Publication for KIF4A and KIF18A

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	KIF4A	kinesin family member 4A	24137			[link]
hsa	KIF18A	kinesin family member 18A	81930

Pubmed ID	Priority	Text
22595673	0.98	Kif4A also had opposite effects on centromere alignment when depleted in combination with Kif18A.
	0.98	Kif18A, Kid and Kif4A spatially regulate centromere switch rates
	0.97	Kif4A); 3) plus-end directed motility along microtubules via 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.
	0.97	Kif18A and Kif4A restored the correlation between switch rate and position to a level similar to that observed in control-depleted cells (Figure 3B and Figure S3B).
	0.97	Kif18A and Kif4A, respectively, is due to direct activities of these motors.
	0.97	Kif18A, GFP-Kif4A and GFP-Kid (Figure S5) on dynamic microtubules were evaluated using an in vitro total internal reflection fluorescence (TIRF) microscopy assay (Figure 6 A-B).
	0.97	Kif4A and Kif18A.
	0.96	Kif4A oppositely tune centromere switch rates and intercentromere distance as a function of position in the absence of Kif18A activity.
	0.96	Kif18A and GFP-Kif4A increased the proportion of time microtubules spent paused in a dose dependent manner.
	0.96	Kif18A/Kif4A depleted cells (bottom) switch rates are also dependent on position, but switching is now influenced by kinetochore tension.
	0.93	Kif4A relative to those in control, Kid or Kif18A depleted cells (Figure 5D).
	0.92	Kif18A and Kif4A directly suppress microtubule plus-end dynamics
	0.91	Kif18A and Kif4A had less severe alignment defects than those depleted of Kif18A alone (r = 0.19 +- 0.01 and p = 0.14 compared to controls, Figure 1B and Figure S1B), confirming that Kif4A-depletion increases centromere alignment.
	0.91	Kif18A and Kif4A led to oscillatory movements that were similar to those observed in Kif18A-depleted cells, but these oscillations were on average positioned significantly closer to the metaphase plate compared to those in cells depleted of Kif18A alone (Figure 2 A-C and Table 1).
	0.91	Kif18A, Kid or Kif4A (Figure 3C and Figure S3 C-D).
	0.90	Kif18A, Kid and Kif4A affect centromere movements, we imaged and tracked the movements of EGFP-CENP-B labeled centromeres with high temporal resolution (2 second intervals) in cells treated with siRNAs specifically targeting these motors (Figure 2 A-B, Figure S1A and supplemental movies S1-S2).
	0.90	Kif4A function effectively confines centromere movements in the absence of Kif18A, indicating that Kid and Kif4A oppositely affect the positioning of bioriented centromeres near the metaphase plate.
	0.89	Kif18A, Kid and Kif4A on mitotic centromere alignment in a large population of cells, we developed an assay to measure the spatial distribution of centromeres along the pole-to-pole axis of the spindle.
	0.87	Kif18A or GFP-Kif4A at the plus-ends of microtubules (Figure 6 C-D and supplemental movies S5-S7).
	0.86	Kif18A-Kid co-depleted cells, consistent with the idea that the increase in alignment caused by Kif4A-depletion requires Kid activity (r = 0.40 +- 0.02 and p = 1.0 x 10-12 compared to controls, Figure 1B and Figure S1B).
	0.84	Kif18A, Kid and Kif4A activity.
	0.79	Kif18A or Kif4A depletion (Figure 1C).
	0.70	Kif18A and Kif4A robustly suppressed microtubule dynamics and promoted microtubule pausing in a concentration-dependent manner (Figure 6E and supplemental movies S5-S7).
	0.57	Kif18A, Kif4A and Kid do not remain bound to the ends of microtubules during depolymerization.
32322170	0.98	KIF4A: P < 0.0001; KIF18A: P = 0.0003; KIF20A: P = 0.0022), which in accordance with bioinformatics results (Fig. 4a).
	0.98	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	KIF18A, KIF18B, KIF20A, KIF20B, KIF22, KIF23, KIF24, KIF26B, KIF2C, KIF3B, KIF4A, KIFC1) with survival analyses regarding OS, RFS and DMFS using chip-seq data.
	0.97	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).
	0.95	KIF18A, KIF18B, KIF20A, KIF20B, KIF22, KIF23, KIF24, KIF26B, KIF2C, KIF3B, KIF4A, KIFC1) overexpressed.
	0.95	KIF18A, KIF18B, KIF20A, KIF23, KIF2C, KIF4A, KIFC1).
	0.95	KIF18A, KIF18B, KIF20A, KIF4A were included (Fig. 3b) and a 6-KIFs-based risk score was generated as below:
	0.93	KIF18A, KIF15 and KIF4A were demonstrated prognostic biomarkers for prediction of clinical outcomes.
	0.92	KIF18A, KIF18B, KIF20A, KIF4A) identified by LASSO regression regarding RFS, OS and DMFS (Additional file 5).
	0.91	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.
	0.85	KIF18A, KIF18B, KIF20A, KIF4A) were testified by quantitative RT-PCR and immunohistochemistry.
	0.59	KIF18A, KIF18B, KIF20A, KIF4A) was generated by LASSO regression with a nomogram validated an accurate predictive efficacy.
25208566	0.97	Kif4A and Kif18A attenuate microtubule dynamics through distinct mechanisms.
	0.94	Kif18A (kinesin-8) localizes to the plus ends of the relatively slowly growing kinetochore fibers (K-fibers) and attenuates their dynamics, whereas Kif4A (kinesin-4) localizes to mitotic chromatin and suppresses the growth of highly dynamic, nonkinetochore microtubules.
	0.91	Kif18A and Kif4A are not functionally equivalent for chromosome alignment, and Kif18A's function in this process depends on its loop2 region.
	0.89	Kif4A and Kif18A motor domains are not functionally equivalent for spindle microtubule length control and likely attenuate microtubule dynamics through distinct mechanisms.
	0.87	Kif18A and Kif4A display a similar ability to attenuate the dynamics of microtubules but function to control the lengths of distinct subsets of spindle microtubules during mitosis.
	0.87	Kif4A and Kif18A directly attenuate microtubule dynamic instability.
	0.82	Kif18A tail is sufficient to facilitate the concentration of other plus end-directed kinesins at K-fiber ends, we engineered chimeric kinesins consisting of the motor and neck-linker domains of Kif18B (kinesin-8), Kif4A (kinesin-4), and Kif5B (kinesin-1) fused to the Kif18A C-terminus (Figure 1A).
	0.77	Kif4A-L2-18A were also significantly different from those measured for Kif18A-FL, they were comparable to the values obtained from FRAP analyses of Kif18B-18A.
	0.77	Kif4A-18A, Kif4A-L2-18A, and Kif5B-18A chimeras were not capable of aligning chromosomes or reducing spindle length compared with GFP-expressing cells depleted of Kif18A (Figure 6, C and D).
	0.66	Kif18A are sufficient for the stable association of plus end-directed motors with K-fiber ends, we inserted the loop2 region of Kif18A into the Kif4A-18A chimera (Kif4A-L2-18A; Figure 4A).
	0.58	Kif18A and Kif18B contain an extended loop2 region compared with Kif4A and Kif5B (Figure 4A).
	0.57	Kif18A and Kif4A are plus end-directed motors that accumulate at microtubule ends, where they suppress both polymerization and depolymerization.
	0.56	Kif4A, Kif18B, and Kif5B (kinesin-1) motor domains to functionally substitute for Kif18A during mitotic chromosome alignment.
30872592	0.97	KIF4A, KIF9, KIF18A, and KIF23 were elevated in LGG patients with a higher histological grade and astrocytoma histologic type than in those with a lower histological grade and histologic type, including oligoastrocytoma and oligodendroglioma.
	0.96	KIF4A, 18A, 23, and 9 were significantly associated with a poor prognosis (KIF4A Hazard ratio [HR]: 3.4 [95% CI 2.38-4.86], KIF18A [HR]: 3.09 [95% CI 2.17-4.4], KIF23 [HR] 3.62 [95% CI 2.52-5.21], KIF9 [HR] 2.17 [95% CI 1.39-3.41]).
	0.96	KIF4A, KIF18A, and KIF23 alterations showed a poorer prognosis than those lacking these alterations in LGG.
	0.94	KIF4A, KIF18A, and KIF23 levels in LGG and GBM patients are correlated with E2F transcription factor activity, the G2M checkpoint, Myc targets, and the mitotic spindle.
	0.91	KIF4A, 18A, 23, and 9 were significantly associated with a poor prognosis (KIF4A Hazard ratio [HR]: 1.36 [95% CI 1.02-1.82], KIF18A [HR]: 1.38 [95% CI 1.02-1.87], KIF23 [HR] 1.31 [95% CI 1.05-1.62], KIF9 [HR] 2.53 [95% CI 1.61-3.99]).
24391143	0.97	Kif4A/4B, Kif5A/5B, 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.
	0.95	Kif4A, Kif4B, Kif5B, Kif10/CENPE, Kif11/EG5, Kif15, Kif16A, Kif18A, Kif18B, Kif20A, Kif20B, Kif21A, Kif23, Kif24, Kif25 and KifC1 (Fig. 1A).
	0.95	Kif4A, 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.
	0.75	Kif4A, Kif4B, Kif5B, Kif10/CENPE, Kif11/EG5, Kif15, Kif16A, Kif18A, Kif18B, Kif20A, Kif20B, Kif21A, Kif23, Kif25 and KifC1.
22839103	0.97	KIF4A, KIF15, KIF18A, KIF18B, KIF20, NUSAP1, and PRC1, of which five were annotated to microtubule-based movement), and six genes were annotated to DNA binding (E2F8, HJURP, EXO1, ERCC6L, KIF15, KIF4A, NUSAP1), whereas no genes in the mitotic checkpoint module were annotated to these categories.
23264559	0.97	KIF4A, KIF7, KIF11, KIF13B, KIF14, KIF15, KIF18A, KIF20A, KIF20B, KIF23, KIFC1, KIFC2).
24327603	0.97	KIF4A and KIF18A may play roles in tumor progression.
28615236	0.97	Kif4), Kinesin-7 (Kif10), Kinesin-8 (Kif18A), Kinesin-10 (Kif22), Kinesin-13 (Kif2B, Kif2C) and Kinesin-14 (KifC1).
28789343	0.94	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.
26912793	0.93	Kif18A depletion leads to significantly increased MT assembly rates, similar to Kif4A.
	0.58	Kif4A and Kif18A rescues the Kif18A congression defect, restoring proper spindle structure and function.
27829144	0.93	KIF4A KO (n=12) *p=0.0225; KIF18A RNAi (n=5) *p=0.0285; Ska1DeltaMTBD (n=5) **p=0.0096.
	0.86	KIF4A KO (n=12) n.s. p=0.854; KIF18A RNAi (n=5) ****p<0.0001; Ska1DeltaMTBD (n=5) ****p<0.0001 and for anti-poleward motion: KID+KIF4A KO (n=12) **p=0.0033; KIF18A RNAi (n=5) n.s. p=0.3492; Ska1DeltaMTBD (n=5) ****p<0.0001.
29346445	0.93	KIF4A, KIF18A, KIF11, and KIF15 (Fig 2C).
	0.75	KIF4A, KIF11, KIF15, KIF18A, KIF20A, which play a pivotal role in cell movements and intracellular trafficking, including chromosome and centrosome positioning during mitosis.
21390237	0.91	Kif18a, Kif22, Kif4), segregation (Aspm Cenpe, Ckap2, Incenp, Jub, Kif20a, Kif23, Lats2, Prc1), and/or cytokinesis (Incenp, Kif20a, Kif23, Prc1) (Table 4).
30906836	0.90	KIF4A, BUB1, PRC1, CDCA8, CCNA2, CDC20, BIRC5, BUB1B, MAD2L1, ZWILCH, CKAP5, KIF18A, KIF2C, CENPE, CENPF, CENPK, KIF20A, CCNB1 are the genes found in the top cluster with high interaction.
31392101	0.87	KIF4A, ANLN, KIF15, KIF18A, FANCI, NEK2, ECT2 and RAD51AP1 (Table 5).
22945934	0.86	KIF4A or KIF18A, or by inhibition of NUMA.
25708751	0.85	Kif4/Xklp-1), Kinesin-8 (Kif18A).
26437877	0.74	KIF4, and the mammalian kinesin-8, KIF18A, localize to microtubule plus ends and suppress microtubule dynamics.
29581135	0.71	KIF4A, KIF18A, DIAPH3, TPX2) have been causally associated with resistance to chemotherapy (20,21,.