1.14.18.1	tyrosinase	B-16 cell	-	685452, 689442, 696686	
1.14.18.1	tyrosinase	B-16 cell	B16 melanoma cell	688041	
2.4.1.80	ceramide glucosyltransferase	B-16 cell	-	735591	
2.4.2.12	nicotinamide phosphoribosyltransferase	B-16 cell	-	735872, 759035	
2.4.3.1	beta-galactoside alpha-(2,6)-sialyltransferase	B-16 cell	-	637260	
2.4.3.8	alpha-N-acetylneuraminate alpha-2,8-sialyltransferase	B-16 cell	-	764085	
2.5.1.132	3-deoxy-D-glycero-D-galacto-nonulopyranosonate 9-phosphate synthase	B-16 cell	-	737585	
2.7.1.40	pyruvate kinase	B-16 cell	-	761609	
2.7.11.25	mitogen-activated protein kinase kinase kinase	B-16 cell	-	680887	
2.7.7.1	nicotinamide-nucleotide adenylyltransferase	B-16 cell	-	642811	
3.1.4.11	phosphoinositide phospholipase C	B-16 cell	-	679976	
3.1.4.4	phospholipase D	B-16 cell	-	665531	
3.1.4.4	phospholipase D	B-16 cell	melanoma cell	679775	
3.2.1.166	heparanase	B-16 cell	-	732954	
3.4.21.B2	granzyme M	B-16 cell	-	754951	
3.4.22.1	cathepsin B	B-16 cell	a melanoma cell line	708276	
3.4.22.26	cancer procoagulant	B-16 cell	-	30157, 30159	
4.1.1.17	ornithine decarboxylase	B-16 cell	melanoma cell line	677508	
4.1.1.33	diphosphomevalonate decarboxylase	B-16 cell	-	693443	
6.2.1.1	acetate-CoA ligase	B-16 cell	cells express higher levels of cytosolic acetyl-CoA synthetase ACSS2 under hypoxia than normoxia. Knockdown of ACSS2 by RNA interference in tumor cells enhances tumor cell death under long-term hypoxia in vitro. The ACSS2 suppression slows tumor growth in vivo. Tumor cells excrete acetate and the quantity increases under hypoxia, the pattern of acetate excretion follows the expression pattern of ACSS2. The ACSS2 knockdown leads to a corresponding reduction in the acetate excretion in tumor cells	703038	
6.3.2.17	tetrahydrofolate synthase	B-16 cell	-	1068, 1074