Publication for KIF15 and KIF18A

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	KIF15	kinesin family member 15	56992			[link]
hsa	KIF18A	kinesin family member 18A	81930

Pubmed ID	Priority	Text
30709852	0.98	KIF18A-N480 and KIF15-N420 (Fig. 3 C).
	0.98	KIF18A and KIF15, it is likely that these lagging chromosomes are caused, at least in part, by merotelic attachments.
	0.98	KIF18A and KIF15 activity that are lower than fourfold.
	0.98	KIF18A and KIF15 motor activity within the spindle.
	0.97	KIF18A and KIF15 during mitosis.
	0.97	KIF18A), and kinesin-12 (KIF15).
	0.97	KIF18A, while the shorter spindles in cells expressing higher levels of mCherry-KBP could result from KIF15 inhibition (Fig. 1 E, right).
	0.97	KIF18A and KIF15 by fourfold compared with endogenous levels (Fig. 9 G).
	0.96	KIF18A and KIF15 coinhibition, we knocked down KIF18A, KIF15, or KIF18A and KIF15 using previously validated siRNAs.
	0.96	KIF18A-N480-GFP-His6 (D) and His6-KIF15-N420 (E) in the presence and absence of GST-KBP and/or MTs.
	0.95	KIF18A and KIF15 as metaphase KBP substrates.
	0.95	KIF18A and/or KIF15 display multiple lagging chromosomes in anaphase.
	0.94	KIF18A and KIF15 suggests that KBP may also play an important role in regulating cell division, as both of these motors have established mitotic functions.
	0.94	KIF18A (A) or endogenous KIF15 (B).
	0.94	KIF18A and KIF15, we preincubated motors with KBP to allow complex formation and then measured their ability to bind MTs in the presence of AMPPNP.
	0.93	KIF18A and KIF15 by KBP is required to prevent lagging chromosomes in anaphase.
	0.92	KIF18A's influence of chromosome alignment and KIF15's effects on spindle length are well established, a role for KIF14 in metaphase has not been documented.
	0.91	KIF18A, GFP-KIF15, or both mCherry-KIF18A and GFP-KIF15.
	0.89	KIF18A and KIF15 during metaphase.
	0.84	KIF18A accumulation is abolished in even the faintest mCherry-KBP-expressing cells, KIF15 distribution correlates with mCherry-KBP expression level in the cell (Fig. 4 E).
	0.82	KIF18A and KIF15 in combination produced cells with normal spindle lengths (Fig. 2 C).
	0.79	KIF18A and KIF15 within the spindle.
	0.79	KIF18A (28), and GFP-KIF15 (49).
	0.77	KIF18A and KIF15 by blocking the MT binding activity of their motor domains but may not prevent MT interaction when secondary nonmotor MT-binding elements are present.
	0.65	KIF15 and KIF18A, and this inhibition occurs in a dose-dependent manner (Fig. 3, A and B), with KIF18A showing enhanced sensitivity to KBP levels (~80% inhibition of KIF18A activity achieved with 100 nM KBP compared with 250 nM KBP for KIF15).
	0.63	KIF18A or GFP-KIF15 alone or in combination were much more likely to have multipolar spindles in addition to multiple lagging chromosomes, particularly in the double motor overexpression condition (Fig. 9 F).
	0.57	KIF18A knockdown resulted in unaligned chromosomes (large FWHM values), and this phenotype remained unchanged in combination with KIF15 knockdown (Fig. 2 C, left).
	0.56	KIF18A-N480-GFP-His6 (top) or 50 nM His6-KIF15-N420 (bottom) with 250 nM GST-KBP probed with antibodies targeting 6xHis (alpha His) and KBP (alpha KBP).
	0.51	KIF15 and KIF18A motor function in vitro.
26295306	0.98	KIF15, MPP6, KIF18A, EZH2, DEPDC1, HMMR, P2RY5, FAM118A, and FNDC3B) correlated with the least favorable survival (Supplementary Figure S6A).
	0.98	KIF18A, DEPDC1, KIF15, NOL4 and FAM118A from protein cluster 1 positively correlated with the increment in levels of MTOR, DLL3 (Notch), PDGFB and STAT3.
	0.97	KIF15, MPP6, KIF18A, EZH2, HMMR, FAM118A, FNDC3B and MDM1 (Figure 5A, Supplementary Figure S7).
	0.95	KIF15 (E-E"), anti-CDC6 (G-G'), anti-KIF18A (H-H'), and HMMR (J-O) were visualized with green fluorescence.
	0.94	KIF15, DEPDC1, CDC6, DLG7, KIF18A, EZH2 and HMMR) in GSCs and GBM tissues was confirmed with all experimental and bioinformatic methods.
	0.94	KIF15, KIF18A, EZH2, DEPDC1, HMMR, FILIP1L and FNDC3B) (Supplementary Table S2).
	0.94	KIF15, MPP6, KIF18A, EZH2, HMMR, FAM118A, FNDC3B and MDM1.
	0.94	KIF15, PBK, CDC6 and KIF18A in the cerebral cortex (A'-H') and in GBM tissues A-H. and against MPP6 and HMMR in NSCs (I', J-L. and GSCs I, M-O. is shown.
	0.91	KIF15, DEPDC1, CDC6, DLG7/DLGAP5/HURP, KIF18A, EZH2, HMMR/RHAMM/CD168, NOL4, MPP6, MDM1, RAPGEF4, RHBDD1, FNDC3B, FILIP1L, MCC, ATXN7L4/ATXN7L1, P2RY5/LPAR6 and FAM118A (Figure 1A, Table 1 and Supplementary Figure S1).
	0.90	KIF15, DEPDC1, CDC6, DLG7, KIF18A, EZH2, HMMR, MPP6, RHBDD1, FNDC3B, MCC, and FAM118A) were functionally interconnected and built a protein interaction network (Figure 6, Table 2, Supplementary Figure S8).
	0.83	KIF15, DEPDC1, CDC6, DLG7, KIF18A, EZH2, HMMR, NOL4, MCC, MPP6, RAPGEF4, ATXN7L4 and MDM1) were significantly up-regulated while FAM118A and P2RY5 were down-regulated (Figure 1C-1C').
	0.67	KIF15, DEPDC1, CDC6, DLG7, KIF18A, EZH2, and HMMR) whose expression was confirmed using all experimental and bioinformatics verification methods (Table 1).
	0.54	KIF15, KIF18A, EZH2, DEPDC1 and HMMR), the second eight genes (FILIP1L, MCC, MPP6, ATXN7L4, P2RY5, FAM118A, FNDC3B and MADM1), and the third two genes (NOL4, RAPGEF4) (Figure 3A).
24391143	0.96	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.
	0.95	Kif15, Kif16A, Kif18A, Kif18B, Kif20A, Kif20B, Kif21A, Kif23, Kif24, Kif25 and KifC1 (Fig. 1A).
	0.85	Kif15, Kif16A, Kif18A, Kif18B, Kif20A, Kif20B, Kif21A, Kif23, Kif25 and KifC1.
	0.65	Kif15, Kif18A/18B, Kif20A/20B, Kif21, Kif23, Kif24, Kif25 and KifC1 while suppresses the expression of 7 others including Kif1A, Kif1C, Kif7 and KifC3.
30593585	0.96	KIF15 (I), KIF18A (J), and KIF26B (K).
30655363	0.92	KIF15 are kinesin motors that stabilize the spindle and occupy the same microtubule-binding site as KIF18A.
31392101	0.78	KIF15, KIF18A, FANCI, NEK2, ECT2 and RAD51AP1 (Table 5).
	0.55	KIF15, KIF18A, FANCI, NEK2, ECT2, and RAD51AP1.
23264559	0.73	KIF15, KIF18A, KIF20A, KIF20B, KIF23, KIFC1, KIFC2).
28061449	0.70	KIF18A, KIF15) that were independent of MMB and FOXM1 were also included in the signature.