Publication for DLGAP5 and KIF18A

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	DLGAP5	DLG associated protein 5	9787			[link]
hsa	KIF18A	kinesin family member 18A	81930

Pubmed ID	Priority	Text
26295306	0.98	DLG7, PBK, CDC6, KIF15, KIF18A, EZH2, DEPDC1, HMMR) and the two genes from cluster III, (NOL4 and RAPGEF4) were highly expressed in the majority of proneural samples.
	0.97	DLG7, KIF18A, EZH2, HMMR, NOL4, MPP6, MDM1, FNDC3B, FILIP1L, ATXN7L4, P2RY5 and FAM118A), we found good correlation (r = 0.64 + 021) between the RNA and the corresponding protein levels (Table 1).
	0.97	DLG7 (A-A'), anti-CENPA (B-B'), anti-EZH (D-D'), anti-KIF15 (E-E"), anti-CDC6 (G-G'), anti-KIF18A (H-H'), and HMMR (J-O) were visualized with green fluorescence.
	0.97	DLG7, KIF18A, EZH2, and HMMR) whose expression was confirmed using all experimental and bioinformatics verification methods (Table 1).
	0.97	DLG7, KIF18A, EZH2, and HMMR) in GSCs, but also in the range of independent methods used to verify the results.
	0.96	DLG7, PBK, CDC6, KIF15, KIF18A, EZH2, DEPDC1, HMMR, FILIP1L and FNDC3B) (Supplementary Table S2).
	0.95	DLG7 also regulates KIF18A localization in the cell.
	0.93	KIF18A and EZH2 shared common interactants with DLL3 and that DLG7, DEPDC1 and CENPA shared common interactants with STAT3.
	0.92	DLG7, PBK, CDC6, 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).
	0.89	DLG7, and KIF18A as up-regulated in GBM and classified them as mitosis, DNA replication, and chromosome (MRC) organization genes.
	0.86	DLG7, KIF15, KIF18A, EZH2 and DEPDC1) were highly co-expressed and were arranged within protein cluster 1 together with signaling pathway reporters such as MTOR, pSTAT3 (Ser727), DLL3 and PDGFB (Figure 5B).
	0.85	DLG7, PBK, MCC, MPPG, KIF18A and DEPDC1.
	0.77	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').
	0.72	DLG7, PBK, FILIPL1, DEPDC1, NOL4, CDC6, KIF15, MPP6, KIF18A, EZH2, HMMR, FAM118A, FNDC3B and MDM1.
	0.70	DLG7, EZH2, KIF18A, DEPDC1, KIF15, NOL4 and FAM118A from protein cluster 1 positively correlated with the increment in levels of MTOR, DLL3 (Notch), PDGFB and STAT3.
	0.63	KIF18A, HMMR and DLG7) were shown to be up-regulated in GBM, thus underscoring the relevance of our study.
	0.54	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).
30655363	0.98	HURP overexpression in cells stabilizes K-fibers but also reduces WT KIF18A accumulation at plus-ends.
	0.97	KIF18A's neck linker in cells, reducing the microtubule-bundling protein HURP or the kinetochore mesh component TACC3 allows KIF18A sNL to accumulate at the plus-ends of central K-fibers, whereas increased hepatoma-upregulated protein (HURP) expression inhibits accumulation of the wild-type motor.
	0.97	HURP regulates KIF18A's localization and function in mitotic cells.
	0.97	KIF18A siRNA and transfected with GFP-WT or GFP-sNL1 before fixation and staining with anti-HURP antibodies.
	0.97	KIF18A's neck linker length is important for navigating K-fibers, there are certainly additional obstacles that KIF18A must contend with on K-fibers beyond HURP and TACC3.
	0.94	HURP or TACC3 knockdown reduces K-fiber stability and WT KIF18A accumulation at K-fiber plus-ends.
	0.91	KIF18A and then co-expressed GFP-HURP, which led to increased tubulin immunofluorescence in K-fibers (Fig S4), with either mCherry-tagged KIF18A WT or sNL1 (Fig 5B), WT KIF18A accumulation was reduced at the ends of K-fibers at the center of the spindle (Fig 5C, bottom).
	0.90	HURP-depleted cells, KIF18A displays a tighter accumulation at K-fiber plus-ends, whereas overexpression of HURP's microtubule-binding domain disrupts KIF18A's localization and function.
	0.90	KIF18A or KIF18A and HURP, then transfected GFP-WT KIF18A or GFP-sNL1.
	0.86	KIF18A is also consistent with previously published data showing that overexpression of HURP or the microtubule-binding domain of HURP inhibits KIF18A accumulation at K-fiber plus-ends.
	0.78	HURP and KIF18A do not co-localize on peripheral K-fibers.
	0.75	KIF18A WT is ideally suited to navigate obstacles, such as HURP or TACC3, on K-fibers.
	0.58	KIF18A must be agile during its translocation along K-fibers to navigate microtubule-associated proteins such as HURP and TACC3 and accumulate at plus-ends, where it controls chromosome movements (Fig 6B).
	0.57	KIF18A and mitotic microtubule-associated proteins like HURP must be maintained to ensure that chromosome movements are properly controlled and spindle stability is maintained.
24039047	0.98	Kif18a has been reported recently to interact with HURP, a K-fiber associated protein important for spindle assembly [Ye et al., ].
	0.96	Kif18a localization through HURP mislocalization.
25364424	0.97	Kif18A function by HURP results in the regulation of chromosome congression.
	0.97	HURP expression leads to increased Kif18A sequestration at the K-MTs and a chromosome congression defect is more likely to occur.
25576382	0.96	Kif18A localizes to the plus ends of K-fibers through an association with HURP (Hepatoma UpRegulated Protein).
	0.94	HURP fragment that prevents Kif18A plus end localization leads to decreased association of Kif18A and an increased amplitude of kinetochore oscillations, ultimately leading to a delay in chromosome congression, similar to the phenotype of Kif18A knockdown.
25264249	0.96	Kif18A, and HURP.
30906836	0.96	DLGAP5, AURKB, ECT2, CDCA5, RAD21, CASC5, ZWINT, KIF23, RACGAP1, CCNB2, MLF1IP, AURKA, TOP2A, CENPA, CDK1, NCAPG, NDC80, NEK2, KIF11, 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.
22235336	0.94	DLGAP5, and KIF18A (Figure S2).