Publication for HMMR and KIF18A

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	HMMR	hyaluronan mediated motility receptor	3161			[link]
hsa	KIF18A	kinesin family member 18A	81930

Pubmed ID	Priority	Text
26295306	0.98	KIF18A, EZH2 and HMMR should be further explored as targets for treatment of GBM.
	0.98	KIF18A, EZH2 and HMMR) in GSCs and GBM tissues was confirmed with all experimental and bioinformatic methods.
	0.98	KIF18A, EZH2, and HMMR) whose expression was confirmed using all experimental and bioinformatics verification methods (Table 1).
	0.97	KIF18A, EZH2, HMMR/RHAMM/CD168, NOL4, MPP6, MDM1, RAPGEF4, RHBDD1, FNDC3B, FILIP1L, MCC, ATXN7L4/ATXN7L1, P2RY5/LPAR6 and FAM118A) that were consistently expressed in GSC cultures and consistently not expressed in NSC cultures.
	0.97	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	KIF18A (H-H'), and HMMR (J-O) were visualized with green fluorescence.
	0.96	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.
	0.95	HMMR, KIF18A, MPP6 and FAM118A) as well as DLL3 and NF1.
	0.94	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).
	0.91	KIF18A, EZH2, and HMMR) were all part of the same protein-protein interaction network (Figure 6).
	0.76	KIF18A, EZH2, DEPDC1 and HMMR (red text) were highly co-expressed in all four subtypes.
	0.72	KIF18A, EZH2, HMMR, MPP6, RHBDD1 and FNDC3B (Figure 6, Supplementary Figures S8-S9) as well as with products of BMI1, MTOR, STAT3, HIF1A, EGFR, NF1, POU3F2 and SALL2.
	0.66	HMMR, KIF18A, MPP6 and FAM118A) to one another and to DLL3 and NF1.
	0.51	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).