| 2001 |
Human PFTAIRE1 (CDK14) protein is localized to the cytoplasm when expressed as a GFP fusion in HeLa cells, as determined by fluorescence microscopy. |
GFP fusion protein expression and fluorescence microscopy in HeLa cells |
Gene |
Medium |
11313143
|
| 1998 |
Mouse Pftaire-1 (CDK14 ortholog) is expressed in late pachytene spermatocytes in the testis and in post-mitotic neuronal cells in the brain and embryo, suggesting roles in meiosis and neuron differentiation, as established by in situ hybridization. |
Northern blot and in situ hybridization in mouse tissues |
Molecular reproduction and development |
Medium |
9547506
|
| 2007 |
Human PFTK1 (CDK14) specifically interacts with cyclin D3 (CCND3) and forms a ternary complex with p21(Cip1); CCND3 is required for PFTK1 kinase activity, which is negatively regulated by p21(Cip1); Rb is a downstream phosphorylation substrate of the PFTK1/CCND3 complex; siRNA knockdown of PFTK1 causes G1 cell cycle arrest. |
Co-immunoprecipitation, siRNA knockdown, cell cycle analysis (flow cytometry), kinase assays in mammalian cells |
Proceedings of the National Academy of Sciences of the United States of America |
High |
17517622
|
| 2009 |
Cyclin Y (CCNY) is a novel interacting partner of PFTK1 (CDK14) identified by yeast two-hybrid screen; the cyclin box of CCNY and the PFTAIRE motif of PFTK1 are both required for the interaction; binding of CCNY to PFTK1 enhances PFTK1 kinase activity and changes its intracellular localization; CCNY is enriched at the plasma membrane via an N-terminal myristoylation signal. |
Yeast two-hybrid screen, in vivo and in vitro binding assays, Northern blot, subcellular localization studies |
FEBS letters |
High |
19524571
|
| 2010 |
Caldesmon (CaD) is a downstream phosphorylation substrate of PFTK1 (CDK14); PFTK1 knockdown reduces CaD phosphorylation and causes dissociation of CaD from F-actin fibers, loss of actin stress fibers, and altered CaD subcellular localization in hepatocellular carcinoma cells. |
siRNA knockdown, immunofluorescence, co-localization analysis, phosphorylation assays in HCC cells |
Molecular and cellular biochemistry |
Medium |
21184254
|
| 2011 |
PFTK1 (CDK14) phosphorylates TAGLN2 (transgelin2) at residues S83 and S163, inactivating its actin-binding function; in PFTK1-suppressed cells, unphosphorylated TAGLN2 exhibits strong actin-binding ability that inhibits actin cytoskeleton dynamics and cell motility; knockdown of TAGLN2 in PFTK1-suppressed cells rescues cell invasion and motility and restores actin polymerization. β-actin (ACTB) tyrosine phosphorylation is also affected by PFTK1. |
2D-PAGE mass spectrometry, siRNA knockdown, site-directed mutagenesis of TAGLN2, cell invasion/motility assays, actin polymerization assays |
Oncogene |
High |
21577206
|
| 2014 |
PFTK1 (CDK14) forms a direct complex with cyclin Y (CCNY) in HCC cells; this complex upregulates key components of noncanonical Wnt signaling (Dvl2 and Naked1) and activates Rho GTPases, leading to actin polymerization. |
Co-immunoprecipitation, exogenous expression, Rho GTPase activation assays, actin polymerization assays in HCC cells |
Biochemical and biophysical research communications |
Medium |
24824184
|
| 2014 |
CDK14 phosphorylates cyclin Y (CCNY) at Ser-71 and Ser-73, creating a phospho-degron that triggers CCNY ubiquitination by an SCF-Cul1 complex and its proteasomal degradation; mutation of these serines to alanine stabilizes CCNY and enhances CCNY/CDK14 activity on LRP6 phosphorylation, representing autoregulation of the cyclin Y/CDK14 pair. |
In vivo and in vitro phosphorylation mapping by mass spectrometry, Cul1 inactivation, site-directed mutagenesis (S71A/S73A), ubiquitination assays, LRP6 phosphorylation assays |
FEBS letters |
High |
24794231
|
| 2014 |
14-3-3 proteins (ε, β, η, τ isoforms) interact with cyclin Y (CCNY) via Ser-100 and Ser-326 residues, and this binding significantly enhances the association between CCNY and CDK14. |
Yeast two-hybrid screen, in vitro and in vivo binding assays, site-directed mutagenesis |
Acta biochimica et biophysica Sinica |
Medium |
24618387
|
| 2015 |
CDK14 interacts with cyclin Y in spinal cord injury (SCI) rat model; CDK14 expression increases and peaks at 3 days post-SCI; CDK14 co-localizes with cyclin Y and with PCNA in astrocytes/glial cells, suggesting a role in reactive gliosis. |
Western blot, immunohistochemistry, double immunofluorescence, Co-immunoprecipitation in rat SCI model |
Journal of molecular neuroscience : MN |
Medium |
26315607
|
| 2015 |
PFTK1 (CDK14) knockdown in breast cancer cells attenuates Wnt/β-catenin signaling by reducing DVL2 levels and inhibiting β-catenin transcriptional targets (cyclin D1, MMP9, HEF1); PFTK1 interacts with cyclin B, and this complex increases DVL2 levels. |
Co-immunoprecipitation (cyclin B interaction), siRNA knockdown, Western blot, proliferation/migration/invasion assays in breast cancer cells |
Medical oncology |
Medium |
26033031
|
| 2015 |
PFTK1 (CDK14) knockdown in oligodendrocyte progenitor cell-derived OLN-93 cells promotes oligodendrocyte differentiation (increased CNPase, MOG, CGT, MBP markers); this effect is mediated through activation of the PI3K/AKT pathway but not the MAPK/ERK pathway, as AKT-specific inhibitor abrogates the differentiation-promoting effect of PFTK1 silencing. |
siRNA knockdown, qPCR, Western blot, AKT inhibitor epistasis in OLN-93 cells |
Journal of molecular neuroscience : MN |
Medium |
25355490
|
| 2016 |
Caprin-2 positively regulates constitutive LRP5/6 Ser-1490 phosphorylation in a cell cycle-dependent manner (G2/M) by forming a quaternary complex with CDK14, Cyclin Y, and LRP5/6; Caprin-2 knockdown disrupts the CDK14–Cyclin Y interaction and the CDK14/Cyclin Y–LRP6 interaction. |
Co-immunoprecipitation, siRNA knockdown, cell cycle-dependent phosphorylation assays |
The Journal of biological chemistry |
High |
27821587
|
| 2019 |
FMF-04-159-2 is a potent covalent CDK14 inhibitor with TAIRE kinase-biased selectivity; covalent CDK14 inhibition affects cell-cycle regulation, particularly mitotic progression; phospho-proteomics under washout conditions identified putative CDK14-specific substrates. |
Covalent inhibitor development, phospho-proteomics, cell-cycle analysis with washout conditions |
Cell chemical biology |
High |
30930164
|
| 2019 |
Synthesis and SAR of covalent 4-amino-1H-pyrazole CDK14 inhibitors culminated in FMF-04-159-2, a potent, covalent CDK14 inhibitor with TAIRE kinase-biased selectivity profile. |
Medicinal chemistry synthesis, structure-activity relationship analysis, biochemical kinase selectivity profiling |
Bioorganic & medicinal chemistry letters |
Medium |
31175010
|
| 2021 |
In C. elegans, CDK-14 (mammalian CDK14 homolog) promotes axon regeneration via noncanonical Wnt signaling in a kinase-independent manner: CDK-14 binds MIG-5/Disheveled and activates EPHX-1 (ephexin RhoGEF), which activates CDC-42, inhibiting myosin phosphatase and maintaining MLC-4 phosphorylation. EGL-20/Wnt and MIG-1/Frizzled are required for efficient axon regeneration. |
Genetic epistasis (C. elegans), binding studies, GEF activity assays, phospho-mimetic rescue experiments in motor neurons |
The Journal of neuroscience |
High |
34429379
|
| 2022 |
CDK14 knockdown or pharmacological inhibition (FMF-04-159-2) reduces mammary basal cell colony-formation and regeneration capacity, inhibits MMTV-Wnt-1 mammary tumor progression, and suppresses TNBC progression and metastasis by attenuating Wnt/β-catenin signaling. |
Genetic knockdown, pharmacological inhibition (FMF-04-159-2), in vivo MMTV-Wnt-1 mouse model, in vitro colony-formation assays, Wnt signaling readouts |
Cell reports |
High |
36103813
|
| 2022 |
CDK7/cyclin H (CAK complex) physically interacts with CDK14 in the cell nucleus and increases CDK14 phosphorylation; this activates CDK14 to phosphorylate Rb, inhibiting Rb function; overexpression of CDK7 with CDK14 strengthens colony formation and cisplatin resistance in ESCC cells. |
Co-immunoprecipitation, immunofluorescence co-localization, truncation mutant analysis, colony formation assays in ESCC cells |
Annals of translational medicine |
Medium |
31930082
|
| 2023 |
In Drosophila, Eip63E (CDK14 ortholog) regulates axogenesis; PFTK1 knockout mice show increased axonal outgrowth; PFTK1 phosphorylates GDP-bound inactive RhoA and this phosphorylation is required for RhoA activity, establishing RhoA as a CDK14 substrate mediating axon development. |
Drosophila genetic loss-of-function, PFTK1 knockout mouse model, RhoA phosphorylation assays in primary neuronal cultures, functional interaction studies |
BMC biology |
High |
37907898
|
| 2023 |
METTL1 adds internal m7G modifications to CDK14 mRNA, enhancing its stability and thereby promoting CRPC progression; the P300/SP1 complex binds the METTL1 promoter via SP1, mediating METTL1 transcriptional upregulation in CRPC. |
ChIP-qPCR, Co-IP, luciferase reporter assay, m7G AlkAniline-Seq, mRNA degradation assays, transcriptome sequencing |
Journal of experimental & clinical cancer research |
High |
37599359
|
| 2024 |
CDK14 loss in the preformed fibrils (PFF) mouse model of Parkinson's disease mitigates grip strength deficits and reduces pS129 α-synuclein pathology in the cortex; Cdk14 depletion in primary neurons protects against propagation of toxic α-Syn species; pharmacological CDK14 inhibition (FMF-04-159-2) decreases total and pathologically aggregated α-Syn in human neurons, PFF-challenged rat neurons, and α-Syn-humanized mouse brains. |
Genetic Cdk14 knockout in PFF mouse model, primary neuron depletion assays, pharmacological inhibition in multiple model systems, pS129 α-Syn immunostaining |
Cell death & disease |
High |
38575601
|
| 2024 |
IGF2BP2 interacts with CDK14 mRNA, stabilizing it by inhibiting its degradation; CDK14 facilitates LRP6 and GSK3β phosphorylation, thereby regulating β-catenin levels and Wnt/β-catenin signaling during osteogenic differentiation. |
Co-IP (IGF2BP2-CDK14 mRNA interaction), siRNA knockdown, CDK14 inhibitor (FMF-04-159-2), Western blot for LRP6/GSK3β/β-catenin phosphorylation, osteogenesis assays |
Life sciences |
Medium |
39447733
|
| 2024 |
Gefitinib suppresses PFTK1 (CDK14) promoter methylation in a DNMT3B-dependent manner, upregulating CDK14 expression; CDK14 interacts with LRP6 and activates Wnt/β-catenin signaling to attenuate gefitinib-induced apoptosis and confer gefitinib resistance in NSCLC; FMF-04-159-2 reverses CDK14-mediated gefitinib resistance in vitro and in vivo. |
Promoter methylation analysis, DNMT3B manipulation, Co-IP (CDK14-LRP6), gain/loss-of-function assays, pharmacological inhibition in vitro and in vivo |
Communications biology |
Medium |
39702755
|
| 2025 |
Genetic ablation of Cdk14 in mice impairs pulmonary vascular endothelial and alveolar epithelial cell proliferation, causes G2/M cell cycle arrest, and increases mortality and severity of bleomycin- or LPS-induced lung injury; RNA-seq reveals CDK14 knockdown controls STAT1 expression and interferon-signaling-associated genes; CDK14 disruption interferes with IFN-γ-induced lung repair. |
Cdk14 knockout mouse model, CDK14 covalent inhibitor FMF-04-159-2, RNA-seq, cell cycle analysis, in vivo lung injury models |
Cell death discovery |
High |
39827158
|
| 2025 |
RNF213 ubiquitinates CDK14, inhibiting the CDK14-Pdgfrβ signaling pathway; maltol upregulates RNF213, thereby suppressing CDK14-Pdgfrβ signaling, M1 macrophage polarization, and NF-κB phosphorylation. |
In vitro and in vivo macrophage polarization assays, Western blot for CDK14-Pdgfrβ pathway, RNF213 overexpression/knockdown |
Journal of agricultural and food chemistry |
Medium |
40315161
|
| 2025 |
IRX3 promotes CDK14 transcription by binding to its promoter (ChIP-confirmed); CDK14 then stabilizes β-catenin by restraining its ubiquitination and degradation, activating canonical Wnt/β-catenin signaling; LRP6 is identified as a crucial regulatory factor in IRX3-CDK14-mediated β-catenin stabilization in glioblastoma. |
ChIP assay, luciferase reporter assay, gain/loss-of-function in GBM cells, Western blot for β-catenin ubiquitination/stability |
Cell death & disease |
Medium |
41436436
|