PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26883802-0	2016	UDP-sugar substrates of HAS3 regulate its O-GlcNAcylation, intracellular traffic, extracellular shedding and correlate with melanoma progression.	Uridine Diphosphate Sugars	0-9	hyaluronan synthase 3	Homo sapiens	24-28	
26883802-2	2016	Hyaluronan synthesis requires the transport of hyaluronan synthases (HAS1-3) from Golgi to plasma membrane (PM), where the enzymes are activated.	Hyaluronic Acid	0-10	hyaluronan synthase 1	Homo sapiens	69-75	
26883802-3	2016	For the very first time, the present study demonstrated a rapid recycling of HAS3 between PM and endosomes, controlled by the cytosolic levels of the HAS substrates UDP-GlcUA and UDP-GlcNAc.	Uridine Diphosphate Glucuronic Acid	165-174	hyaluronan synthase 3	Homo sapiens	77-81	
26883802-3	2016	For the very first time, the present study demonstrated a rapid recycling of HAS3 between PM and endosomes, controlled by the cytosolic levels of the HAS substrates UDP-GlcUA and UDP-GlcNAc.	Uridine Diphosphate N-Acetylglucosamine	179-189	hyaluronan synthase 3	Homo sapiens	77-81	
26883802-4	2016	Depletion of UDP-GlcNAc or UDP-GlcUA shifted the balance towards HAS3 endocytosis, and inhibition of hyaluronan synthesis.	Uridine Diphosphate N-Acetylglucosamine	13-23	hyaluronan synthase 3	Homo sapiens	65-69	
26883802-4	2016	Depletion of UDP-GlcNAc or UDP-GlcUA shifted the balance towards HAS3 endocytosis, and inhibition of hyaluronan synthesis.	Uridine Diphosphate Glucuronic Acid	27-36	hyaluronan synthase 3	Homo sapiens	65-69	
26883802-5	2016	In contrast, UDP-GlcNAc surplus suppressed endocytosis and lysosomal decay of HAS3, favoring its retention in PM, stimulating hyaluronan synthesis, and HAS3 shedding in extracellular vesicles.	Uridine Diphosphate N-Acetylglucosamine	13-23	hyaluronan synthase 3	Homo sapiens	78-82	
26883802-5	2016	In contrast, UDP-GlcNAc surplus suppressed endocytosis and lysosomal decay of HAS3, favoring its retention in PM, stimulating hyaluronan synthesis, and HAS3 shedding in extracellular vesicles.	Uridine Diphosphate N-Acetylglucosamine	13-23	hyaluronan synthase 3	Homo sapiens	152-156	
26883802-5	2016	In contrast, UDP-GlcNAc surplus suppressed endocytosis and lysosomal decay of HAS3, favoring its retention in PM, stimulating hyaluronan synthesis, and HAS3 shedding in extracellular vesicles.	Hyaluronic Acid	126-136	hyaluronan synthase 3	Homo sapiens	78-82	
26883802-6	2016	The concentration of UDP-GlcNAc also controlled the level of O-GlcNAc modification of HAS3.	Uridine Diphosphate N-Acetylglucosamine	21-31	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	61-69	
26883802-6	2016	The concentration of UDP-GlcNAc also controlled the level of O-GlcNAc modification of HAS3.	Uridine Diphosphate N-Acetylglucosamine	21-31	hyaluronan synthase 3	Homo sapiens	86-90	
26883802-7	2016	Increasing O-GlcNAcylation reproduced the effects of UDP-GlcNAc surplus on HAS3 trafficking, while its suppression showed the opposite effects, indicating that O-GlcNAc signaling is associated to UDP-GlcNAc supply.	Uridine Diphosphate N-Acetylglucosamine	53-63	hyaluronan synthase 3	Homo sapiens	75-79	
26883802-7	2016	Increasing O-GlcNAcylation reproduced the effects of UDP-GlcNAc surplus on HAS3 trafficking, while its suppression showed the opposite effects, indicating that O-GlcNAc signaling is associated to UDP-GlcNAc supply.	Uridine Diphosphate N-Acetylglucosamine	53-63	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	11-19	
26883802-7	2016	Increasing O-GlcNAcylation reproduced the effects of UDP-GlcNAc surplus on HAS3 trafficking, while its suppression showed the opposite effects, indicating that O-GlcNAc signaling is associated to UDP-GlcNAc supply.	Uridine Diphosphate N-Acetylglucosamine	196-206	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	11-19	
26883802-8	2016	Importantly, a similar correlation existed between the expression of GFAT1 (the rate limiting enzyme in UDP-GlcNAc synthesis) and hyaluronan content in early and deep human melanomas, suggesting the association of UDP-sugar metabolism in initiation of melanomagenesis.	Uridine Diphosphate N-Acetylglucosamine	104-114	glutamine--fructose-6-phosphate transaminase 1	Homo sapiens	69-74	
26883802-8	2016	Importantly, a similar correlation existed between the expression of GFAT1 (the rate limiting enzyme in UDP-GlcNAc synthesis) and hyaluronan content in early and deep human melanomas, suggesting the association of UDP-sugar metabolism in initiation of melanomagenesis.	Hyaluronic Acid	130-140	glutamine--fructose-6-phosphate transaminase 1	Homo sapiens	69-74	
26883802-8	2016	Importantly, a similar correlation existed between the expression of GFAT1 (the rate limiting enzyme in UDP-GlcNAc synthesis) and hyaluronan content in early and deep human melanomas, suggesting the association of UDP-sugar metabolism in initiation of melanomagenesis.	Uridine Diphosphate Sugars	214-223	glutamine--fructose-6-phosphate transaminase 1	Homo sapiens	69-74	
26883802-9	2016	In general, changes in glucose metabolism, realized through UDP-sugar contents and O-GlcNAc signaling, are important in HAS3 trafficking, hyaluronan synthesis, and correlates with melanoma progression.	Glucose	23-30	O-linked N-acetylglucosamine (GlcNAc) transferase	Homo sapiens	83-91	
26883802-9	2016	In general, changes in glucose metabolism, realized through UDP-sugar contents and O-GlcNAc signaling, are important in HAS3 trafficking, hyaluronan synthesis, and correlates with melanoma progression.	Glucose	23-30	hyaluronan synthase 3	Homo sapiens	120-124