| 1995 |
PLK1 (Plk) physically interacts with CHO1/MKLP1 (KIF23) in vivo during late M phase, colocalizing at the midbody, and CHO1/MKLP1 is phosphorylated by Plk-associated kinase activity in vitro. CHO1/MKLP1 induces microtubule bundling and antiparallel movement in vitro. |
Co-immunoprecipitation, in vitro kinase assay, immunofluorescence colocalization |
Molecular and cellular biology |
High |
8524282
|
| 2004 |
PLK1 binds CHO1/MKLP1 (KIF23) via its Polo-box domain, while the stalk domain of CHO1/MKLP1 mediates binding to PLK1. Ser904 and Ser905 are the two major PLK1 phosphorylation sites on CHO1/MKLP1. Depletion of CHO1/MKLP1 causes multinucleation and mislocalizes PLK1 during late mitosis; overexpression of a non-phosphorylatable mutant causes cytokinesis defects; rescue requires the phosphorylatable form. |
Transient transfection domain-mapping, in vitro kinase assay with phosphosite mutagenesis, siRNA knockdown, immunofluorescence, rescue experiments |
Journal of cell science |
High |
15199097
|
| 2005 |
Aurora B phosphorylates MKLP1 (KIF23) on conserved C-terminal serine residues in vitro and in vivo. A non-phosphorylatable MKLP1 mutant localizes properly but fails to support completion of cytokinesis. Aurora B inhibition in late anaphase attenuates MKLP1 phosphorylation and causes cytokinesis failure without disrupting the central spindle. |
In vitro kinase assay, phosphosite mutagenesis, Aurora kinase inhibitor treatment, live-cell imaging, C. elegans genetics and human cell culture |
Current biology : CB |
High |
15854913
|
| 2005 |
INCENP is required for recruiting MKLP1 (KIF23) to the spindle midzone/midbody. MKLP1 depletion by siRNA does not disrupt chromosome segregation or midzone formation but abrogates midbody formation and completion of cytokinesis. INCENP depletion disrupts midzone/midbody formation and causes binucleation. |
RNAi/siRNA knockdown, immunofluorescence, live-cell imaging, 3D reconstruction |
The Biochemical journal |
High |
15796717
|
| 1999 |
GTP-bound (activated) Arf proteins directly bind the C-terminal tail domain of MKLP1 (KIF23) via switch I and switch II regions. An 88-amino acid domain in the MKLP1 C-terminus is sufficient for GTP-dependent Arf binding, and all human Arf isoforms interact with this domain. |
Yeast two-hybrid screen, deletion mapping, GST pull-down assay, point mutagenesis of Arf switch regions |
Cell motility and the cytoskeleton |
High |
10506747
|
| 2012 |
Arf6 directly interacts with MKLP1 (KIF23) at the Flemming body/midbody. Crystal structure of the Arf6-MKLP1 complex shows MKLP1 forms a homodimer flanked by two Arf6 molecules (2:2 heterotetramer) with an extended β-sheet spanning the complex, suitable for membrane interaction at the cleavage furrow. Structure-based mutagenesis and siRNA knockdowns confirm that complex formation is required for completion of cytokinesis. |
Crystal structure determination, structure-based mutagenesis, siRNA knockdown, immunofluorescence |
The EMBO journal |
High |
22522702
|
| 2007 |
Centralspindlin is a heterotetrameric complex composed of two CYK-4/MgcRacGAP homodimers (via parallel coiled coil) and two ZEN-4/MKLP1 homodimers (via parallel coiled coil), assembled through two low-affinity interactions. Centralspindlin (but not individual subunits alone) is sufficient to bundle microtubules in vitro. |
Biochemical dissection, in vitro microtubule bundling assay, conditional genetic mutations and suppressor screen in C. elegans |
Molecular biology of the cell |
High |
17942600
|
| 2013 |
TRAF6 E3 ubiquitin ligase mediates ubiquitination of KIF23/MKLP1 at the midbody ring. SQSTM1/p62 and WDFY3/ALFY form a complex with TRAF6, and these proteins plus NBR1 are required for clearance of midbody ring derivatives by selective autophagy. TRAF6 depletion reduces ubiquitinated midbody ring derivatives. |
siRNA knockdown, immunofluorescence, autophagy assays |
Autophagy |
Medium |
24128730
|
| 2013 |
A missense mutation in KIF23 (p.P916R) causes autosomal dominant congenital dyserythropoietic anemia type III (CDA III). RNAi-based knockdown and rescue experiments in HeLa cells demonstrate that the p.P916R mutation causes cytokinesis failure, consistent with large multinucleated erythroblasts observed in patients. |
Targeted next-generation sequencing, RNAi knockdown, mutant rescue in HeLa cells, haplotype analysis |
Blood |
High |
23570799
|
| 1998 |
CHO1/MKLP1 (KIF23) is required for establishing nonuniform microtubule polarity in podocyte processes. Antisense oligonucleotide treatment in differentiating podocytes abolishes both process formation and nonuniform MT polarity. CHO1/MKLP1 associates with microtubules in podocytes during process formation. |
Antisense oligonucleotide treatment, hook-decoration MT polarity assay, immunofluorescence, taxol/nocodazole recovery experiments |
The Journal of cell biology |
High |
9864367
|
| 1998 |
CHO1/MKLP1 (KIF23) is expressed in postmitotic neurons (in vivo and in vitro), with mRNA levels peaking prior to dendritic development and declining after dendrites differentiate. Dorsal root ganglion neurons (axon-only) express significantly lower levels, consistent with a role in establishing the dendritic minus-end-distal microtubule polarity pattern. |
In situ hybridization in rodent brain, in vitro hippocampal neuron culture, quantitative expression analysis |
The European journal of neuroscience |
Medium |
9749792
|
| 2006 |
MKLP1 (KIF23) nuclear localization during interphase requires two NLS sequences (899SRKRRSST906 and 949KRKKP953) in its tail domain. Expression of an NLS-deleted mutant causes cell cycle arrest at cytokinesis. Phosphomimetic mutations at two serines within the first NLS attenuate nuclear localization, suggesting phosphorylation-regulated nuclear import. |
Domain mapping by mutagenesis, ectopic expression of NLS mutants, cell cycle analysis |
Biochemical and biophysical research communications |
Medium |
17198681
|
| 2006 |
The motor and tail domains of MKLP1 (KIF23) are required for its dendritic targeting in hippocampal neurons. Deletion of the motor domain prevents dendritic distribution; deletion of the tail domain causes axonal mislocalization; deletion of the stalk domain still permits dendritic targeting. |
eGFP-tagged domain deletion mutants expressed in primary hippocampal neurons, fluorescence microscopy |
Journal of cell science |
Medium |
16418225
|
| 2015 |
Kif23 isoform CHO1 (but not the shorter MKLP1 isoform) contains two NDR/LATS kinase consensus sites (S716 and S814) that are phosphorylated by NDR and LATS kinases in vitro. Phosphorylation at S814 creates a 14-3-3 binding site important for Kif23 clustering during cytokinesis. Sequential phosphorylation occurs: S716 phosphorylation is required for efficient S814 phosphorylation. LATS1/2 participate in S814 phosphorylation in vivo. |
In vitro kinase assay with NDR/LATS, site-directed mutagenesis, 14-3-3 binding assay, in vivo phosphorylation analysis |
PloS one |
High |
25658096
|
| 2016 |
p120-catenin binds MKLP1 (KIF23) via its N-terminal coiled-coil domain (isoform 1A) at the cleavage furrow during anaphase to spatially control RhoA GTPase cycling. This binding is independent of cadherin association. Loss of p120 leads to multinucleation due to cytokinesis failure. |
Co-immunoprecipitation, domain mutagenesis, immunofluorescence, siRNA knockdown with multinucleation readout |
Nature communications |
High |
28004812
|
| 2013 |
KIF23 transcription is regulated by p53 via p21(WAF1/CIP1)-dependent repression. The cell cycle genes homology region (CHR) element in the KIF23 promoter is required for both p53-dependent repression and cell cycle-dependent expression. DREAM and MMB complexes differentially bind the CHR element to control cell cycle- and p53-dependent regulation of KIF23. |
Promoter reporter assays, qRT-PCR, Western blot, chromatin immunoprecipitation |
PloS one |
Medium |
23650552
|
| 2008 |
CUX1 and E2F1 transcription factors cooperatively bind the MKLP1 (KIF23) promoter upon S-phase entry, driving its transcriptional activation. The KIF23 promoter contains CHR sites, E2F binding elements, and CUX1 binding sites. CUX1 or E2F1 overexpression increases endogenous MKLP1 protein; E2F1 knockdown reduces it. |
Chromatin immunoprecipitation, promoter-luciferase reporter assays, dominant negative/overexpression of transcription factors, siRNA |
Molecular and cellular biology |
High |
19015243
|
| 2024 |
SIRT7 physically interacts with KIF23 and inhibits its succinylation at K537, thereby enhancing KIF23 protein stability. Overexpression of SIRT7 increases KIF23 protein levels in HEK-293T cells, and SIRT7 knockdown blocks the pro-proliferative and pro-migratory effects of KIF23 overexpression in anaplastic thyroid cancer cells. |
Co-immunoprecipitation, Western blot for succinylation, protein stability assay, siRNA knockdown, overexpression |
BMC cancer |
Medium |
38360598
|
| 2020 |
KIF23 activates Wnt/β-catenin signaling in gastric cancer by directly interacting with Amer1, competitively blocking Amer1-APC association, and relocating Amer1 from the membrane/cytoplasm to the nucleus, thereby attenuating Amer1's negative regulation of Wnt/β-catenin signaling. |
Co-immunoprecipitation, immunofluorescence, siRNA knockdown, cell function assays, TCGA/GEO data analysis |
Aging |
Medium |
32365332
|
| 2020 |
The tail domain of MKLP1 (KIF23) exhibits an autoinhibitory effect on its motor activity; overexpression of the tail domain alone blocks cytokinesis and causes binucleation. PAK2 (p21-activated kinase 2) binds the MKLP1 tail domain, and PAK2 knockdown causes loss of MKLP1 midbody localization and cytokinesis failure, suggesting PAK2 binding relieves autoinhibition. |
GST pull-down, LC-MS/MS interactome, co-immunoprecipitation, FRET, siRNA knockdown, overexpression in HEK293 cells |
BioMed research international |
Low |
33204722
|
| 2022 |
FOXM1 epigenetically activates KIF23 expression in hepatocellular carcinoma by increasing RNA polymerase II occupancy and histone H3K27 acetylation at the KIF23 promoter. FOXM1 suppression reduces KIF23 levels and reverses sorafenib resistance. |
ChIP for RNA Pol II and H3K27ac at KIF23 promoter, Western blot, siRNA knockdown |
Biochemical and biophysical research communications |
Medium |
36940637
|
| 2022 |
NAT10 binds the 3'UTR of KIF23 mRNA and up-regulates its ac4C modification, stabilizing KIF23 mRNA and increasing KIF23 protein levels, which in turn activates Wnt/β-catenin signaling via GSK-3β/β-catenin to promote colorectal cancer progression. |
RIP-seq, acRIP-seq, RNA stability assays, luciferase reporter assay, Western blot, in vitro and in vivo cancer models |
Journal of experimental & clinical cancer research : CR |
Medium |
36522719
|
| 2024 |
KIF23 depletion in mice disrupts mitotic spindle orientation and impairs cytokinesis in neural stem and progenitor cells (NSPCs), leading to precocious neurogenesis, neuronal apoptosis, accelerated cell cycle exit, and disrupted apical junction protein localization. Phenotypes are rescued by wild-type human KIF23 but not by a microcephaly-associated variant, establishing KIF23 as required for spindle orientation and apical surface maintenance in cortical NSPCs. |
Kif23 knockdown in mouse cortex, rescue with WT vs. disease-variant human KIF23, live imaging, immunofluorescence for spindle orientation and apical junction proteins |
The EMBO journal |
High |
39632980
|
| 2022 |
Centralspindlin (Cyk4/MKLP1) and its partner RhoGEF Ect2 are required for exclusion of NuMA/dynein/dynactin from the equatorial cell membrane during anaphase. Ect2-based and NuMA-based complexes occupy mutually exclusive membrane domains; equatorial enrichment of the Ect2/Cyk4/Mklp1 complex is essential for proper spindle elongation and cleavage furrow formation. |
siRNA knockdown, immunofluorescence, live-cell imaging of membrane compartmentalization |
The Journal of cell biology |
Medium |
36197340
|
| 2025 |
Kif23 promotes cardiac fibroblast proliferation and myofibroblast transdifferentiation following myocardial infarction by activating RhoA and suppressing Ces1d-mediated fatty acid β-oxidation via the RhoA/ROCK1 signaling axis, causing pathological lipid accumulation and fibrosis. Kif23 knockdown (via AAV-shRNA) attenuated post-MI fibrosis in mice. |
AAV-mediated shRNA knockdown in vivo, TGF-β1-stimulated cardiac fibroblasts, proteomic profiling, lipid droplet analysis, Western blot for RhoA/ROCK1 |
Hypertension (Dallas, Tex. : 1979) |
Medium |
41078122
|
| 2023 |
In hepatocellular carcinoma, the TAZ-TEAD2 transcriptional pathway promotes tumor cell proliferation via increased expression of KIF23 (and ANLN) as direct transcriptional targets. CRISPRi knockdown of KIF23 in mice reduced HCC tumor growth, and TAZ deletion consistently decreased HCC growth and mortality. |
CRISPRi screen, ChIP to confirm TAZ target genes, RNA sequencing, genetic deletion of TAZ in floxed mice, AAV8-Cre delivery |
Gastroenterology |
Medium |
36894036
|
| 2016 |
In Drosophila motoneurons, Toll-6/dSARM/FoxO signaling represses Pavarotti/MKLP1 (ortholog of KIF23) expression. Elevated MKLP1 attenuates microtubule dynamics. Pathway loss-of-function phenotypes in axon transport and structural plasticity are rescued by reducing Pav-KLP expression, placing MKLP1 downstream of Toll-6-FoxO signaling. |
Drosophila genetic epistasis (suppressor analysis), in vivo imaging, Western blot |
The Journal of cell biology |
Medium |
27502486
|
| 2026 |
The C-terminal domain of KIF23 directly binds the myosin tail domain of MYH9. This interaction stabilizes MYH9 by recruiting deubiquitinase USP7 to remove K48-linked ubiquitin chains from MYH9. Stabilized MYH9 then recruits USP15 to deubiquitinate MCM2 at K469, preventing MCM2 degradation. Elevated MCM2 enhances binding to PCNA, promoting cervical cancer cell proliferation and cisplatin resistance. |
Co-immunoprecipitation, CRISPR/Cas9 knockout, protein half-life assay, ubiquitination assay, domain mapping |
Clinical and translational medicine |
Medium |
41940421
|
| 2025 |
CDK1 and Aurora B phosphorylation of Citron kinase (CIT-K) at S440 and S699 reduces CIT-K's ability to interact with its midbody partners including KIF23/MKLP1 (and KIF14 and AURKB), thereby regulating midbody formation and post-mitotic midbody remnant stability. |
Phosphosite mutagenesis, Co-immunoprecipitation, in vitro kinase assay, live-cell imaging |
bioRxivpreprint |
Medium |
|