PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
22627736-2	2012	We and others previously demonstrated that glucose activates CD38/ADP-ribosyl cyclase (ADPR-cyclase) to produce two Ca(2+) second messengers, cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP).	Glucose	43-50	CD38 molecule	Homo sapiens	61-65	
22627736-6	2012	Pretreatment with jasplakinolide, an actin polymerizing agent, or a myosin heavy chain IIA (MHCIIA) blocker, blebbistatin, inhibited glucose-induced CD38 internalization, an essential step for cADPR formation.	Glucose	133-140	CD38 molecule	Homo sapiens	149-153	
22627736-8	2012	These results indicate that actin filaments along with MHCIIA play an important role in CD38 internalization for the generation of Ca(2+) mobilizing messengers for glucose-induced Ca(2+) signaling in pancreatic beta-cells.	Glucose	164-171	CD38 molecule	Homo sapiens	88-92	
10580418-8	1999	The anti-CD38+ sera potentiated insulin release both at low [95 (64) vs. 23 (12) microU/ml of control incubations, respectively, P < 0.0001] and high [271 (336) vs. a control of 55 (37) microU/ml, respectively, P = 0.001] medium glucose concentrations, whereas the anti-CD38- sera did not.	Glucose	232-239	CD38 molecule	Homo sapiens	9-13	
19087393-2	2003	On the other hand, ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase (CD38) synthesizes cyclic ADP-ribose from NAD+, which acts as a second messenger, mobilizing intracellular Ca2+ for insulin secretion in response to glucose in beta-cells.	Glucose	216-223	CD38 molecule	Homo sapiens	68-72	
11334442-8	2001	In cultured human islets, anti-CD38-positive sera exhibiting [Ca2+]i-mobilizing activity in Jurkat T-cells (n = 6) significantly stimulated insulin release at 3.3 mmol/l glucose (median [interquartile range] 738 microU/ml [234], P = 0.0001 vs. 320 [52] microU/ml of control), whereas 6 anti-CD38-positive sera without [Ca2+]i-mobilizing activity and 10 anti-CD38-negative did not.	Glucose	170-177	CD38 molecule	Homo sapiens	31-35	
21387169-8	2011	MIN6 cells transfected with human CD38 exhibited increased glucose-induced insulin release.	Glucose	59-66	CD38 molecule	Homo sapiens	34-38	
11334442-9	2001	In further incubations, the five anti-CD38-positive sera displaying [Ca2+]i-mobilizing activity in dispersed islet cells significantly stimulated insulin release at both 3.3 mmol/l glucose (2.2 +/- 0.3% of insulin islet content, P < 0.002 vs. 1.2 +/- 0.1% of control) and 16.7 mmol/l glucose (3.7 +/- 0.3 vs. 2.3 +/- 0.3%, P < 0.002).	Glucose	181-188	CD38 molecule	Homo sapiens	38-42	
11334442-9	2001	In further incubations, the five anti-CD38-positive sera displaying [Ca2+]i-mobilizing activity in dispersed islet cells significantly stimulated insulin release at both 3.3 mmol/l glucose (2.2 +/- 0.3% of insulin islet content, P < 0.002 vs. 1.2 +/- 0.1% of control) and 16.7 mmol/l glucose (3.7 +/- 0.3 vs. 2.3 +/- 0.3%, P < 0.002).	Glucose	287-294	CD38 molecule	Homo sapiens	38-42	
10553576-3	1999	ATP, produced by glucose metabolism, competes with cADPR for the binding site, Lys-129, of CD38, resulting in the inhibition of the hydrolysis of cADPR and thereby causing cADPR accumulation in beta-cells.	Glucose	17-24	CD38 molecule	Homo sapiens	91-95	
32319590-6	2020	Further experiments using an ATP test kit and lactate test kit revealed that CD38 promotes glucose consumption, increases lactate accumulation and increases ATP production.	Glucose	91-98	CD38 molecule	Homo sapiens	77-81	
9754820-2	1998	As human lymphocyte antigen CD38 has both ADP-ribosyl cyclase and cADPR hydrolase activity, it may be important in glucose-induced insulin secretion in islets.	Glucose	115-122	CD38 molecule	Homo sapiens	28-32	
9664081-0	1998	Autoantibodies against CD38 (ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase) that impair glucose-induced insulin secretion in noninsulin- dependent diabetes patients.	Glucose	90-97	CD38 molecule	Homo sapiens	23-27	
9664081-3	1998	Insulin secretion from pancreatic islets by glucose is significantly inhibited by the addition of the NIDDM sera with anti-CD38 antibodies (P </= 0.04-0.0001), and the inhibition of insulin secretion is abolished by the addition of recombinant CD38 (P </= 0.02).	Glucose	44-51	CD38 molecule	Homo sapiens	123-127	
9664081-3	1998	Insulin secretion from pancreatic islets by glucose is significantly inhibited by the addition of the NIDDM sera with anti-CD38 antibodies (P </= 0.04-0.0001), and the inhibition of insulin secretion is abolished by the addition of recombinant CD38 (P </= 0.02).	Glucose	44-51	CD38 molecule	Homo sapiens	247-251	
8527489-1	1995	Cyclic ADP-ribose is generated from NAD+ in glucose-stimulated beta-cells by CD38.	Glucose	44-51	CD38 molecule	Homo sapiens	77-81	
10331647-3	1999	ATP, produced by glucose metabolism, competes with cADPR for the binding site, Lys-129, of CD38, resulting in the inhibition of the hydrolysis of cADPR and thereby causing cADPR accumulation in beta-cells.	Glucose	17-24	CD38 molecule	Homo sapiens	91-95	
31465774-2	2019	AHR targets of the latter function are PARPs/ARTs and CD38 that are regulating glucose and lipid metabolism via NAD-dependent sirtuins.	Glucose	79-86	CD38 molecule	Homo sapiens	54-58