Developmental biology Medium 21740898

Source papers

Stage 0 corpus · 43 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1994 c-Abl kinase regulates the protein binding activity of c-Crk. The EMBO journal 349 8194526
1996 The proto-oncogene product p120CBL and the adaptor proteins CRKL and c-CRK link c-ABL, p190BCR/ABL and p210BCR/ABL to the phosphatidylinositol-3' kinase pathway. Oncogene 251 8632906
1995 Structural basis for the specific interaction of lysine-containing proline-rich peptides with the N-terminal SH3 domain of c-Crk. Structure (London, England : 1993) 221 7735837
2023 AlphaFold accelerates artificial intelligence powered drug discovery: efficient discovery of a novel CDK20 small molecule inhibitor. Chemical science 208 36794205
2017 Hepatoma-intrinsic CCRK inhibition diminishes myeloid-derived suppressor cell immunosuppression and enhances immune-checkpoint blockade efficacy. Gut 178 28939663
1995 Insulin-like growth factor-I stimulates tyrosine phosphorylation of endogenous c-Crk. The Journal of biological chemistry 106 7534289
1995 Cellular proteins binding to the first Src homology 3 (SH3) domain of the proto-oncogene product c-Crk indicate Crk-specific signaling pathways. Oncogene 106 7731701
2013 CCRK depletion inhibits glioblastoma cell proliferation in a cilium-dependent manner. EMBO reports 87 23743448
2018 An inflammatory-CCRK circuitry drives mTORC1-dependent metabolic and immunosuppressive reprogramming in obesity-associated hepatocellular carcinoma. Nature communications 81 30523261
1996 The proto-oncogene product c-Crk associates with insulin receptor substrate-1 and 4PS. Modulation by insulin growth factor-I (IGF) and enhanced IGF-I signaling. The Journal of biological chemistry 77 8621590
2017 CDK20 interacts with KEAP1 to activate NRF2 and promotes radiochemoresistance in lung cancer cells. Oncogene 76 28534518
2011 Transcriptional profiling of C. elegans DAF-19 uncovers a ciliary base-associated protein and a CDK/CCRK/LF2p-related kinase required for intraflagellar transport. Developmental biology 54 21740898
1994 The C-terminal SH3 domain of the mouse c-Crk protein negatively regulates tyrosine-phosphorylation of Crk associated p130 in rat 3Y1 cells. Oncogene 50 8183562
2006 The cyclin-dependent kinase (CDK) family member PNQALRE/CCRK supports cell proliferation but has no intrinsic CDK-activating kinase (CAK) activity. Cell cycle (Georgetown, Tex.) 49 16552187
2000 Phosphorylation of c-Crk II on the negative regulatory Tyr222 mediates nerve growth factor-induced cell spreading and morphogenesis. The Journal of biological chemistry 45 10825157
2018 CCRK is a novel signalling hub exploitable in cancer immunotherapy. Pharmacology & therapeutics 43 29360538
2000 c-Crk, a substrate of the insulin-like growth factor-1 receptor tyrosine kinase, functions as an early signal mediator in the adipocyte differentiation process. The Journal of biological chemistry 42 10926934
2009 Differences in DNA methylation patterns and expression of the CCRK gene in human and nonhuman primate cortices. Molecular biology and evolution 41 19282513
2014 Role of electrostatic interactions in binding of peptides and intrinsically disordered proteins to their folded targets. 1. NMR and MD characterization of the complex between the c-Crk N-SH3 domain and the peptide Sos. Biochemistry 39 25207671
2017 Cell Cycle-Related Kinase (CCRK) regulates ciliogenesis and Hedgehog signaling in mice. PLoS genetics 38 28817564
2003 Identification of Tyr900 in the kinase domain of c-Kit as a Src-dependent phosphorylation site mediating interaction with c-Crk. Experimental cell research 38 12878163
2019 A CCRK and a MAK Kinase Modulate Cilia Branching and Length via Regulation of Axonemal Microtubule Dynamics in Caenorhabditis elegans. Current biology : CB 36 30955935
2001 Activation of the focal adhesion kinase signaling pathway by structural alterations in the carboxyl-terminal region of c-Crk II. Oncogene 32 11314030
1997 Ligation of the T cell antigen receptor induces tyrosine phosphorylation of p105CasL, a member of the p130Cas-related docking protein family, and its subsequent binding to the Src homology 2 domain of c-Crk. European journal of immunology 31 9295052
1998 Tyrosine phosphorylation and association of p130Cas and c-Crk II by ANG II in vascular smooth muscle cells. The American journal of physiology 27 9575907
1993 A 31-amino-acid N-terminal extension regulates c-Crk binding to tyrosine-phosphorylated proteins. Molecular and cellular biology 26 7504172
2010 Functional characterisation of cell cycle-related kinase (CCRK) in colorectal cancer carcinogenesis. European journal of cancer (Oxford, England : 1990) 23 20466538
2016 Role of Electrostatic Interactions in Binding of Peptides and Intrinsically Disordered Proteins to Their Folded Targets: 2. The Model of Encounter Complex Involving the Double Mutant of the c-Crk N-SH3 Domain and Peptide Sos. Biochemistry 15 26910732
2022 BROMI/TBC1D32 together with CCRK/CDK20 and FAM149B1/JBTS36 contributes to intraflagellar transport turnaround involving ICK/CILK1. Molecular biology of the cell 12 35609210
2011 c-Crk proto-oncogene contributes to transcriptional repression of p120-catenin in non-small cell lung cancer cells. Clinical & experimental metastasis 12 21336985
2021 CCRK/CDK20 regulates ciliary retrograde protein trafficking via interacting with BROMI/TBC1D32. PloS one 10 34624068
2001 C3G, a guanine nucleotide exchange factor bound to adapter molecule c-Crk, has two alternative splicing forms. Biochemical and biophysical research communications 9 11485308
1998 Downregulated expression of the signaling molecules Nck, c-Crk, Grb2/Ash, PI 3-kinase p110 alpha and WRN during fibroblast aging in vitro. Biochimica et biophysica acta 9 9531977
1997 Phosphorylation of a 72-kDa protein in PDGF-stimulated cells which forms complex with c-Crk, c-Fyn and Eps15. FEBS letters 9 9202144
2023 The Role of CDK20 Protein in Carcinogenesis. Current drug targets 8 37469151
2021 xbx-4, a homolog of the Joubert syndrome gene FAM149B1, acts via the CCRK and RCK kinase cascade to regulate cilia morphology. Current biology : CB 8 34731674
2004 Mutational analysis of the interaction between insulin receptor and IGF-I receptor with c-Crk and Crk-L in a yeast two-hybrid system. Biochemical and biophysical research communications 8 15522217
2024 Ccrk-Mak/Ick signaling is a ciliary transport regulator essential for retinal photoreceptor survival. Life science alliance 5 39293864
2026 AlphaFold2 Insights into c-Abl Transactivation by Adaptor c-Crk or Abi-1: Structural Forms, Active Site Types, and Multiple SH3-PxxPxK/R Interactions. Genes to cells : devoted to molecular & cellular mechanisms 0 41618774
2025 Quantum chemical optimization and residue-specific stabilization of CDK20 inhibitors in hepatocellular carcinoma. Molecular diversity 0 40928680
2025 BQ323636.1 Employs the AR-CCRK Axis to Modulate the Expression of KU70 to Interfere with Non-Homologous End Joining Mediated DNA Repair Mechanism. Cells 0 40940753
2025 Activation of the ciliary kinase CDKL5 is mediated by the cyclin-dependent kinase CDK20/LF2 to control flagellar length. PLoS biology 0 41385589
2022 Effects of the Targeted Regulation of CCRK by miR-335-5p on the Proliferation and Tumorigenicity of Human Renal Carcinoma Cells. Journal of oncology 0 36276294

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