PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26875731-5	2016	Our results showed that: (a) S100B at physiological levels decreases glucose uptake, through the multiligand receptor RAGE and mitogen-activated protein kinase/ERK signaling, and (b) insulin stimulated S100B secretion via PI3K signaling.	Glucose	69-76	S100 calcium binding protein B	Homo sapiens	29-34	
26875731-6	2016	Our findings indicate the existence of insulin-S100B modulation of glucose utilization in the brain tissue, and may improve our understanding of glucose metabolism in several conditions such as ketosis, streptozotocin-induced dementia and pharmacological exposure to antipsychotics, situations that lead to changes in insulin signaling and extracellular levels of S100B.	Glucose	67-74	S100 calcium binding protein B	Homo sapiens	47-52	
26875731-6	2016	Our findings indicate the existence of insulin-S100B modulation of glucose utilization in the brain tissue, and may improve our understanding of glucose metabolism in several conditions such as ketosis, streptozotocin-induced dementia and pharmacological exposure to antipsychotics, situations that lead to changes in insulin signaling and extracellular levels of S100B.	Glucose	67-74	S100 calcium binding protein B	Homo sapiens	364-369	
26875731-6	2016	Our findings indicate the existence of insulin-S100B modulation of glucose utilization in the brain tissue, and may improve our understanding of glucose metabolism in several conditions such as ketosis, streptozotocin-induced dementia and pharmacological exposure to antipsychotics, situations that lead to changes in insulin signaling and extracellular levels of S100B.	Glucose	145-152	S100 calcium binding protein B	Homo sapiens	47-52	
19467712-6	2009	RESULTS: Significantly, we demonstrate the improved recovery of the protein S100B using a larger molecular weight (MW) cut-off catheter (20 kDa range: 0.1-9%; 100 kDa range: 1.7-18.3%) while maintaining comparable performance for the conventional markers glucose, lactate and pyruvate.	Glucose	255-262	S100 calcium binding protein B	Homo sapiens	76-81	
26316432-7	2015	CONCLUSION: We believe that long-term exposure to high blood glucose concentrations leads to an increase in TOL in patients with DKA and that the neurotransmitter changes that develop in response to this exposure lead to an increase in S100B levels, which is an indicator of neuronal damage.	Glucose	61-68	S100 calcium binding protein B	Homo sapiens	236-241	
24275002-0	2014	Decrease of serum S100B during an oral glucose tolerance test correlates inversely with the insulin response.	Glucose	39-46	S100 calcium binding protein B	Homo sapiens	18-23	
24275002-4	2014	Therefore, we assumed that dynamic changes of S100B could be observed by challenging healthy subjects with an oral glucose tolerance test (OGTT).	Glucose	115-122	S100 calcium binding protein B	Homo sapiens	46-51	
24275002-9	2014	However, the decrease of serum-S100B 1h after glucose ingestion correlated inversely with the respective changes of serum-insulin (r = -0.484, P=0.049) and serum-C-peptide (r = -0.570, P = 0.017).	Glucose	46-53	S100 calcium binding protein B	Homo sapiens	31-36	
26875731-3	2016	Changes in cerebrospinal fluid levels of S100B (an astrocyte-derived protein) have been associated with alterations in glucose metabolism; however, there is no evidence whether insulin modulates glucose metabolism and S100B secretion.	Glucose	119-126	S100 calcium binding protein B	Homo sapiens	41-46	
26875731-4	2016	Herein, we investigated the effect of S100B on glucose metabolism, measuring D-(3)H-glucose incorporation in two preparations, C6 glioma cells and acute hippocampal slices, and we also investigated the effect of insulin on S100B secretion.	Glucose	47-54	S100 calcium binding protein B	Homo sapiens	38-43	
24275002-7	2014	Mean S100B concentrations decreased about 20% during the first hour after glucose ingestion (P<0.001).	Glucose	74-81	S100 calcium binding protein B	Homo sapiens	5-10	
20835858-10	2010	Exposure of MIO-M1 cells to high glucose induced increased production of RAGE and S100B.	Glucose	33-40	S100 calcium binding protein B	Homo sapiens	82-87	
17383127-5	2007	The increase in VEGF expression by HG or S100b was dose- and time-dependently prevented by KIOM-79 (p<0.05 versus 25mM glucose; p<0.01 versus S100b).	Glucose	122-129	S100 calcium binding protein B	Homo sapiens	41-46	
18390927-6	2008	This premature p47phox translocation and preassembly with p22phox were also observed in HL-60 cells cultured with high glucose (HG; 25 mM) and with the specific ligand for the receptor for advanced glycation end products (RAGE), S100B.	Glucose	119-126	S100 calcium binding protein B	Homo sapiens	229-234	
18390927-8	2008	HL-60 cells cultured in HG and S100B exhibited a 1.8-fold increase in fMLP-induced superoxide generation compared with those cultured in normal glucose (5.5 mM).	Glucose	144-151	S100 calcium binding protein B	Homo sapiens	31-36	
31009650-7	2019	Glucose levels and glucose metabolism differentially modulated S100B secretion in astrocytes and BDNF secretion in neurons, when evaluated under specific conditions (high-potassium medium, presence of tetrodotoxin or fluorocitrate).	Glucose	0-7	S100 calcium binding protein B	Homo sapiens	63-68	
34073816-9	2021	In this paper, we have shown that S100B secretion decreases in neurons cultured in a high-glucose or high-insulin medium, while levels in cell lysates are increased with statistical significance.	Glucose	90-97	S100 calcium binding protein B	Homo sapiens	34-39	
32326589-7	2020	It is therefore necessary to clarify the relationship between the concentration of the S100B protein and glucose and insulin levels.	Glucose	105-112	S100 calcium binding protein B	Homo sapiens	87-92	
31009650-7	2019	Glucose levels and glucose metabolism differentially modulated S100B secretion in astrocytes and BDNF secretion in neurons, when evaluated under specific conditions (high-potassium medium, presence of tetrodotoxin or fluorocitrate).	Glucose	19-26	S100 calcium binding protein B	Homo sapiens	63-68	
30854054-0	2019	Long non-coding RNA-NEF targets glucose transportation to inhibit the proliferation of non-small-cell lung cancer cells.	Glucose	32-39	S100 calcium binding protein B	Homo sapiens	20-23	
30854054-8	2019	Overexpression of lncRNA-NEF inhibited NSCLC cell proliferation and glucose uptake, and downregulated GLUT1 expression.	Glucose	68-75	S100 calcium binding protein B	Homo sapiens	25-28	
30854054-9	2019	Therefore, it can be concluded that lncRNA-NEF can target glucose transportation to inhibit the proliferation of NSCLC cells.	Glucose	58-65	S100 calcium binding protein B	Homo sapiens	43-46