| 2006 |
KIF14 interacts with PRC1 (protein-regulating cytokinesis 1) and targets to the central spindle via this interaction. KIF14 depletion causes citron kinase to fail to localize to the central spindle and midbody. KIF14 and citron kinase localization to the central spindle and midbody is codependent, and they form a complex depending on the activation state of citron kinase. |
Co-immunoprecipitation of endogenous proteins, RNAi depletion, immunofluorescence localization |
The Journal of cell biology |
High |
16431929
|
| 2006 |
RNAi-mediated silencing of KIF14 induces cytokinesis failure, causing endoreduplication and multinucleated cells. KIF14 accumulates at spindle poles, spindle microtubules, and the midbody during mitosis. Partial KIF14 depletion (hypomorphic) causes multiple cell cycle phenotypes and acute apoptosis, while strong depletion causes cytokinesis failure. |
RNAi knockdown, time-lapse microscopy, immunofluorescence |
Molecular and cellular biology |
High |
16648480
|
| 2012 |
KIF14 associates with the PDZ domain of Radil and negatively regulates Rap1-mediated inside-out integrin activation by tethering Radil on microtubules. Depletion of KIF14 leads to increased cell spreading, altered focal adhesion dynamics, and inhibition of cell migration and invasion. |
Co-immunoprecipitation, pulldown assay, RNAi knockdown with cell spreading/migration assays, integrin activation assay |
The Journal of cell biology |
High |
23209302
|
| 2014 |
The mouse KIF14 motor domain binds tightly to microtubules and does not display typical nucleotide-dependent changes in microtubule affinity. It has robust ATPase activity but very slow motility. Crystal structure of the ADP-bound motor domain reveals a dramatically opened ATP-binding pocket with central β-sheet twisted ~10° beyond the maximal amount seen in other kinesins (rigor-like state). Cryo-EM fitting shows a distinct binding configuration to microtubules. |
Crystal structure (X-ray crystallography), cryo-electron microscopy, in vitro ATPase assay, microtubule co-sedimentation assay, motility assay |
Journal of molecular biology |
High |
24949858
|
| 2014 |
KIF14 knockdown in hepatocellular carcinoma cells decreases Skp2 and Cks1 levels, leading to accumulation of p27(Kip1) protein by inhibiting its proteasome-dependent degradation. Overexpression of Skp2 in KIF14 knockdown cells attenuates cytokinesis failure, placing KIF14 upstream of the SCF(Skp2) complex in regulating p27(Kip1) ubiquitination. |
RNAi knockdown, western blot for SCF complex components, overexpression rescue, cell cycle analysis |
Experimental & molecular medicine |
Medium |
24854087
|
| 2014 |
KIF14 ectopic expression promotes AKT phosphorylation and activity. Live-cell imaging confirmed an insulin-induced temporal colocalization of KIF14 and AKT at the plasma membrane. KIF14 knockdown correlates with decreased AKT phosphorylation. A small-molecule inhibitor of KIF14 reduces AKT activation. |
Live-cell imaging (colocalization), western blot (AKT phosphorylation), RNAi knockdown, overexpression, small-molecule inhibitor treatment |
Neoplasia (New York, N.Y.) |
Medium |
24784001
|
| 2013 |
KIF14 loss-of-function mutations (autosomal recessive truncating mutations) cause a lethal fetal ciliopathy syndrome in humans with IUGR, microcephaly, renal cystic dysplasia, and brain malformations. Phenotype links KIF14 function in cell division/cytokinesis to primary cilia. |
Whole-exome sequencing, genetic segregation analysis in families |
Clinical genetics |
Medium |
24128419
|
| 2017 |
Homozygous loss-of-function mutations in KIF14 cause primary microcephaly (MCPH) in humans. Patient-derived fibroblasts show impaired localization of both KIF14 and CRIK (citron kinase) at the midbody, and exhibit binucleated and apoptotic cells—hallmarks of failed cytokinesis. KIF14-depleted cells recapitulate these cytokinesis defects. Kif14 knockout mice also show primary microcephaly. |
Whole-exome sequencing, immunofluorescence of patient fibroblasts, RNAi depletion in cells, Kif14 knockout mouse model |
Annals of neurology |
High |
28892560
|
| 2013 |
Kif14 splice-site mutation in mice (laggard) causes severe brain malformation, hypomyelination, and reduced expression of myelin-related genes. Kif14 knockout mice phenocopy laggard. Transgenic complementation with wild-type Kif14 cDNA rescues ataxic phenotype. Disrupted cytoarchitecture of cerebellar and cerebral cortices results from apoptotic cell death. |
Positional cloning, transgenic complementation, Kif14 knockout mouse generation, gene expression analysis, histology |
PloS one |
High |
23308235
|
| 2020 |
The intrinsically disordered N-terminal domain of KIF14 enables unique functional diversity: (1) enables diffusibility of monomeric KIF14, (2) renders dimeric KIF14 super-processive and enables passage through crowded areas, (3) enables autonomous tracking of growing microtubule tips independent of EB proteins, and (4) is sufficient for crosslinking parallel microtubules and necessary for driving sliding of antiparallel microtubules. The disordered domain interacts diffusibly with the microtubule lattice and shows increased affinity for GTP-bound tubulin. |
Single-molecule TIRF microscopy in vitro, domain deletion/truncation analysis, microtubule tip-tracking assays, microtubule sliding assays |
Current biology : CB |
High |
32649913
|
| 2020 |
KIF14 depletion leads to defects in primary ciliogenesis and basal body biogenesis, impairing efficiency of primary cilium formation and elongation dynamics, and disrupting localization of distal appendage proteins SCLT1 and FBF1 and IFT-B complex components. Deregulated Aurora A activity is identified as a mechanism contributing to cilia and basal body formation defects after KIF14 depletion. Primary cilia in KIF14-depleted cells are also defective in response to Hedgehog pathway activation, independently of Aurora A. |
RNAi depletion, immunofluorescence, live-cell imaging, epistasis with Aurora A inhibition, Hedgehog pathway reporter assay |
The Journal of cell biology |
High |
32348467
|
| 2013 |
KIF14 overexpression inhibits anchorage-independent growth in vitro and xenograft tumor growth in vivo in lung adenocarcinoma, and modulates cancer cell migration, invasion, and adhesion to extracellular matrix. Cadherins CDH11 and MCAM were detected as cargo on KIF14; KIF14 overexpression enhances recruitment of CDH11 to the membrane fraction, suggesting KIF14 transports adhesion molecules to the cell membrane. |
Co-immunoprecipitation (cargo identification), cell fractionation (membrane fraction), overexpression and knockdown functional assays, xenograft mouse model |
PloS one |
Medium |
23626713
|
| 2023 |
KIF14 binds the G3BP1/YBX1 complex and facilitates their interaction, causing increased NF-κB promoter activity and activation of the NF-κB pathway in cholangiocarcinoma cells. |
Co-immunoprecipitation, NF-κB promoter reporter assay, gain- and loss-of-function studies |
Oncogene |
Medium |
36922675
|
| 2024 |
BUB1 phosphorylates KIF14 at serine 1292 (Ser1292). Overexpression of the KIF14-ΔSer1292 mutant (non-phosphorylatable) fails to facilitate aggressiveness of anaplastic thyroid cancer cells compared to wild-type KIF14, demonstrating that BUB1-mediated phosphorylation of KIF14 at Ser1292 is required for the BUB1/KIF14 complex to drive chromosome instability. |
Phosphorylation site identification, phospho-mutant overexpression, cell viability and invasion assays, xenograft model |
Journal of cellular and molecular medicine |
Medium |
38498903
|
| 2021 |
LETM1 physically binds KIF14 (demonstrated by co-immunoprecipitation). Interference with LETM1 causes downregulation of KIF14 expression and leads to inhibition of proliferation, invasion, migration, and angiogenesis in esophageal squamous cell carcinoma cells. |
Co-immunoprecipitation, RNAi knockdown, proliferation/invasion/migration/tubule formation assays |
Bioengineered |
Low |
34605738
|
| 2025 |
KIF14 binds directly to the focal adhesion protein vinculin and mediates its delivery to the leading edge of migrating colorectal cancer cells. KIF14 overexpression promotes focal adhesion assembly while KIF14 knockdown disrupts it. The transcription factor E2F1 directly binds the KIF14 promoter to drive its transcription, and E2F1 effects on metastasis are mediated through KIF14. |
Co-immunoprecipitation (KIF14-vinculin), chromatin immunoprecipitation (E2F1-KIF14 promoter), transcriptomic analysis, overexpression/knockdown functional assays, in vivo metastasis model |
Acta biochimica et biophysica Sinica |
Medium |
40931756
|
| 2026 |
MYCBP2 (a ubiquitin E3 ligase) regulates KIF14 protein stability through ubiquitination. KIF14 expression is associated with better overall survival in AML, and KIF14 knockdown partially reverses the effects of MYCBP2 knockdown on cell viability and apoptosis, placing KIF14 downstream of MYCBP2-mediated ubiquitin-proteasome regulation. |
Gene Set Enrichment Analysis, siRNA knockdown, flow cytometry, co-immunoprecipitation (implied), in vivo xenograft model |
The Journal of biological chemistry |
Low |
42036047
|
| 2025 |
Phosphorylation of citron kinase (CIT-K) at S699 by CDK1/Aurora B reduces its ability to interact with KIF14 at the midbody. This phosphorylation-dependent regulation of the CIT-K/KIF14 interaction controls midbody formation and stability. |
Phospho-mutant analysis, co-immunoprecipitation, immunofluorescence, cytokinesis functional assays |
bioRxivpreprint |
Medium |
bio_10.1101_2025.08.25.672096
|
| 2025 |
KIF14 localizes within primary cilia and drives processive runs along the ciliary axoneme. KIF14 depletion impairs intraflagellar transport (IFT). The motor domain drives processive ciliary motility in cooperation with the C-terminal CC1 domain. C-terminal truncations of KIF14 (including patient mutation Q1380x) cause traffic-jam-like accumulations of ciliary components in the distal cilia, leading to bulged cilia tips. |
Live-cell imaging, expansion microscopy, TIRF microscopy (in vitro and in cells), RNAi depletion, domain truncation analysis, patient mutation functional characterization |
bioRxivpreprint |
Medium |
bio_10.1101_2025.03.20.644298
|
| 2014 |
Transcriptional regulation of KIF14 overexpression in ovarian cancer involves Sp1 and YY1 transcription factors binding to the KIF14 promoter. ChIP confirmed enrichment of Sp1 and YY1 at the endogenous KIF14 promoter in high-KIF14-expressing ovarian cancer cell lines. siRNA knockdown of Sp1 and YY1 reduced endogenous KIF14 expression. miR-93, miR-144, and miR-382 post-transcriptionally regulate KIF14 mRNA levels. |
Promoter deletion analysis, ChIP, siRNA knockdown, miRNA mimic/inhibitor treatment |
PloS one |
Medium |
24626475
|
| 2026 |
KIF14 depletion reduces AKT phosphorylation, decreases GPX4 and SLC7A11 expression, increases ACSL4, and sensitizes triple-negative breast cancer cells to ferroptosis. Reciprocal co-immunoprecipitation supports a physical association between endogenous KIF14 and AKT. AKT activator SC79 partially reverses the biochemical and ferroptosis phenotypes caused by KIF14 depletion. |
Reciprocal co-immunoprecipitation (KIF14-AKT), RNAi knockdown, western blot, ferroptosis assays (MDA, Fe2+, ferrostatin-1 rescue), AKT activator rescue |
Open life sciences |
Medium |
42083583
|