PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
32838757-3	2020	Recently, SGLT2 inhibitors such as empagliflozin that reduce the plasma levels of 1,5-anhydroglucitol have been described as a new treatment option for the neutropenia and neutrophil dysfunction in patients with GSD Ib.	1,5-anhydroglucitol	82-101	solute carrier family 5 member 2	Homo sapiens	10-15
32686804-3	2020	We developed a one-step paper-based sensor for detecting 1,5-AG using glucose oxidase, catalase, and mutarotase that eliminates excess glucose, which interferes with 1,5-AG detection.	1,5-anhydroglucitol	57-63	catalase	Homo sapiens	87-95
32686804-3	2020	We developed a one-step paper-based sensor for detecting 1,5-AG using glucose oxidase, catalase, and mutarotase that eliminates excess glucose, which interferes with 1,5-AG detection.	1,5-anhydroglucitol	166-172	catalase	Homo sapiens	87-95
32294159-3	2020	Off-label use of empagliflozin in four GSD-Ib patients with incomplete response to granulocyte colony stimulating factor (GCSF) treatment decreased serum 1,5-anhydroglucitol and neutrophil 1,5-anhydroglucitol-6-phosphate levels within one month.	1,5-anhydroglucitol	154-173	colony stimulating factor 3	Homo sapiens	83-120
32294159-3	2020	Off-label use of empagliflozin in four GSD-Ib patients with incomplete response to granulocyte colony stimulating factor (GCSF) treatment decreased serum 1,5-anhydroglucitol and neutrophil 1,5-anhydroglucitol-6-phosphate levels within one month.	1,5-anhydroglucitol	154-173	colony stimulating factor 3	Homo sapiens	122-126
31396338-2	2019	We recently demonstrated that miR-223 is significantly upregulated both in atherosclerotic arteries and in the serum sample of ASO patients.	1,5-anhydroglucitol	127-130	microRNA 223	Homo sapiens	30-37
32904185-0	2020	1,5-anhydroglucitol is a good predictor for the treatment effect of the Sodium-Glucose cotransporter 2 inhibitor in Japanese patients with type 2 diabetes mellitus.	1,5-anhydroglucitol	0-19	solute carrier family 5 member 2	Homo sapiens	72-102
32904185-12	2020	Conclusion: The use of SGLT2 inhibitors in patients with T2DM, 1,5-AG was identified as the most reliable indicator for predicting HbA1c reduction.	1,5-anhydroglucitol	63-69	solute carrier family 5 member 2	Homo sapiens	23-28
32253031-2	2020	The reactive AF is metabolized to non-reactive 1,5-anhydro-D-glucitol by AF reductase in animal tissues and human cells.	1,5-anhydroglucitol	47-69	aldo-keto reductase family 1 member E2	Homo sapiens	73-85
32280712-0	2020	Serum 1,5-Anhydroglucitol to Glycated Albumin Ratio Can Help Early Distinguish Fulminant Type 1 Diabetes Mellitus from Newly Onset Type 1A Diabetes Mellitus.	1,5-anhydroglucitol	6-25	albumin	Homo sapiens	38-45
31443163-10	2019	Intervention with TXNIP-ASO prevented ischemia-induced glial activation and neuro-vascular degeneration, and improved visual function compared to untreated WT.	1,5-anhydroglucitol	24-27	thioredoxin interacting protein	Mus musculus	18-23
29625129-15	2018	Additional knockdown of up-regulated Nrf1 offset the effects of miR-378-ASO, suggesting that Nrf1 mediated the inhibitory effect of miR-378-ASO on hepatosteatosis.	1,5-anhydroglucitol	72-75	microRNA 378a	Mus musculus	132-139
30668377-7	2019	Anti-proliferative activity of ASO was studied by Sulforhodamine B (SRB) assay using HaCaT cell lines.	1,5-anhydroglucitol	31-34	chaperonin containing TCP1 subunit 4	Homo sapiens	50-66
30668377-7	2019	Anti-proliferative activity of ASO was studied by Sulforhodamine B (SRB) assay using HaCaT cell lines.	1,5-anhydroglucitol	31-34	chaperonin containing TCP1 subunit 4	Homo sapiens	68-71
30626647-7	2019	Treating G6PC3-deficient mice with an inhibitor of the kidney glucose transporter SGLT2 to lower their blood level of 1,5-anhydroglucitol restored a normal neutrophil count, while administration of 1,5-anhydroglucitol had the opposite effect.	1,5-anhydroglucitol	118-137	solute carrier family 5 (sodium/glucose cotransporter), member 2	Mus musculus	82-87
30626647-7	2019	Treating G6PC3-deficient mice with an inhibitor of the kidney glucose transporter SGLT2 to lower their blood level of 1,5-anhydroglucitol restored a normal neutrophil count, while administration of 1,5-anhydroglucitol had the opposite effect.	1,5-anhydroglucitol	198-217	solute carrier family 5 (sodium/glucose cotransporter), member 2	Mus musculus	82-87
29625129-14	2018	Antagonizing miR-378 via injecting miR-378-ASO into HFD-treated mice led to increased expression of Nrf1, improved FAO and decreased hepatosteatosis.	1,5-anhydroglucitol	43-46	microRNA 378a	Mus musculus	13-20
30976018-0	2019	Rare variants in SLC5A10 are associated with serum 1,5-anhydroglucitol (1,5-AG) in the Atherosclerosis Risk in Communities (ARIC) Study.	1,5-anhydroglucitol	51-70	solute carrier family 5 member 10	Homo sapiens	17-24
30976018-0	2019	Rare variants in SLC5A10 are associated with serum 1,5-anhydroglucitol (1,5-AG) in the Atherosclerosis Risk in Communities (ARIC) Study.	1,5-anhydroglucitol	72-78	solute carrier family 5 member 10	Homo sapiens	17-24
30778899-6	2019	The level of 1,5-AG was lowest in type 1 diabetes and HNF1A MODY, 3.8 and 4.7 mug/ml, respectively, and highest (11.2 mug/ml) in GCK MODY.	1,5-anhydroglucitol	13-19	HNF1 homeobox A	Homo sapiens	54-59
30778899-8	2019	Finally, 1,5-AG and hsCRP in conjunction yielded a C-statistic of 0.86 in discriminating HNF1A from GCK MODY.	1,5-anhydroglucitol	9-15	HNF1 homeobox A	Homo sapiens	89-94
29625129-14	2018	Antagonizing miR-378 via injecting miR-378-ASO into HFD-treated mice led to increased expression of Nrf1, improved FAO and decreased hepatosteatosis.	1,5-anhydroglucitol	43-46	microRNA 378a	Mus musculus	35-42
28820081-4	2017	1,5-AG strongly inhibited trehalase and lactase, whereas d-sorbose inhibited them very weakly.	1,5-anhydroglucitol	0-6	trehalase	Rattus norvegicus	26-35
29625129-14	2018	Antagonizing miR-378 via injecting miR-378-ASO into HFD-treated mice led to increased expression of Nrf1, improved FAO and decreased hepatosteatosis.	1,5-anhydroglucitol	43-46	nuclear respiratory factor 1	Mus musculus	100-104
29625129-15	2018	Additional knockdown of up-regulated Nrf1 offset the effects of miR-378-ASO, suggesting that Nrf1 mediated the inhibitory effect of miR-378-ASO on hepatosteatosis.	1,5-anhydroglucitol	72-75	nuclear respiratory factor 1	Mus musculus	37-41
29625129-15	2018	Additional knockdown of up-regulated Nrf1 offset the effects of miR-378-ASO, suggesting that Nrf1 mediated the inhibitory effect of miR-378-ASO on hepatosteatosis.	1,5-anhydroglucitol	72-75	microRNA 378a	Mus musculus	64-71
30220274-10	2018	The mature miR-155 expression in lung tissue in pmiR-155-ASO group was significantly lower than that in pmiR-cont group (2-DeltaDeltaCt: 4.92+-0.72 vs. 15.38+-0.60, P < 0.05).	1,5-anhydroglucitol	57-60	microRNA 155	Mus musculus	11-18
28820081-4	2017	1,5-AG strongly inhibited trehalase and lactase, whereas d-sorbose inhibited them very weakly.	1,5-anhydroglucitol	0-6	lactase	Rattus norvegicus	40-47
27907860-1	2017	Present study describes the preparation of a polyethylene glycol-grafted oxidized multi-walled carbon nanotubes (oMWCNTs-PEG) hybrid nanosystem as a carrier of etoposide (VP-16) and Bcl-2 phosphorothioate antisense deoxyoligonucleotides (Aso) to achieve a superior cytostastic efficacy in non-small and small cell lung cancer in vitro.	1,5-anhydroglucitol	238-241	host cell factor C1	Homo sapiens	171-176
28483016-5	2017	Results Compared to the control group,the ASO group presented with significantly higher level of plasma Angptl2 [(13.55+-9.17) mug/L vs. (9.04+-4.79) mug/L,P=0.010].	1,5-anhydroglucitol	42-45	angiopoietin like 2	Homo sapiens	104-111
28483016-8	2017	In addition,type 2 diabetes mellitus patients with ASO exhibited significantly higher serum Angptl2 levels [(18.67+-9.84)mug/L] than those without ASO [(13.01+-3.47) mug/L] (P=0.021).	1,5-anhydroglucitol	51-54	angiopoietin like 2	Homo sapiens	92-99
28483016-9	2017	In ASO group,serum Angptl2 levels were negatively correlated with ankle brachial index (r=-0.244,P=0.035).	1,5-anhydroglucitol	3-6	angiopoietin like 2	Homo sapiens	19-26
27907860-7	2017	Moreover, Aso specifically binding to the first six codons of the Bcl-2 mRNA gave a satisfactorily decrease in Bcl-2 translation and an increase in NCIH2135 chemosensitivity towards VP-16.	1,5-anhydroglucitol	10-13	BCL2 apoptosis regulator	Homo sapiens	66-71
27907860-7	2017	Moreover, Aso specifically binding to the first six codons of the Bcl-2 mRNA gave a satisfactorily decrease in Bcl-2 translation and an increase in NCIH2135 chemosensitivity towards VP-16.	1,5-anhydroglucitol	10-13	BCL2 apoptosis regulator	Homo sapiens	111-116
27907860-7	2017	Moreover, Aso specifically binding to the first six codons of the Bcl-2 mRNA gave a satisfactorily decrease in Bcl-2 translation and an increase in NCIH2135 chemosensitivity towards VP-16.	1,5-anhydroglucitol	10-13	host cell factor C1	Homo sapiens	182-187
27995982-7	2016	Intrathecal administration of c-fos antisense oligodeoxynucleotides (ASO) or minocycline (a specific microglia inhibitor) attenuated mechanical allodynia.	1,5-anhydroglucitol	69-72	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	30-35
28000561-8	2017	Molecular docking against 1,5-anhydrosorbitol was performed for functional characterization of RGN.	1,5-anhydroglucitol	26-45	regucalcin	Bubalus bubalis	95-98
28000561-11	2017	Molecular docking of 1,5-anhydrosorbitol reveals information regarding important binding site residues of RGN.	1,5-anhydroglucitol	21-40	regucalcin	Bubalus bubalis	106-109
28000561-14	2017	CONCLUSION: Three dimensional structure of RGN was generated and its interactions with 1,5- anhydrosorbitol, demonstrates the role of key binding residues.	1,5-anhydroglucitol	87-107	regucalcin	Bubalus bubalis	43-46
27847472-6	2016	Intracerebroventricular administration of astroglial toxin L-a-aminoadipate (L-AA) and c-Fos antisense oligodeoxy nucleotides (ASO) both decreased RWIS-induced gastric mucosal damage.	1,5-anhydroglucitol	127-130	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	87-92
27246285-0	2016	1,5-Anhydro-D-Glucitol Could Reflect Hypoglycemia Risk in Patients with Type 2 Diabetes Receiving Insulin Therapy.	1,5-anhydroglucitol	0-22	insulin	Homo sapiens	98-105
26282675-4	2016	METHODS: Wildtype mice maintained on a high fat diet (HFD) received tail vein injections of microRNA-21-anti-sense oligonucleotide (ASO) or miR-21 mismatched ASO for 4 or 8 weeks.	1,5-anhydroglucitol	132-135	microRNA 21a	Mus musculus	92-103
26172028-9	2015	All levels of measurable C-peptide were responsive to acute fluctuations in blood glucose levels as assessed by 1,5-Anhydroglucitol (P < 0.0001).	1,5-anhydroglucitol	112-131	insulin	Homo sapiens	25-34
26477861-4	2015	The miR-1271 expression in cells was overexpressed by miRNA-mimic transfection and reduced by miRNA-antisense-oligonucleotide (ASO) transfection.	1,5-anhydroglucitol	127-130	membrane associated ring-CH-type finger 8	Homo sapiens	4-7
26881967-7	2016	In all cases, the treatment with miR-10b ASO led to targets" derepression, and attenuated growth and progression of established intracranial GBM.	1,5-anhydroglucitol	41-44	microRNA 10b	Mus musculus	33-40
24247359-13	2013	Administration of miR-124 ASO for two weeks significantly reduced urinary podocytic nephrin, podocin and albumin excretion and up-regulate integrin alpha3 expression.	1,5-anhydroglucitol	26-29	NPHS1 adhesion molecule, nephrin	Rattus norvegicus	84-91
23481354-12	2013	This work has contributed to the development of a BRCA2-targeting antisense oligdeoxynucleotide (ASO) "BR-1" which we will test in vivo in combination with our TS-targeting ASO "SARI 83" and attempt early clinical trials in the future.Molecular Therapy - Nucleic Acids (2013) 2, e78; doi:10.1038/mtna.2013.7 published online 12 March 2013.	1,5-anhydroglucitol	97-100	BRCA2 DNA repair associated	Homo sapiens	50-55
24326128-1	2014	BACKGROUND: To assess the relationship between the serum level of 1,5-anhydroglucitol (1,5-AG), a marker of postprandial hyperglycemia, and the ratio of the urinary activity of N-acetyl-beta-d-glucosaminidase to creatinine (NAG index) in subjects without diabetes mellitus (DM).	1,5-anhydroglucitol	66-85	O-GlcNAcase	Homo sapiens	177-208
24326128-1	2014	BACKGROUND: To assess the relationship between the serum level of 1,5-anhydroglucitol (1,5-AG), a marker of postprandial hyperglycemia, and the ratio of the urinary activity of N-acetyl-beta-d-glucosaminidase to creatinine (NAG index) in subjects without diabetes mellitus (DM).	1,5-anhydroglucitol	66-85	N-acetyl-alpha-glucosaminidase	Homo sapiens	224-227
24326128-1	2014	BACKGROUND: To assess the relationship between the serum level of 1,5-anhydroglucitol (1,5-AG), a marker of postprandial hyperglycemia, and the ratio of the urinary activity of N-acetyl-beta-d-glucosaminidase to creatinine (NAG index) in subjects without diabetes mellitus (DM).	1,5-anhydroglucitol	87-93	O-GlcNAcase	Homo sapiens	177-208
24326128-1	2014	BACKGROUND: To assess the relationship between the serum level of 1,5-anhydroglucitol (1,5-AG), a marker of postprandial hyperglycemia, and the ratio of the urinary activity of N-acetyl-beta-d-glucosaminidase to creatinine (NAG index) in subjects without diabetes mellitus (DM).	1,5-anhydroglucitol	87-93	N-acetyl-alpha-glucosaminidase	Homo sapiens	224-227
24898602-11	2014	The administration of miR-30b ASO for two weeks significantly reduced alpha-SMA excretion and upregulated E-cadherin and BMP-7 expression.	1,5-anhydroglucitol	30-33	microRNA 30b	Rattus norvegicus	22-29
24898602-11	2014	The administration of miR-30b ASO for two weeks significantly reduced alpha-SMA excretion and upregulated E-cadherin and BMP-7 expression.	1,5-anhydroglucitol	30-33	cadherin 1	Rattus norvegicus	106-116
24898602-11	2014	The administration of miR-30b ASO for two weeks significantly reduced alpha-SMA excretion and upregulated E-cadherin and BMP-7 expression.	1,5-anhydroglucitol	30-33	bone morphogenetic protein 7	Rattus norvegicus	121-126
24111861-1	2014	BACKGROUND: This study assessed the relationship between the serum level of 1,5-anhydroglucitol (1,5-AG), a marker of postprandial hyperglycemia, and the ratio of the urinary activity of N-acetyl-beta-D-glucosaminidase (NAG) to creatinine (NAG index) in patients with type 2 diabetes mellitus.	1,5-anhydroglucitol	76-95	O-GlcNAcase	Homo sapiens	187-218
24111861-1	2014	BACKGROUND: This study assessed the relationship between the serum level of 1,5-anhydroglucitol (1,5-AG), a marker of postprandial hyperglycemia, and the ratio of the urinary activity of N-acetyl-beta-D-glucosaminidase (NAG) to creatinine (NAG index) in patients with type 2 diabetes mellitus.	1,5-anhydroglucitol	76-95	O-GlcNAcase	Homo sapiens	220-223
24111861-1	2014	BACKGROUND: This study assessed the relationship between the serum level of 1,5-anhydroglucitol (1,5-AG), a marker of postprandial hyperglycemia, and the ratio of the urinary activity of N-acetyl-beta-D-glucosaminidase (NAG) to creatinine (NAG index) in patients with type 2 diabetes mellitus.	1,5-anhydroglucitol	76-95	O-GlcNAcase	Homo sapiens	240-243
24111861-1	2014	BACKGROUND: This study assessed the relationship between the serum level of 1,5-anhydroglucitol (1,5-AG), a marker of postprandial hyperglycemia, and the ratio of the urinary activity of N-acetyl-beta-D-glucosaminidase (NAG) to creatinine (NAG index) in patients with type 2 diabetes mellitus.	1,5-anhydroglucitol	97-103	O-GlcNAcase	Homo sapiens	187-218
24111861-1	2014	BACKGROUND: This study assessed the relationship between the serum level of 1,5-anhydroglucitol (1,5-AG), a marker of postprandial hyperglycemia, and the ratio of the urinary activity of N-acetyl-beta-D-glucosaminidase (NAG) to creatinine (NAG index) in patients with type 2 diabetes mellitus.	1,5-anhydroglucitol	97-103	O-GlcNAcase	Homo sapiens	220-223
24111861-1	2014	BACKGROUND: This study assessed the relationship between the serum level of 1,5-anhydroglucitol (1,5-AG), a marker of postprandial hyperglycemia, and the ratio of the urinary activity of N-acetyl-beta-D-glucosaminidase (NAG) to creatinine (NAG index) in patients with type 2 diabetes mellitus.	1,5-anhydroglucitol	97-103	O-GlcNAcase	Homo sapiens	240-243
24247359-13	2013	Administration of miR-124 ASO for two weeks significantly reduced urinary podocytic nephrin, podocin and albumin excretion and up-regulate integrin alpha3 expression.	1,5-anhydroglucitol	26-29	NPHS2 stomatin family member, podocin	Rattus norvegicus	93-100
24247359-13	2013	Administration of miR-124 ASO for two weeks significantly reduced urinary podocytic nephrin, podocin and albumin excretion and up-regulate integrin alpha3 expression.	1,5-anhydroglucitol	26-29	integrin subunit alpha 3	Rattus norvegicus	139-154
23349732-4	2013	Here, we report the crystal structures of mouse SMP30/GNL and its complex with xylitol, a substrate analogue, and those with 1,5-anhydro-D-glucitol and D-glucose, product analogues.	1,5-anhydroglucitol	125-147	regucalcin	Mus musculus	48-53
23349732-4	2013	Here, we report the crystal structures of mouse SMP30/GNL and its complex with xylitol, a substrate analogue, and those with 1,5-anhydro-D-glucitol and D-glucose, product analogues.	1,5-anhydroglucitol	125-147	regucalcin	Mus musculus	54-57
22731793-0	2012	Increased 1,5-anhydroglucitol predicts glycemic remission in patients with newly diagnosed type 2 diabetes treated with short-term intensive insulin therapy.	1,5-anhydroglucitol	10-29	insulin	Homo sapiens	141-148
22906840-4	2012	Local infusion of antisense oligodeoxynucleotide (ASO) to specifically knockdown Egr-1 in the dorsal hippocampus 8 h posttraining impairs LTM tested 7 days, but not 1 day after training, indicating that a delayed learning-associated expression of Egr-1 is necessary for the persistence of LTM storage.	1,5-anhydroglucitol	50-53	early growth response 1	Rattus norvegicus	81-86
22906840-4	2012	Local infusion of antisense oligodeoxynucleotide (ASO) to specifically knockdown Egr-1 in the dorsal hippocampus 8 h posttraining impairs LTM tested 7 days, but not 1 day after training, indicating that a delayed learning-associated expression of Egr-1 is necessary for the persistence of LTM storage.	1,5-anhydroglucitol	50-53	early growth response 1	Rattus norvegicus	247-252
22906840-6	2012	Local infusion of egr-1 ASO 30 min before training in the dorsal hippocampus persistently hinders memory formation measured 1 and 7 days after IA training, indicating the crucial role of Egr-1 in memory formation.	1,5-anhydroglucitol	24-27	early growth response 1	Rattus norvegicus	18-23
22906840-6	2012	Local infusion of egr-1 ASO 30 min before training in the dorsal hippocampus persistently hinders memory formation measured 1 and 7 days after IA training, indicating the crucial role of Egr-1 in memory formation.	1,5-anhydroglucitol	24-27	early growth response 1	Rattus norvegicus	187-192
22395091-9	2012	Finally, correlation analysis was applied to establish quantitative linkages between the 5 individual metabolite 3-hydroxybutyric acid, L-valine, L-threonine, 1-deoxyglucose, and glycine and the 5 individual proteins MACF1, APOH, A2M, IGL@, and VDB.	1,5-anhydroglucitol	159-173	microtubule actin crosslinking factor 1	Homo sapiens	217-222
22421598-0	2012	Potential for use of 1,5-anhydroglucitol when initiating insulin therapy in people with type 2 diabetes and suboptimal control with oral antidiabetic drugs.	1,5-anhydroglucitol	21-40	insulin	Homo sapiens	57-64
22746391-7	2012	Moreover, high expression levels of both CgA and Ki67 in mucosal crypt epithelia favor ASO as compared to NA (P < 0.001  =  3.4 x 10(-6) and 3.1 x 10(-5), respectively).	1,5-anhydroglucitol	87-90	chromogranin A	Homo sapiens	41-44
22060802-9	2012	1,5-AG was significantly correlated to HbA1c in patients, but not controls.	1,5-anhydroglucitol	0-6	hemoglobin subunit alpha 1	Homo sapiens	39-43
22490356-10	2012	The low level of heat shock protein 27 (HSP27) in ASO was verified by IHC and western-blot in accord with the result of MS.	1,5-anhydroglucitol	50-53	heat shock protein family B (small) member 1	Homo sapiens	17-38
22490356-10	2012	The low level of heat shock protein 27 (HSP27) in ASO was verified by IHC and western-blot in accord with the result of MS.	1,5-anhydroglucitol	50-53	heat shock protein family B (small) member 1	Homo sapiens	40-45
21595282-5	2011	Two-week intranasal administration of GLP-1 just before meals significantly decreased serum glycoalbumin level and significantly increased 1,5-AG (1,5-anhydro-D-glucitol) level.	1,5-anhydroglucitol	139-145	glucagon	Homo sapiens	38-43
19576799-5	2011	Interestingly, targeting Bcl-2 with ASO resulted in the inhibition of in vitro tube formation and inhibition of angiogenesis in Matrigel plugs similar to treatment with bevacizumab.	1,5-anhydroglucitol	36-39	BCL2 apoptosis regulator	Homo sapiens	25-30
21595282-5	2011	Two-week intranasal administration of GLP-1 just before meals significantly decreased serum glycoalbumin level and significantly increased 1,5-AG (1,5-anhydro-D-glucitol) level.	1,5-anhydroglucitol	147-169	glucagon	Homo sapiens	38-43
21342497-8	2011	Infusion with TLR3 antisense oligodeoxynucleotide (ASO) dose-dependently attenuated CP-induced allodynia.	1,5-anhydroglucitol	51-54	toll-like receptor 3	Rattus norvegicus	14-18
20109509-2	2010	We conjugated antisense-HIF1alpha-oligonucleotide (ASO) with low molecular weight protamine (LMWP), a cell-penetrating peptide, to enhance its ability to block hypoxic-angiogenesis, thereby eliciting an anti-obesity effect.	1,5-anhydroglucitol	51-54	hypoxia inducible factor 1, alpha subunit	Mus musculus	24-33
20709052-5	2010	On the other hand, serum 1,5-AG levels were significantly lower in the FT1DM patients than in the T2DM patients.	1,5-anhydroglucitol	25-31	AKT interacting protein	Homo sapiens	71-74
20802017-5	2010	Antisense oligodeoxynucleotides (ASO) were infused into each structure to knock down the expression of the immediate-early gene zif268, which is known to be required for memory reconsolidation.	1,5-anhydroglucitol	33-36	early growth response 1	Homo sapiens	128-134
20802017-8	2010	The results show that both intranucleus accumbens core and intrabasolateral amygdala zif268 ASO infusions at memory reactivation impaired the reconsolidation of the memory underlying a cocaine-conditioned place preference.	1,5-anhydroglucitol	92-95	early growth response 1	Homo sapiens	85-91
19379550-2	2009	After bcr3/abl2 antisense oligodeoxynucleotide (ASO) was introduced into CML cell line K562 cells by liposomal transfection, the cell viability was detected by MTT assay, the cell apoptosis was determined by flow cytometry (FCM), the mitochondrial membrane potential (DeltaPsi) was labeled by Rhodamine 123 and examined by FCM, and the expression of mitochondrial apoptosis signal transduction pathway related proteins cytochrome C was analyzed by Western blot.	1,5-anhydroglucitol	48-51	BCR pseudogene 3	Homo sapiens	6-10
20377999-8	2010	In addition, 1,5-AG suppressed cytokine release and iNOS expression by suppressing Akt/NF-kB activity in RAW264.7 cells.	1,5-anhydroglucitol	13-19	nitric oxide synthase 2, inducible	Mus musculus	52-56
20377999-8	2010	In addition, 1,5-AG suppressed cytokine release and iNOS expression by suppressing Akt/NF-kB activity in RAW264.7 cells.	1,5-anhydroglucitol	13-19	thymoma viral proto-oncogene 1	Mus musculus	83-86
19759893-6	2009	Intrathecal administration of c-fos antisense oligodeoxynucleotides (ASO) or astroglial toxin L-alpha-aminoadipate (L-AA) reversed the mechanical allodynia, respectively.	1,5-anhydroglucitol	69-72	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	30-35
19620188-12	2009	HbA1c and 1,5-anhydroglucitol are excellent predictors of T2DM in insulin-resistant obese children.	1,5-anhydroglucitol	10-29	insulin	Homo sapiens	66-73
19379550-3	2009	The results showed that after K562 cells were exposed to 2 micromol/L of bcr3/abl2 ASO for 24 hours, bcr3/abl2 ASO significantly inhibited cell viability with inhibitory rate of 65.7%, induced the apoptosis of K562 cell line with apoptotic rate of 16.9%, and decreased mitochondrial Deltapsi of K562 cells with the reducing rate of 38.33%, enhanced the expression of cytochrome C with increase of optical density value from 2.33 +/- 0.3 to 4.78 +/- 0.1 by laser photometric scanning.	1,5-anhydroglucitol	83-86	BCR pseudogene 3	Homo sapiens	73-77
19933992-3	2010	Serum 1,5 anhydroglucitol (1,5AG) levels were reported to differentiate maturity-onset diabetes of the young due to HNF1A mutations (HNF1A-MODY) from type 2 diabetes, but this requires further validation.	1,5-anhydroglucitol	6-25	HNF1 homeobox A	Homo sapiens	116-121
19933992-3	2010	Serum 1,5 anhydroglucitol (1,5AG) levels were reported to differentiate maturity-onset diabetes of the young due to HNF1A mutations (HNF1A-MODY) from type 2 diabetes, but this requires further validation.	1,5-anhydroglucitol	6-25	HNF1 homeobox A	Homo sapiens	133-143
19933992-3	2010	Serum 1,5 anhydroglucitol (1,5AG) levels were reported to differentiate maturity-onset diabetes of the young due to HNF1A mutations (HNF1A-MODY) from type 2 diabetes, but this requires further validation.	1,5-anhydroglucitol	27-32	HNF1 homeobox A	Homo sapiens	116-121
19933992-3	2010	Serum 1,5 anhydroglucitol (1,5AG) levels were reported to differentiate maturity-onset diabetes of the young due to HNF1A mutations (HNF1A-MODY) from type 2 diabetes, but this requires further validation.	1,5-anhydroglucitol	27-32	HNF1 homeobox A	Homo sapiens	133-143
19429157-4	2009	Furthermore, we observed the behavioral changes following intracisternal injection of KCC2 antisense oligodeoxynucleotides (ASO) into naive mice.	1,5-anhydroglucitol	124-127	solute carrier family 12, member 5	Mus musculus	86-90
19429157-7	2009	Intracisternal injection of KCC2 ASO into naive mice led to behavioral hypersensitivity similar to the hyperalgesia observed in formalin experiments.	1,5-anhydroglucitol	33-36	solute carrier family 12, member 5	Mus musculus	28-32
19379550-3	2009	The results showed that after K562 cells were exposed to 2 micromol/L of bcr3/abl2 ASO for 24 hours, bcr3/abl2 ASO significantly inhibited cell viability with inhibitory rate of 65.7%, induced the apoptosis of K562 cell line with apoptotic rate of 16.9%, and decreased mitochondrial Deltapsi of K562 cells with the reducing rate of 38.33%, enhanced the expression of cytochrome C with increase of optical density value from 2.33 +/- 0.3 to 4.78 +/- 0.1 by laser photometric scanning.	1,5-anhydroglucitol	83-86	BCR pseudogene 3	Homo sapiens	101-105
19379550-3	2009	The results showed that after K562 cells were exposed to 2 micromol/L of bcr3/abl2 ASO for 24 hours, bcr3/abl2 ASO significantly inhibited cell viability with inhibitory rate of 65.7%, induced the apoptosis of K562 cell line with apoptotic rate of 16.9%, and decreased mitochondrial Deltapsi of K562 cells with the reducing rate of 38.33%, enhanced the expression of cytochrome C with increase of optical density value from 2.33 +/- 0.3 to 4.78 +/- 0.1 by laser photometric scanning.	1,5-anhydroglucitol	83-86	cytochrome c, somatic	Homo sapiens	367-379
19379550-3	2009	The results showed that after K562 cells were exposed to 2 micromol/L of bcr3/abl2 ASO for 24 hours, bcr3/abl2 ASO significantly inhibited cell viability with inhibitory rate of 65.7%, induced the apoptosis of K562 cell line with apoptotic rate of 16.9%, and decreased mitochondrial Deltapsi of K562 cells with the reducing rate of 38.33%, enhanced the expression of cytochrome C with increase of optical density value from 2.33 +/- 0.3 to 4.78 +/- 0.1 by laser photometric scanning.	1,5-anhydroglucitol	111-114	BCR pseudogene 3	Homo sapiens	73-77
19379550-3	2009	The results showed that after K562 cells were exposed to 2 micromol/L of bcr3/abl2 ASO for 24 hours, bcr3/abl2 ASO significantly inhibited cell viability with inhibitory rate of 65.7%, induced the apoptosis of K562 cell line with apoptotic rate of 16.9%, and decreased mitochondrial Deltapsi of K562 cells with the reducing rate of 38.33%, enhanced the expression of cytochrome C with increase of optical density value from 2.33 +/- 0.3 to 4.78 +/- 0.1 by laser photometric scanning.	1,5-anhydroglucitol	111-114	BCR pseudogene 3	Homo sapiens	101-105
19379550-3	2009	The results showed that after K562 cells were exposed to 2 micromol/L of bcr3/abl2 ASO for 24 hours, bcr3/abl2 ASO significantly inhibited cell viability with inhibitory rate of 65.7%, induced the apoptosis of K562 cell line with apoptotic rate of 16.9%, and decreased mitochondrial Deltapsi of K562 cells with the reducing rate of 38.33%, enhanced the expression of cytochrome C with increase of optical density value from 2.33 +/- 0.3 to 4.78 +/- 0.1 by laser photometric scanning.	1,5-anhydroglucitol	111-114	cytochrome c, somatic	Homo sapiens	367-379
18703105-6	2008	Therefore, our data suggest a role of the IL-10 gene on ASO susceptibility.	1,5-anhydroglucitol	56-59	interleukin 10	Homo sapiens	42-47
19254570-2	2009	Here, we evaluated the role of PGC-1beta in the pathogenesis of fructose-induced insulin resistance by using an antisense oligonucletoide (ASO) to knockdown PGC-1beta in liver and adipose tissue.	1,5-anhydroglucitol	139-142	insulin	Homo sapiens	81-88
19254570-2	2009	Here, we evaluated the role of PGC-1beta in the pathogenesis of fructose-induced insulin resistance by using an antisense oligonucletoide (ASO) to knockdown PGC-1beta in liver and adipose tissue.	1,5-anhydroglucitol	139-142	PPARG coactivator 1 beta	Homo sapiens	157-166
18575865-9	2008	In JAK2 V671F allelo-specific-oligonucleotide (ASO) quantitative PCR (qPCR), cutoff point of 1% was established by receiving operating characteristic (ROC) curves.	1,5-anhydroglucitol	47-50	Janus kinase 2	Homo sapiens	3-7
19099802-4	2008	Allele specific oligonucleotide (ASO) upstream primers were designed complementary to the V-D-J or D-J junctional region of TCRbeta gene rearrangements.	1,5-anhydroglucitol	33-36	T cell receptor beta locus	Homo sapiens	124-131
18335175-2	2008	We have determined glucose and 1,5-AG, based on glucokinase (GK) converting glucose to G6P, a compound that can be catalyzed ultimately into 6-PGA by G-6PD and its coenzyme NADP(+), and then calculated glucose concentration according to absorbance variety.	1,5-anhydroglucitol	31-37	glucose-6-phosphate dehydrogenase	Homo sapiens	150-155
18492944-0	2008	Clinical application of 1,5-anhydroglucitol measurements in patients with hepatocyte nuclear factor-1alpha maturity-onset diabetes of the young.	1,5-anhydroglucitol	24-43	HNF1 homeobox A	Homo sapiens	74-106
18492944-4	2008	The purpose of this study was to assess the 1,5-AG levels in patients with HNF-1alpha MODY and in type 2 diabetic subjects with a similar degree of metabolic control.	1,5-anhydroglucitol	44-50	HNF1 homeobox A	Homo sapiens	75-85
17207885-7	2007	By means of analysis of covariance, it was revealed that 1,5-anhydro-d-glucitol plasma levels are associated with SUR1 exon 16-3c/t polymorphism.	1,5-anhydroglucitol	57-79	ATP binding cassette subfamily C member 8	Homo sapiens	114-118
21176444-2	2006	The aim of this study is to use c-fos antisense oligodeoxynucleotide (ASO) to block c-fos expression and to explore whether c-fos can directly regulate VIP-induced VEGF expression in small cell lung cancer (SCLC) cells.	1,5-anhydroglucitol	70-73	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	32-37
16548352-2	2006	METHODS: Flow cytometery analysis was used to detect the expression of CD11b/CD18 in peripheral neutrophils of 30 patients with ASO and 30 healthy subjects by direct immunofluroscent technique.	1,5-anhydroglucitol	128-131	integrin subunit alpha M	Homo sapiens	71-76
16548352-2	2006	METHODS: Flow cytometery analysis was used to detect the expression of CD11b/CD18 in peripheral neutrophils of 30 patients with ASO and 30 healthy subjects by direct immunofluroscent technique.	1,5-anhydroglucitol	128-131	integrin subunit beta 2	Homo sapiens	77-81
16548352-7	2006	The possible mechanism of XZOL in treating and preventing ASO might be through reducing the expression of CD11b/CD18 in peripheral neutrophils to interfere the adhesive function of them.	1,5-anhydroglucitol	58-61	integrin subunit alpha M	Homo sapiens	106-111
16548352-7	2006	The possible mechanism of XZOL in treating and preventing ASO might be through reducing the expression of CD11b/CD18 in peripheral neutrophils to interfere the adhesive function of them.	1,5-anhydroglucitol	58-61	integrin subunit beta 2	Homo sapiens	112-116
16741579-3	2006	To examine whether Scd1 activity is required for the development of diet-induced hepatic insulin resistance, we used a sequence-specific antisense oligodeoxynucleotide (ASO) to lower hepatic Scd1 expression in rats and mice with diet-induced insulin resistance.	1,5-anhydroglucitol	169-172	stearoyl-CoA desaturase	Rattus norvegicus	19-23
16741579-3	2006	To examine whether Scd1 activity is required for the development of diet-induced hepatic insulin resistance, we used a sequence-specific antisense oligodeoxynucleotide (ASO) to lower hepatic Scd1 expression in rats and mice with diet-induced insulin resistance.	1,5-anhydroglucitol	169-172	stearoyl-CoA desaturase	Rattus norvegicus	191-195
16741579-4	2006	Treatment of rats with Scd1 ASO markedly decreased liver Scd1 expression (approximately 80%) and total Scd activity (approximately 50%) compared with that in rats treated with scrambled ASO (control).	1,5-anhydroglucitol	28-31	stearoyl-CoA desaturase	Rattus norvegicus	23-27
16741579-4	2006	Treatment of rats with Scd1 ASO markedly decreased liver Scd1 expression (approximately 80%) and total Scd activity (approximately 50%) compared with that in rats treated with scrambled ASO (control).	1,5-anhydroglucitol	28-31	stearoyl-CoA desaturase	Rattus norvegicus	57-61
16741579-4	2006	Treatment of rats with Scd1 ASO markedly decreased liver Scd1 expression (approximately 80%) and total Scd activity (approximately 50%) compared with that in rats treated with scrambled ASO (control).	1,5-anhydroglucitol	28-31	stearoyl-Coenzyme A desaturase 1	Mus musculus	23-26
16741579-5	2006	Insulin clamp studies revealed severe hepatic insulin resistance in high-fat-fed rats and mice that was completely reversed by 5 days of treatment with Scd1 ASO.	1,5-anhydroglucitol	157-160	stearoyl-Coenzyme A desaturase 1	Mus musculus	152-156
21176444-2	2006	The aim of this study is to use c-fos antisense oligodeoxynucleotide (ASO) to block c-fos expression and to explore whether c-fos can directly regulate VIP-induced VEGF expression in small cell lung cancer (SCLC) cells.	1,5-anhydroglucitol	70-73	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	84-89
21176444-2	2006	The aim of this study is to use c-fos antisense oligodeoxynucleotide (ASO) to block c-fos expression and to explore whether c-fos can directly regulate VIP-induced VEGF expression in small cell lung cancer (SCLC) cells.	1,5-anhydroglucitol	70-73	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	84-89
12948285-5	2003	HFE genotyping was performed by PCR and allele-specific oligonucleotide (ASO) hybridization.	1,5-anhydroglucitol	73-76	homeostatic iron regulator	Homo sapiens	0-3
15864350-5	2005	administration (2 injections over 1 week) of an antisense oligodeoxynucleotide (ASO) directed to reduce insulin expression downregulated hepatic IR expression in C57BL6J mice.	1,5-anhydroglucitol	80-83	insulin receptor	Mus musculus	145-147
15864350-9	2005	The rate of glucose infusion during the clamp studies was comparable in control-ASO- and IR-ASO-treated mice.	1,5-anhydroglucitol	92-95	insulin receptor	Mus musculus	89-91
15135449-5	2004	In addition, the reactions included four differentially labeled ASO probes for the specific detection of the different FVL/PT G20210A genotypes.	1,5-anhydroglucitol	64-67	coagulation factor V	Homo sapiens	119-122
15607332-0	2005	SLC5A9/SGLT4, a new Na+-dependent glucose transporter, is an essential transporter for mannose, 1,5-anhydro-D-glucitol, and fructose.	1,5-anhydroglucitol	96-118	solute carrier family 5 member 9	Homo sapiens	0-6
15607332-0	2005	SLC5A9/SGLT4, a new Na+-dependent glucose transporter, is an essential transporter for mannose, 1,5-anhydro-D-glucitol, and fructose.	1,5-anhydroglucitol	96-118	solute carrier family 5 member 9	Homo sapiens	7-12
15463917-2	2004	We present here the basic tools to allow a thorough investigation of the CFTR gene, beginning with the identification of potential regulatory regions using DNase I hypersensitive sites, and continuing with methods for the detection of mutations: denaturing High Performance Liquid Chromatography (dHPLC), Single Strand Conformation Polymorphism (SSCP), and allele-specific oligonucleotide (ASO) hybridisation.	1,5-anhydroglucitol	390-393	CF transmembrane conductance regulator	Homo sapiens	73-77
15145332-0	2004	Different effects of two alpha-glucosidase inhibitors, acarbose and voglibose, on serum 1,5-anhydroglucitol (1,5AG) level.	1,5-anhydroglucitol	88-107	sucrase-isomaltase	Homo sapiens	25-42
15145332-1	2004	Serum 1,5-anhydroglucitol (1,5AG) is a useful glycemic marker in the control of diabetes; however, treated with alpha-glucosidase inhibitors (alpha-GIs), acarbose (Aca) and voglibose (Vog), it tends to show the discrepancy between serum 1,5AG and related glucose levels.	1,5-anhydroglucitol	6-25	sucrase-isomaltase	Homo sapiens	112-129
15145332-1	2004	Serum 1,5-anhydroglucitol (1,5AG) is a useful glycemic marker in the control of diabetes; however, treated with alpha-glucosidase inhibitors (alpha-GIs), acarbose (Aca) and voglibose (Vog), it tends to show the discrepancy between serum 1,5AG and related glucose levels.	1,5-anhydroglucitol	27-32	sucrase-isomaltase	Homo sapiens	112-129
12794695-7	2003	Protein-coding DNA fragments from the CFTR gene were amplified in vitro by the polymerase chain reaction (PCR) and analyzed for mutations using allele-specific oligonucleotide (ASO) probes.	1,5-anhydroglucitol	177-180	CF transmembrane conductance regulator	Homo sapiens	38-42
10826855-7	2000	Plasma concentrations of TIMP-1 in patients with AAA (293.8 +/- 61.2 ng/mL) or ASO (327.6 +/- 54.9 ng/mL) were significantly higher than in HC (227.3 +/- 60.2 ng/mL; both p < 0.01).	1,5-anhydroglucitol	79-82	TIMP metallopeptidase inhibitor 1	Homo sapiens	25-31
12800253-3	2003	In order to facilitate the detection of the known SNPs of CYP2C9, an allele-specific oligonucleotide (ASO) based microarray was made.	1,5-anhydroglucitol	102-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	58-64
12393948-5	2002	At the same time, ASO treatment also significantly decreased the expression of Fos protein within the lumbar region of the spinal cord ipsilateral to the injection.	1,5-anhydroglucitol	18-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-82
10866322-3	2000	We designed and adapted allele-specific oligonucleotide (ASO)-PCR protocols that enabled the detection of >90% of the IGH, IGK, TCRD, and TCRG rearrangements observed in ALL patients.	1,5-anhydroglucitol	57-60	immunoglobulin heavy locus	Homo sapiens	121-124
10866322-3	2000	We designed and adapted allele-specific oligonucleotide (ASO)-PCR protocols that enabled the detection of >90% of the IGH, IGK, TCRD, and TCRG rearrangements observed in ALL patients.	1,5-anhydroglucitol	57-60	immunoglobulin kappa locus	Homo sapiens	126-129
10866322-3	2000	We designed and adapted allele-specific oligonucleotide (ASO)-PCR protocols that enabled the detection of >90% of the IGH, IGK, TCRD, and TCRG rearrangements observed in ALL patients.	1,5-anhydroglucitol	57-60	T cell receptor delta constant	Homo sapiens	131-135
10866322-3	2000	We designed and adapted allele-specific oligonucleotide (ASO)-PCR protocols that enabled the detection of >90% of the IGH, IGK, TCRD, and TCRG rearrangements observed in ALL patients.	1,5-anhydroglucitol	57-60	T cell receptor gamma locus	Homo sapiens	141-145
14633785-13	2003	Similar clinical trials with Bcl-2 ASO molecules alone and in combination with doxorubicin and dexamethasone or thalidomide showed promising results.	1,5-anhydroglucitol	35-38	BCL2 apoptosis regulator	Homo sapiens	29-34
12097411-2	2002	We reported previously that aerosolized Syk antisense oligodeoxynucleotides (ASO) depresses Syk expression in inflammatory cells, the release of mediators from alveolar macrophages, and pulmonary inflammation.	1,5-anhydroglucitol	77-80	spleen associated tyrosine kinase	Rattus norvegicus	40-43
12097411-2	2002	We reported previously that aerosolized Syk antisense oligodeoxynucleotides (ASO) depresses Syk expression in inflammatory cells, the release of mediators from alveolar macrophages, and pulmonary inflammation.	1,5-anhydroglucitol	77-80	spleen associated tyrosine kinase	Rattus norvegicus	92-95
12097411-4	2002	Syk ASO, delivered in a liposome, carrier/lipid complex by aerosol to rats, significantly inhibited the Ag-induced inflammatory cell infiltrate in the bronchoalveolar space, decreasing both neutrophilia and eosinophilia.	1,5-anhydroglucitol	4-7	spleen associated tyrosine kinase	Rattus norvegicus	0-3
12097411-6	2002	Syk ASO also depressed up-regulation of the expression of beta(2) integrins, alpha(4) integrin, and ICAM-1 in bronchoalveolar lavage leukocytes and reversed the Ag-induced decrease in CD62L expression on neutrophils.	1,5-anhydroglucitol	4-7	spleen associated tyrosine kinase	Rattus norvegicus	0-3
12097411-6	2002	Syk ASO also depressed up-regulation of the expression of beta(2) integrins, alpha(4) integrin, and ICAM-1 in bronchoalveolar lavage leukocytes and reversed the Ag-induced decrease in CD62L expression on neutrophils.	1,5-anhydroglucitol	4-7	intercellular adhesion molecule 1	Rattus norvegicus	100-106
12097411-8	2002	Syk ASO also suppressed Ag-mediated contraction of the trachea in a complementary model.	1,5-anhydroglucitol	4-7	spleen associated tyrosine kinase	Rattus norvegicus	0-3
12097411-9	2002	Thus, aerosolized Syk ASO suppresses many of the central components of allergic asthma and inflammation and may provide a new therapeutic approach.	1,5-anhydroglucitol	22-25	spleen associated tyrosine kinase	Rattus norvegicus	18-21
11953033-6	2001	Depletion efficacy was measured by semi-quantitative allele-specific oligonucleotide (ASO)-PCR amplification of patients" clonotypic IgH gene.	1,5-anhydroglucitol	86-89	immunoglobulin heavy locus	Homo sapiens	133-136
9808706-7	1998	ASO treatment caused a 15% to 25% decrease of specific [3H]flunitrazepam binding in most brain areas, with statistically significant decreases in frontal cortex, cerebellar molecular layer, zona reticulata of substantia nigra and CA3 of hippocampus.	1,5-anhydroglucitol	0-3	carbonic anhydrase 3	Rattus norvegicus	230-233
10725739-3	2000	We hypothesized that Syk antisense oligodeoxynucleotides (ASO) delivered by aerosol to rat lungs in vivo would depress Syk PTK expression, mediator release from alveolar macrophages, and Syk-dependent pulmonary inflammation.	1,5-anhydroglucitol	58-61	spleen associated tyrosine kinase	Rattus norvegicus	21-24
10725739-3	2000	We hypothesized that Syk antisense oligodeoxynucleotides (ASO) delivered by aerosol to rat lungs in vivo would depress Syk PTK expression, mediator release from alveolar macrophages, and Syk-dependent pulmonary inflammation.	1,5-anhydroglucitol	58-61	spleen associated tyrosine kinase	Rattus norvegicus	119-122
10725739-3	2000	We hypothesized that Syk antisense oligodeoxynucleotides (ASO) delivered by aerosol to rat lungs in vivo would depress Syk PTK expression, mediator release from alveolar macrophages, and Syk-dependent pulmonary inflammation.	1,5-anhydroglucitol	58-61	spleen associated tyrosine kinase	Rattus norvegicus	119-122
10725739-4	2000	RT-PCR and RT-in situ PCR demonstrated that aerosolized Syk ASO administration reduced Syk mRNA expression from alveolar macrophages compared with cells isolated from sham-treated rats.	1,5-anhydroglucitol	60-63	spleen associated tyrosine kinase	Rattus norvegicus	56-59
10725739-4	2000	RT-PCR and RT-in situ PCR demonstrated that aerosolized Syk ASO administration reduced Syk mRNA expression from alveolar macrophages compared with cells isolated from sham-treated rats.	1,5-anhydroglucitol	60-63	spleen associated tyrosine kinase	Rattus norvegicus	87-90
10725739-5	2000	Western blot analysis confirmed that Syk PTK expression was reduced after Syk ASO treatment.	1,5-anhydroglucitol	78-81	spleen associated tyrosine kinase	Rattus norvegicus	37-40
10725739-5	2000	Western blot analysis confirmed that Syk PTK expression was reduced after Syk ASO treatment.	1,5-anhydroglucitol	78-81	spleen associated tyrosine kinase	Rattus norvegicus	74-77
10725739-6	2000	Compared with sham-treated rats (scrambled oligodeoxynucleotide), Syk ASO treatment suppressed Fcgamma-receptor-mediated nitric oxide (86.0 +/- 8.3%) and TNF (73.1 +/- 3.1%) production by alveolar macrophages stimulated with IgG-anti-IgG complexes.	1,5-anhydroglucitol	70-73	spleen associated tyrosine kinase	Rattus norvegicus	66-69
10725739-6	2000	Compared with sham-treated rats (scrambled oligodeoxynucleotide), Syk ASO treatment suppressed Fcgamma-receptor-mediated nitric oxide (86.0 +/- 8.3%) and TNF (73.1 +/- 3.1%) production by alveolar macrophages stimulated with IgG-anti-IgG complexes.	1,5-anhydroglucitol	70-73	tumor necrosis factor	Rattus norvegicus	154-157
10725739-8	2000	Additionally, Syk ASO suppressed Ag-induced pulmonary inflammation, suggesting that Syk ASO may prove useful as an anti-inflammatory therapy in disorders such as asthma.	1,5-anhydroglucitol	18-21	spleen associated tyrosine kinase	Rattus norvegicus	14-17
10725739-8	2000	Additionally, Syk ASO suppressed Ag-induced pulmonary inflammation, suggesting that Syk ASO may prove useful as an anti-inflammatory therapy in disorders such as asthma.	1,5-anhydroglucitol	18-21	spleen associated tyrosine kinase	Rattus norvegicus	84-87
10725739-8	2000	Additionally, Syk ASO suppressed Ag-induced pulmonary inflammation, suggesting that Syk ASO may prove useful as an anti-inflammatory therapy in disorders such as asthma.	1,5-anhydroglucitol	88-91	spleen associated tyrosine kinase	Rattus norvegicus	14-17
10725739-8	2000	Additionally, Syk ASO suppressed Ag-induced pulmonary inflammation, suggesting that Syk ASO may prove useful as an anti-inflammatory therapy in disorders such as asthma.	1,5-anhydroglucitol	88-91	spleen associated tyrosine kinase	Rattus norvegicus	84-87
10850552-3	1999	In this study, antisense oligodeoxynucleotides (ASO) targeted at the start codon region of GABA-Transaminase mRNA were used to modify seizure activity.	1,5-anhydroglucitol	48-51	4-aminobutyrate aminotransferase	Mus musculus	91-108
11783195-6	1999	The plasma level of ET-1, NO and apoprotein was positively correlated with the stage altering of ASO, it was normalized gradually when ASO was alleviating effectively.	1,5-anhydroglucitol	97-100	endothelin 1	Homo sapiens	20-24
11783195-6	1999	The plasma level of ET-1, NO and apoprotein was positively correlated with the stage altering of ASO, it was normalized gradually when ASO was alleviating effectively.	1,5-anhydroglucitol	135-138	endothelin 1	Homo sapiens	20-24
10464671-6	1999	This molecular genetic study seeks to verify the Ashkenazi Jewish carrier frequency of the BLM 2281 delta 6ins7 allele using semiautomated allele-specific oligonucleotide (ASO) analysis.	1,5-anhydroglucitol	172-175	BLM RecQ like helicase	Homo sapiens	91-94
10090476-5	1999	Extensive sequence analysis was subsequently performed on 14 samples which either had a CPT2 mutation detected by ASO screening or the residual CPT activity was below that observed in ASO positive samples.	1,5-anhydroglucitol	114-117	carnitine palmitoyltransferase 2	Homo sapiens	88-92
9571353-0	1998	Relationship between serum 1,5-anhydroglucitol and urinary excretion of N-acetylglucosaminidase and albumin determined at onset of NIDDM with 3-year follow-up.	1,5-anhydroglucitol	27-46	N-acetyl-alpha-glucosaminidase	Homo sapiens	72-95
9774222-1	1998	A 15-mer, all-phosphorothioate-modified antisense oligodeoxynucleotide (ASO) targeted against rat dopamine D3 receptor mRNA (4 microM, 5 days) significantly reduced (28%) the amount of binding sites labelled with [3H]spiperone in monolayer cultured Chinese hamster ovary (CHO) cells transfected with the complementary desoxyribonucleic acid (cDNA) for the rat D3 receptor.	1,5-anhydroglucitol	72-75	dopamine receptor D3	Rattus norvegicus	98-118
9571353-6	1998	The abnormal excretion of NAG and albumin was associated with a change in serum 1,5AG and was quickly reversible when the serum 1,5AG improved.	1,5-anhydroglucitol	80-85	N-acetyl-alpha-glucosaminidase	Homo sapiens	26-29
9571353-6	1998	The abnormal excretion of NAG and albumin was associated with a change in serum 1,5AG and was quickly reversible when the serum 1,5AG improved.	1,5-anhydroglucitol	128-133	N-acetyl-alpha-glucosaminidase	Homo sapiens	26-29
9500578-6	1998	The urinary level of TM in diabetic patients was significantly correlated with 24-hour glucose excretion and the serum level of 1,5-anhydroglucitol (1,5-AG) (P < .001).	1,5-anhydroglucitol	128-147	thrombomodulin	Homo sapiens	21-23
9379733-7	1997	Genotyping for deletions and 10 point mutations in the CYP 21B gene was performed by Southern blot analysis and polymerase chain reaction (PCR) allele-specific oligonucleotide (ASO) hybridation technique.	1,5-anhydroglucitol	177-180	cytochrome P450 family 21 subfamily A member 2	Homo sapiens	55-62
9389590-5	1997	injection of antisense olignucleotide (ASO) complementary to OFQ receptor but not mismatch olignucleotide (MSO) resulted in the decrease of pain behavior; in such circumstances, OFQ showed no enhancing effect on formalin nociception.	1,5-anhydroglucitol	39-42	prepronociceptin	Rattus norvegicus	61-64
8606878-1	1995	We successfully assessed a fetus at risk for lethal infantile hypophosphatasia using amniocyte DNA and allele-specific oligonucleotide (ASO) probes for two missense mutations in the tissue-non-specific alkaline phosphatase isoenzyme (TNSALP) gene.	1,5-anhydroglucitol	136-139	alkaline phosphatase, biomineralization associated	Homo sapiens	182-232
9376532-1	1997	We investigated the dose-response and time-course of c-fos antisense oligodeoxynucleotide (ASO) treatment against excitatory amino acid (EAA)-induced neurotoxicity in rat hippocampal neurons.	1,5-anhydroglucitol	91-94	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-58
9376532-4	1997	In vivo, bilateral intrahippocampal injections of c-fos ASO (0.025 nmol/site) was neuroprotective when administered 30 min before or after NMDA treatment.	1,5-anhydroglucitol	56-59	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	50-55
9322121-12	1997	K-ras mutation was studied by single-stranded conformation polymorphism (SSCP) and slot-blot allele-specific oligonucleotide (ASO) hybridization of PCR-amplified DNA product.	1,5-anhydroglucitol	126-129	KRAS proto-oncogene, GTPase	Homo sapiens	0-5
9209954-9	1997	K-ras mutation was determined by single-strand conformation polymorphism (SSCP) and slot-blot allele-specific oligonucleotide (ASO) hybridization of PCR-amplified DNA product p53 expression was scored on the basis of percent nuclear staining with the MAb DO7.	1,5-anhydroglucitol	127-130	KRAS proto-oncogene, GTPase	Homo sapiens	0-5
9209954-9	1997	K-ras mutation was determined by single-strand conformation polymorphism (SSCP) and slot-blot allele-specific oligonucleotide (ASO) hybridization of PCR-amplified DNA product p53 expression was scored on the basis of percent nuclear staining with the MAb DO7.	1,5-anhydroglucitol	127-130	tumor protein p53	Homo sapiens	175-178
9051408-0	1997	Rapid improvement of serum 1,5-anhydroglucitol concentrations after administration of alpha-glucosidase inhibitor.	1,5-anhydroglucitol	27-46	sucrase-isomaltase	Homo sapiens	86-103
8940003-1	1996	We have characterized the mechanism of action of an antisense oligodeoxynucleotide (ASO) targeting human endothelial leukocyte adhesion molecule, E-selectin.	1,5-anhydroglucitol	84-87	selectin E	Homo sapiens	146-156
8650119-5	1996	We have developed an allele-specific oligonucleotide (ASO) method to detect mutations in a large number of GSD 1a patients.	1,5-anhydroglucitol	54-57	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	107-113
7773436-5	1995	ASO strongly reduced the light-induced expression of c-Fos and JunB proteins.	1,5-anhydroglucitol	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	53-58
7773436-5	1995	ASO strongly reduced the light-induced expression of c-Fos and JunB proteins.	1,5-anhydroglucitol	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	63-67
7720346-9	1995	The urinary excretion of 1,5-anhydro-D-glucitol was closely correlated (r = 0.792) with that of N-acetyl-beta-glucosaminidase; but not with the serum creatinine level or of the urinary excretion of microalbumin or of urinary beta 2-microglobulin.	1,5-anhydroglucitol	25-47	O-GlcNAcase	Homo sapiens	96-125
7720346-9	1995	The urinary excretion of 1,5-anhydro-D-glucitol was closely correlated (r = 0.792) with that of N-acetyl-beta-glucosaminidase; but not with the serum creatinine level or of the urinary excretion of microalbumin or of urinary beta 2-microglobulin.	1,5-anhydroglucitol	25-47	beta-2-microglobulin	Homo sapiens	225-245
7955370-1	1994	We have developed a fully enzymatic method to measure 1,5 anhydro-D-glucitol (1,5-AG) in serum through use of pyranose oxidase (PROD: EC 1.1.3.10), glucokinase (EC 2.7.1.2), and an ATP-regenerating system.	1,5-anhydroglucitol	78-84	glucokinase	Homo sapiens	148-159
8047985-4	1994	Antisense oligodeoxynucleotides (ASO) to either RI alpha or RII beta inhibit protein translation of the target mRNA by sequence-specific binding; subsequently, cellular PKA content and the cAMP-mediated growth may be altered.	1,5-anhydroglucitol	33-36	protein kinase cAMP-dependent type II regulatory subunit beta	Homo sapiens	60-68
1472941-5	1992	Allele-specific oligonucleotide (ASO) hybridization analyses have confirmed the selective amplification of CYP21B genes and the identity of the pathological mutations.	1,5-anhydroglucitol	33-36	cytochrome P450 family 21 subfamily A member 2	Homo sapiens	107-113
8297506-8	1993	Glucokinase phosphorylated neither 1,5-anhydro-D-fructose nor 1,5-anhydro-D-glucitol, and the phosphorylation of D-glucose by glucokinase was inhibited by them.	1,5-anhydroglucitol	62-84	glucokinase	Rattus norvegicus	0-11
8321048-2	1993	Recently mutations in codons 301 and 969 of c-fms, preferentially involving TAT-to-TGT at codon 969, have also been identified in these disorders by allele specific oligonucleotide (ASO) hybridization.	1,5-anhydroglucitol	182-185	colony stimulating factor 1 receptor	Homo sapiens	44-49
8316501-1	1993	The polymerase chain reaction (PCR) and allele specific oligonucleotide (ASO) hybridization have been used to investigate the incidence of N-ras mutation in acute myeloid leukemia (AML).	1,5-anhydroglucitol	73-76	NRAS proto-oncogene, GTPase	Homo sapiens	139-144
34479070-5	2021	Under the optimal conditions, the potential shift of the LAPS is linearly related to the concentration of 1,5-AG at 10 microg mL-1 -350 microg mL-1 with the correlation coefficient of 0.97414.	1,5-anhydroglucitol	106-112	L1 cell adhesion molecule	Mus musculus	126-130
2244184-5	1990	In insulin-dependent (type 1) diabetes with a long history of disease the concentration of 1,5-anhydroglucitol remains low in spite of improvement of glycaemic control by intensification of treatment, whereas in non-insulin dependent (type 2) diabetes the concentration gradually increases towards normal levels concomitantly with improvement in glycaemic control.	1,5-anhydroglucitol	91-110	insulin	Homo sapiens	3-10
34479070-5	2021	Under the optimal conditions, the potential shift of the LAPS is linearly related to the concentration of 1,5-AG at 10 microg mL-1 -350 microg mL-1 with the correlation coefficient of 0.97414.	1,5-anhydroglucitol	106-112	L1 cell adhesion molecule	Mus musculus	143-147
35549996-3	2022	Treatment with sodium-glucose co-transporter-2 (SGLT2) inhibitors, such as empagliflozin, is a novel therapy that reduces 1,5-anhydroglucitol (1,5AG) in plasma.	1,5-anhydroglucitol	122-141	solute carrier family 5 member 2	Homo sapiens	15-46
34167955-0	2021	Saliva 1,5-anhydroglucitol is associated with early-phase insulin secretion in Chinese patients with type 2 diabetes.	1,5-anhydroglucitol	7-26	insulin	Homo sapiens	58-65
34167955-3	2021	This study aimed to explore the relationship between saliva 1,5-AG and insulin secretion function and insulin sensitivity.	1,5-anhydroglucitol	60-66	insulin	Homo sapiens	71-78
34167955-3	2021	This study aimed to explore the relationship between saliva 1,5-AG and insulin secretion function and insulin sensitivity.	1,5-anhydroglucitol	60-66	insulin	Homo sapiens	102-109
35512857-0	2022	Effects of 1,5-anhydro-D-glucitol on insulin secretion both in in vitro and ex vivo pancreatic preparations.	1,5-anhydroglucitol	11-33	insulin	Homo sapiens	37-44
35512857-3	2022	1,5-anhydro-D-glucitol (1,5-AG) is found in foods, and exists in humans and rodents; however, whether 1,5-AG stimulates insulin secretion remains unclear.	1,5-anhydroglucitol	0-22	insulin	Homo sapiens	120-127
35512857-3	2022	1,5-anhydro-D-glucitol (1,5-AG) is found in foods, and exists in humans and rodents; however, whether 1,5-AG stimulates insulin secretion remains unclear.	1,5-anhydroglucitol	102-108	insulin	Homo sapiens	120-127
35512857-4	2022	This study aimed to assess the effects of short-term 1,5-AG stimulation on insulin secretion in both ex vivo and in INS-1E (rat-derived) cells in vitro.	1,5-anhydroglucitol	53-59	insulin	Homo sapiens	75-82
34185398-0	2021	Human and mouse non-targeted metabolomics identify 1,5-anhydroglucitol as SGLT2-dependent glycemic marker.	1,5-anhydroglucitol	51-70	solute carrier family 5 (sodium/glucose cotransporter), member 2	Mus musculus	74-79
35549996-3	2022	Treatment with sodium-glucose co-transporter-2 (SGLT2) inhibitors, such as empagliflozin, is a novel therapy that reduces 1,5-anhydroglucitol (1,5AG) in plasma.	1,5-anhydroglucitol	122-141	solute carrier family 5 member 2	Homo sapiens	48-53
35534727-8	2022	Mechanistically, 1,5-AG directly binds the S2 subunit of the SARS-CoV-2 spike protein, thereby interrupting spike-mediated virus-host membrane fusion.	1,5-anhydroglucitol	17-23	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	72-77
35506446-1	2022	Neutropenia and neutrophil dysfunction found in deficiencies in G6PC3 and in the glucose-6-phosphate transporter (G6PT/SLC37A4) are due to accumulation of 1,5-anhydroglucitol-6-phosphate (1,5-AG6P), an inhibitor of hexokinase made from 1,5-anhydroglucitol (1,5-AG), an abundant polyol present in blood.	1,5-anhydroglucitol	236-255	glucose-6-phosphatase catalytic subunit 3	Homo sapiens	64-69
35506446-1	2022	Neutropenia and neutrophil dysfunction found in deficiencies in G6PC3 and in the glucose-6-phosphate transporter (G6PT/SLC37A4) are due to accumulation of 1,5-anhydroglucitol-6-phosphate (1,5-AG6P), an inhibitor of hexokinase made from 1,5-anhydroglucitol (1,5-AG), an abundant polyol present in blood.	1,5-anhydroglucitol	236-255	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	114-118
35506446-1	2022	Neutropenia and neutrophil dysfunction found in deficiencies in G6PC3 and in the glucose-6-phosphate transporter (G6PT/SLC37A4) are due to accumulation of 1,5-anhydroglucitol-6-phosphate (1,5-AG6P), an inhibitor of hexokinase made from 1,5-anhydroglucitol (1,5-AG), an abundant polyol present in blood.	1,5-anhydroglucitol	236-255	solute carrier family 37 member 4	Homo sapiens	119-126
35506446-1	2022	Neutropenia and neutrophil dysfunction found in deficiencies in G6PC3 and in the glucose-6-phosphate transporter (G6PT/SLC37A4) are due to accumulation of 1,5-anhydroglucitol-6-phosphate (1,5-AG6P), an inhibitor of hexokinase made from 1,5-anhydroglucitol (1,5-AG), an abundant polyol present in blood.	1,5-anhydroglucitol	257-263	glucose-6-phosphatase catalytic subunit 3	Homo sapiens	64-69
35506446-1	2022	Neutropenia and neutrophil dysfunction found in deficiencies in G6PC3 and in the glucose-6-phosphate transporter (G6PT/SLC37A4) are due to accumulation of 1,5-anhydroglucitol-6-phosphate (1,5-AG6P), an inhibitor of hexokinase made from 1,5-anhydroglucitol (1,5-AG), an abundant polyol present in blood.	1,5-anhydroglucitol	257-263	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	114-118
35506446-1	2022	Neutropenia and neutrophil dysfunction found in deficiencies in G6PC3 and in the glucose-6-phosphate transporter (G6PT/SLC37A4) are due to accumulation of 1,5-anhydroglucitol-6-phosphate (1,5-AG6P), an inhibitor of hexokinase made from 1,5-anhydroglucitol (1,5-AG), an abundant polyol present in blood.	1,5-anhydroglucitol	257-263	solute carrier family 37 member 4	Homo sapiens	119-126
35506446-2	2022	Lowering blood 1,5-AG with an SGLT2 inhibitor greatly improved neutrophil counts and function in G6PC3-deficient mice and in patients with G6PT-deficiency.	1,5-anhydroglucitol	15-21	solute carrier family 5 (sodium/glucose cotransporter), member 2	Mus musculus	30-35
35534727-8	2022	Mechanistically, 1,5-AG directly binds the S2 subunit of the SARS-CoV-2 spike protein, thereby interrupting spike-mediated virus-host membrane fusion.	1,5-anhydroglucitol	17-23	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	108-113
35428200-9	2022	CONCLUSIONS: Circulating CD4+ T cells in aged patients with ASO may show a distinct molecular signature.	1,5-anhydroglucitol	60-63	CD4 molecule	Homo sapiens	25-28
6360421-0	1984	Serum 1,5-anhydroglucitol concentration in diabetic patients receiving a continuous subcutaneous infusion of insulin.	1,5-anhydroglucitol	6-25	insulin	Homo sapiens	109-116
6345028-3	1983	1-Deoxyglucose was generally not detectable in plasmas of diabetic patients before they received insulin; it was measurable in the patients who had received insulin, although its concentration was low compared with that of healthy subjects.	1,5-anhydroglucitol	0-14	insulin	Homo sapiens	97-104
6345028-3	1983	1-Deoxyglucose was generally not detectable in plasmas of diabetic patients before they received insulin; it was measurable in the patients who had received insulin, although its concentration was low compared with that of healthy subjects.	1,5-anhydroglucitol	0-14	insulin	Homo sapiens	157-164