Publication for CENPE and KIF18A

Species Symbol Function* Entrez Gene ID* Other ID Gene
coexpression		 CoexViewer
hsa CENPE centromere protein E 1062 [link]
hsa KIF18A kinesin family member 18A 81930

Pubmed ID Priority Text
19625775 0.98 KIF18A depletion via RNAi resulted in decreased signals of kinetochore CENP-E, primarily due to its enhanced degradation.
0.98 KIF18A siRNA, CENP-E staining at the kinetochores was either absent or significantly weakened in comparison with those transfected with luciferase siRNA (Fig. 2B and C), thus consistent with the immuno-blotting data.
0.98 KIF18A depletion destabilized CENP-E due to enhanced protein degradation, we examined the half-life of CENP-E and BubR1 in cells transfected with KIF18A siRNA as well as luciferase siRNA.
0.98 CENP-E and BubR1 in control cells was about 18 h in cells transfected with luciferase siRNA; after depletion of KIF18A, the half-life of CENP-E was less than 8 h, significantly shorter than that in the control cells (Fig. 4).
0.98 KIF18A depletion causes downregulation of CENP-E and that KIF18A is physically associated with CENP-E during mitosis.
0.98 CENP-E. We propose that CENP-E is downstream of KIF18A in the regulation of chromosome congression during mitosis.
0.98 KIF18A, CENP-E or luciferase siRNAs for 24 h were fixed and stained with antibodies to p-H3S10 (red) and alpha-tubulin (green).
0.98 KIF18A depletion results in reduced CENP-E levels.
0.98 KIF18A interacts with CENP-E. (A) Equal amounts of interphase (I) and mitotic (M) HeLa cell lysates were immunoprecipitated with KIF18A IgGs or with control IgGs.
0.98 KIF18A siRNA and the plasmid expressing the wild-type CENP-E tail domain or the tail domain with SIM mutation for 48 h. HeLa cells transfected with luciferase siRNA for 48 h were used as control.
0.97 KIF18A depletion is at least in part mediated through destabilizing kinetochore CENP-E.
0.97 KIF18A and CENP-E are microtubule-based motors in mammalian cells that localize at/or around kinetochores during early mitosis.
0.97 KIF18A or CENP-E prompted us to speculate that these two proteins may be in the same regulatory hierarchy during early mitosis.
0.97 CENP-E and KIF18A mRNA levels summarized from three independent experiments are shown.
0.97 KIF18A, CENP-E or beta-actin.
0.97 CENP-E, BubR1, KIF18A and alpha-tubulin.
0.97 KIF18A and CENP-E, respectively.
0.97 KIF18A, CENP-E or luciferase siRNAs for 24 h and were fixed and stained with antibodies to BubR1 (red) and alpha-tubulin (green).
0.96 CENP-E and KIF18A during mitosis, it remains unclear if there are any physical and functional interactions between mitotic kinesins such as KIF18A and CENP-E during chromosome congression and mitotic progression.
0.96 KIF18A, CENP-E or luciferase siRNAs for 24 h were directly analyzed by time-lapse microscopy.
0.96 CENP-E levels in KIF18A-depleted cells are due to enhanced protein degradation.
0.95 KIF18A via RNAi significantly down-regulated CENP-E, the treatment with MG132, a proteasome inhibitor, largely prevented CENP-E reduction (Fig. 3B and C).
0.94 CENP-E after KIF18A silencing.
0.94 CENP-E protein levels in KIF18A depleted cells was not at the transcription level.
0.94 KIF18A cargos can be a factor that regulates phosphorylation and sumoylation of CENP-E because CENP-E phosphorylation and sumoylation are essential for the maintenance of its activity or kinetochore localization.
0.94 KIF18A, CENP-E or luciferase siRNAs for 24 h were fixed and stained with the antibody to p-H3S10.
0.93 KIF18A depletion, cells transfected with CENP-E siRNA also had mitotic defects, manifesting as having unaligned chromosomes that were unable to move to the equator (Fig. 1D).
0.93 KIF18A could be affected by the enforced expression of CENP-E tail or its SIM mutant.
0.93 KIF18A functions to provide the mitotic kinetochores with a constant flow of kinetochore proteins including CENP-E and BubR1.
0.93 KIF18A, CENP-E or beta-actin.
0.93 KIF18A, SGO1, CENP-E or luciferase siRNAs for 48 h were collected for total RNA extraction.
0.92 KIF18A siRNA; the reduced BubR1 staining in centromeric kinetochores was also observed in cells transfected with CENP-E siRNA (Fig. 5C).
0.92 KIF18A depletion does not result in a complete elimination of CENP-E. It is also likely that KIF18A may not be the sole upstream regulator of CENP-E during mitosis.
0.91 CENP-E, also a plus-end motor protein, results in the same mitotic defects as those seen in cells without KIF18A functions, including the presence of unaligned chromosomes, mitotic arrest and mitotic catastrophe.
0.91 KIF18A depletion causes instability of CENP-E remains unclear, the motor protein may keep CENP-E confined to the kinetochores during early mitosis, thus preventing the access of negative regulator(s).
0.90 KIF18A physically interacted with CENP-E during mitosis and that ectopic expression of a functional CENP-E tail domain, but not its mutant, suppressed chromosome congression defects, we propose that the mitotic roles of KIF18A is at least partially mediated by CENP-E.
0.90 KIF18A siRNAs for 24 h and were fixed and stained with antibodies to CENP-E (green).
0.89 CENP-E depletion induces the chromosome congression defect in a higher percentage of mitotic cells than that caused by KIF18A depletion.
0.85 KIF18A siRNA for one day, the levels of CENP-E, were greatly reduced (Fig. 2A).
0.84 KIF18A physically interacted with CENP-E and BubR1 during mitosis.
0.81 KIF18A or CENP-E. (A) HeLa cells cultured in chamber slides were transfected with KIF18A or luciferase siRNAs for 24 h were fixed and stained with antibodies to phosphorylated-serine 10 of histone H3 (p-H3S10).
0.62 KIF18A and CENP-E levels are high during mitosis.
0.59 CENP-E half-life in cells with KIF18A depletion.
0.50 KIF18A depletion caused specific downregulation of CENP-E. Downregulation of CENP-E as the result of KIF18A silencing was not due to reduced transcription but primarily due to the enhanced protein degradation.
32322170 0.98 KIF10, KIF11, KIF14, KIF15, KIF18A, KIF18B, KIF20A, KIF20B, KIF22, KIF23, KIF24, KIF26B, KIF2C, KIF3B, KIF4A, KIFC1) with survival analyses regarding OS, RFS and DMFS using chip-seq data.
0.98 KIF10, KIF11, KIF14, KIF15, KIF18A, KIF18B, KIF20A, KIF23, KIF2C, KIF4A, KIFC1) that demonstrated significant prognostic value in breast cancer were enrolled for LASSO regression to construct a KIFs-based risk score for prediction of OS in breast cancer.
0.98 KIF10, KIF15, KIF18A, KIF18B, KIF20A, KIF4A) were testified by quantitative RT-PCR and immunohistochemistry.
0.98 KIF10, KIF18A and KIF18B are reported to be essential to the progression from metaphase to anaphase with different functions.
0.97 KIF10, KIF11, KIF14, KIF15, KIF18A, KIF18B, KIF20A, KIF20B, KIF22, KIF23, KIF24, KIF26B, KIF2C, KIF3B, KIF4A, KIFC1) using both TCGA-BRCA and matched GTEx-breast normal data (Tumor = 810; Normal = 291); *P < 0.05; **P < 0.001
0.97 KIF10, KIF11, KIF14, KIF15, KIF18A, KIF18B, KIF20A, KIF20B, KIF22, KIF23, KIF24, KIF26B, KIF2C, KIF3B, KIF4A, KIFC1) significantly overexpressed in breast cancer (Fig. 1b, P < 0.001).
0.97 KIF10, KIF11, KIF14, KIF15, KIF18A, KIF18B, KIF20A, KIF20B, KIF23, KIF4A and KIFC1 with significantly high expression in Basal-like and Luminal B subtypes comparing to Luminal A breast cancer (Fig. 1a, Additional file 3).
0.97 KIF10, KIF15, KIF18A, KIF18B, KIF20A, KIF4A were included (Fig. 3b) and a 6-KIFs-based risk score was generated as below:
0.97 KIF10, KIF15, KIF18B, KIF4A: P < 0.0001; KIF18A: P = 0.0003; KIF20A: P = 0.0022), which in accordance with bioinformatics results (Fig. 4a).
0.97 KIF10, KIF15, KIF18A, KIF18B mainly localized to the cytosol and microtubules, besides, localized to the nucleoplasm in normal breast tissue.
0.97 KIF10, KIF11, KIF14, KIF15, KIF18A, KIF18B, KIF20A, KIF23, KIF2C, KIF4A, KIFC1) significantly correlated with worse OS, RFS and DMFS of breast cancer, indicating efficient biomarkers for predicting the prognosis of breast cancer.
0.97 KIF10 and KIF18A were both reported inhibitions to the proliferation of breast cancer cells via deregulating cell division.
0.96 KIF10, KIF11, KIF14, KIF15, KIF18A, KIF18B, KIF20A, KIF20B, KIF22, KIF23, KIF24, KIF26B, KIF2C, KIF3B, KIF4A, KIFC1) overexpressed.
0.96 KIF10, KIF11, KIF14, KIF15, KIF18A, KIF18B, KIF20A, KIF23, KIF2C, KIF4A, KIFC1) were found to be significantly related to worse outcomes regarding OS, RFS and DMFS, indicating that KIFs play important roles in breast cancer and hold the key to the prognosis of patients (Fig. 2a).
0.93 KIF10, KIF15, KIF18A, KIF18B, KIF20A, KIF4A) identified by LASSO regression regarding RFS, OS and DMFS (Additional file 5).
0.92 KIF10 mainly participates in microtubule-kinetochore capture and mitotic checkpoint signaling, therefore plays an important role in chromosome congression and alignment, while KIF18A and KIF18B, two related members of kinesin-8 family, both regulate microtubule dynamics at the plus end, controlling correct chromosome positioning and the length of astral microtubules, respectively.
0.91 KIF10 regulated by KIF18A, which indicates a putative deficiency in singling out any KIFs to analyze alone rather than balancing the interplay between tumor-related KIFs.
0.85 KIF10, KIF11, KIF14, KIF15, KIF18A, KIF18B, KIF20A, KIF23, KIF2C, KIF4A, KIFC1).
0.50 KIF10 inhibitor), Quinazolinedione and phthalimide inhibitors (both KIF15 inhibitors), BTB1 (an inhibitor of KIF18A), Paprotrain (the first known inhibitor of MKLP2).
23955301 0.98 Kif18A tail is 100-times slower than that of the CENP-E tail.
27095104 0.98 CENP-E and Kif18a, have been implicated in kinetochore recruitment of SKAP:Astrin.
28056781 0.98 CENPE, CENPF, CENPI) and motor proteins (KIF11, KIF14, KIF18A, KIF18B, KIF20B, KIF22, KIF23, KIF2C, KIF5B) were included in this cluster.
30446607 0.98 Kif18A, CENP-E, and the Ska complex; however, the exact contribution of these PP1 interactors to SAC silencing is unclear.
24391143 0.97 Kif10, Kif11, Kif15, Kif18A, Kif20A, and Kif23), Kif3B is primarily involved in cell migration and Kif24 is a centriolar kinesin and functions to remodel the local microtubules for cilia assembly.
0.96 Kif10/CENPE, Kif11/EG5, Kif15, Kif16A, Kif18A, Kif18B, Kif20A, Kif20B, Kif21A, Kif23, Kif24, Kif25 and KifC1 (Fig. 1A).
0.93 Kif10, Kif11, Kif15, Kif18A/18B, Kif20A/20B, Kif21, Kif23, Kif24, Kif25 and KifC1 while suppresses the expression of 7 others including Kif1A, Kif1C, Kif7 and KifC3.
0.83 Kif10/CENPE, Kif11/EG5, Kif15, Kif16A, Kif18A, Kif18B, Kif20A, Kif20B, Kif21A, Kif23, Kif25 and KifC1.
0.79 Kif10/CENPE and Kif18A was found in several human cancers including breast cancer (BCa).
28209915 0.97 kif18A binding to the motor protein CENP-E, a plus end-directed motor protein, functioning together with kif18A in kinetochore-microtubule capture during chromosome alignment in the spindle mid-zone (Figure 4A).
28615236 0.97 Kif10), Kinesin-8 (Kif18A), Kinesin-10 (Kif22), Kinesin-13 (Kif2B, Kif2C) and Kinesin-14 (KifC1).
28789343 0.97 centromere protein E (CENPE), KIF2C, KIF3A, KIFAP3, KIF4A, rac GTPase activating protein 1 (RACGAP1), KIF2A, KIF3C, kinesin light chain 1 (KLC1), KIF5A, kinesin light chain 2 (KLC2), KIF5B, KIF5C, KIF11, KIFC1, KIF22, KIF15, KIF18A, KIF3B and KIF23, of which KIF20A and KIF11 were common genes.
29568567 0.97 CENPE, CCNB1, FBXO5, MAD2L1, DLGP5, ANAPC10, CDK1, BRCA2, NUSAP1, CENPF, ANLN, NDC80 and KIF18A belong to the most significant enriched GO terms.
30459823 0.97 Kif18a impairs chromosome congression and dysregulates BubR1 and CENP-E, however, Kif18a knockout females are fertile, and Kif18a knock out ovaries exhibited no apparent histological defects.
20068571 0.96 CENPE KID KIF2A KIF18A KLP1 KLP10A KLP59C MCAK NDC80 RAN SKA1 SKA2 SKA3
22812528 0.95 CENP-E interacting protein CENP-F. Furthermore, BubR1, Nuf2 and CENP-F are known to be required for targeting CENP-E to kinetochores, and they are also assembled onto kinetochores earlier than CENP-E. Therefore, it would be interesting to test whether CENP-F and other known CENP-E interacting proteins, such as the kinetochore-associated microtubule motor protein KIF18A required for CENP-E localization to kinetochores, are also modified by SUMO-2/3 in vivo.
24686554 0.95 Kif18A, MCAK and CENP-E. These proteins exhibit processive tip-tracking, which is fundamentally different from that of the classic tip-tracking proteins like EB1.
31370271 0.95 CENPE/KIF10 and KIF18A, the RNA binding protein NKAP, the Ran GTPase activating protein RanGAP1, the ANAPC4 subunit of the APC/C, along with the protein kinases BUB1B/BubR1 and MPS1/TTK.
25884224 0.94 Kif18A physically interacts with kinetochore fibrous corona components CENP-E and BubR1 during mitosis, consistent with its role in regulating the dynamic connections between kinetochore and spindle microtubules.
0.93 Kif18A may interact with BubR1, a spindle assembly checkpoint component, at the mitotic stage because both proteins are associated with CENP-E. Indeed, GFP-Kif18A accumulated around the kinetochore region where BubR1 signals were also detected in metaphase cells ectopically expressing GFP-WT (Figure 5A, upper panel), suggesting a physical and functional interaction between these two molecules.
0.85 CENP-E. Kif18A sumoylation can potentially affect the switch rate and velocity of kinetochore/chromosome oscillations at metaphase, thus affecting the tension across spindle poles and delaying mitotic progression.
0.62 Kif18A results in chromosome congression defects, which is at least partially mediated through destabilizing another plus-end directed motor protein CENP-E. Mouse genetic study reveals that ablation of KIF18A causes complete sterility.
20212316 0.94 centromere protein E (CENP-E), mitotic centromere-associated kinesin (MCAK), and Kif18A have been implicated in the generation of force at kinetochores.
0.86 CENP-E, MCAK, and Kif18A depletions on sister kinetochore oscillation and breathing.
20232224 0.94 Kif18A, (2) plus-end binding proteins, such EB1, CLASP, and Clip-170, which can favor microtubule growth and could thus regulate the speed of the poleward-moving sister kinetochore, and (3) microtubule-motor proteins, such as CENP-E or dynein, which could mechanically accelerate or slow down microtubule depolymerization.
29078367 0.94 Kif18A is relevant because it collaborates with CENP-E in chromosome alignment and is up-regulated in a subset of cancers.
20981276 0.93 KIF18A or luciferase siRNA for 24 h were fixed and stained with antibodies to CENP-E (green) and CREST (red).
22196931 0.93 CenpE, CenpH, CenpF, CenpS, Cep57, HURP, SKAP, and Kif18a.
28829971 0.93 Kif18A, Dynein, and CENP-E. The MAPs include the Ska complex, Astrin/SKAP, CLASP, EB1, and XMAP215Stu2.
30736436 0.93 KIF18A and CENP-E. Pools of PP1gamma-KIF18A and PP1gamma-CENP-E accumulate at the ends of kinetochore-attached microtubules as cells progress from prometaphase to metaphase, thus providing a localized delivery of PP1gamma to oppose NDC80 phosphorylation and promote attachment stability.
25708751 0.91 Kif10, Kif18A and Kif22.
0.86 Kif10), Kinesin-8 (Kif18A), Kinesin-10 (Kif22), Kinesin-13 (Kif2B, Kif2C) and Kinesin-14 (KifC1).
30733233 0.85 CENP-E and KIF22, a role for KIF18A in promoting proper kinetochore microtubule attachments is cell type specific.
22595673 0.77 CENP-E. Published data unequivocally demonstrates that alignment of bioriented chromosomes is highly dependent on the activity of the kinesin-8 motor, Kif18A, making it a good candidate for controlling position-dependent switching.
25264741 0.68 CENPE, CDC25C, CDCA8, KIF11, ECT2, NEK2, CCNA2, KIF18A, were shown in Table 2.
24244223 0.61 Kif18A also interacts with the Kif10-hBUBR1 complex during mitosis, and the estrogen receptor alpha (ERalpha).



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