PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
19096015-8	2009	Our findings on SLC19A2 and SLC19A3 suggest a potential role of these two genes in the pathophysiology of alcohol-related thiamine deficiency but further studies need to be carried out.	Thiamine	122-130	solute carrier family 19 member 2	Homo sapiens	16-23
19096015-8	2009	Our findings on SLC19A2 and SLC19A3 suggest a potential role of these two genes in the pathophysiology of alcohol-related thiamine deficiency but further studies need to be carried out.	Thiamine	122-130	solute carrier family 19 member 3	Homo sapiens	28-35
19347672-1	2009	Thiamine responsive megaloblastic anemia syndrome (TRMA) is a clinical triad characterized by thiamine-responsive anemia, diabetes mellitus and sensorineural deafness.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	51-55
19347672-1	2009	Thiamine responsive megaloblastic anemia syndrome (TRMA) is a clinical triad characterized by thiamine-responsive anemia, diabetes mellitus and sensorineural deafness.	Thiamine	94-102	solute carrier family 19 member 2	Homo sapiens	51-55
19347672-2	2009	We report a 4-year-old girl with TRMA whose anemia improved following administration of thiamine and this case report sensitizes the early diagnosis and treatment with thiamine in children presenting with anemia, diabetes and deafness.	Thiamine	88-96	solute carrier family 19 member 2	Homo sapiens	33-37
19347672-2	2009	We report a 4-year-old girl with TRMA whose anemia improved following administration of thiamine and this case report sensitizes the early diagnosis and treatment with thiamine in children presenting with anemia, diabetes and deafness.	Thiamine	168-176	solute carrier family 19 member 2	Homo sapiens	33-37
18616671-7	2008	CONCLUSIONS: In both ethanol intoxication and thiamin-deficient glucose metabolism, BCSFB impairment exposes the CSF and hence the brain extracellular fluid to neuroactive substances from the blood.	Thiamine	46-53	colony stimulating factor 2	Rattus norvegicus	85-88
18783638-7	2008	Significant negative correlations were found among St4 between perceived stress and thiamine(r= -0,48; p=0,006) and zinc (r= -0,42; p=0,02).	Thiamine	84-92	ST3 beta-galactoside alpha-2,3-sialyltransferase 4	Homo sapiens	51-54
18581039-3	2008	Thiamine acts as a coenzyme for transketolase (TK) and for the pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes, enzymes which play a fundamental role for intracellular glucose metabolism.	Thiamine	0-8	transketolase	Homo sapiens	32-45
18581039-3	2008	Thiamine acts as a coenzyme for transketolase (TK) and for the pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes, enzymes which play a fundamental role for intracellular glucose metabolism.	Thiamine	0-8	transketolase	Homo sapiens	47-49
19013460-0	2008	Thiamin-dependent transactivation activity of PDC2 in Saccharomyces cerevisiae.	Thiamine	0-7	Pdc2p	Saccharomyces cerevisiae S288C	46-50
19013460-4	2008	We found here that Pdc2p could transactivate gene expression and interact with Thi3p, both of which were enhanced by thiamin starvation.	Thiamine	117-124	Pdc2p	Saccharomyces cerevisiae S288C	19-24
19013460-4	2008	We found here that Pdc2p could transactivate gene expression and interact with Thi3p, both of which were enhanced by thiamin starvation.	Thiamine	117-124	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	79-84
18778100-5	2008	By mimicking the "active aldehyde" nucleophilic acylations in Nature catalyzed by the thiamine-dependent enzyme, transketolase, enantioselective N-heterocyclic carbene-catalyzed benzoin and Stetter reactions have been developed.	Thiamine	86-94	transketolase	Homo sapiens	113-126
18430561-0	2008	A novel biosensor based on activation effect of thiamine on the activity of pyruvate oxidase.	Thiamine	48-56	proline dehydrogenase 1	Homo sapiens	76-92
18430561-1	2008	A biosensor based on pyruvate oxidase (POX) enzyme was developed for the investigation of the effect of thiamine (vitamin B(1)) molecule on the activity of the enzyme.	Thiamine	104-112	proline dehydrogenase 1	Homo sapiens	21-37
18430561-1	2008	A biosensor based on pyruvate oxidase (POX) enzyme was developed for the investigation of the effect of thiamine (vitamin B(1)) molecule on the activity of the enzyme.	Thiamine	104-112	proline dehydrogenase 1	Homo sapiens	39-42
18430561-1	2008	A biosensor based on pyruvate oxidase (POX) enzyme was developed for the investigation of the effect of thiamine (vitamin B(1)) molecule on the activity of the enzyme.	Thiamine	114-123	proline dehydrogenase 1	Homo sapiens	21-37
18430561-1	2008	A biosensor based on pyruvate oxidase (POX) enzyme was developed for the investigation of the effect of thiamine (vitamin B(1)) molecule on the activity of the enzyme.	Thiamine	114-123	proline dehydrogenase 1	Homo sapiens	39-42
18430561-4	2008	Thiamine is an activator for POX enzyme and determination method of the biosensor was based on this effect of thiamine on the activity of the enzyme.	Thiamine	0-8	proline dehydrogenase 1	Homo sapiens	29-32
18430561-4	2008	Thiamine is an activator for POX enzyme and determination method of the biosensor was based on this effect of thiamine on the activity of the enzyme.	Thiamine	110-118	proline dehydrogenase 1	Homo sapiens	29-32
18481165-2	2008	We have investigated cyclooxygenase-2 (COX-2) expression in vulnerable (medial thalamus, inferior colliculus) and spared (frontal cortex) regions of rats with thiamine deficiency.	Thiamine	159-167	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	21-37
18533652-2	2008	In plants, TPP regulates its own production by binding to the 3" untranslated region of the mRNA encoding ThiC, a critical enzyme in thiamine biosynthesis, which promotes the formation of an unstable splicing variant.	Thiamine	133-141	thiaminC	Arabidopsis thaliana	106-110
18384109-3	2008	Owing to a reduced activity of the enzyme transketolase, which requires diphosphorylated thiamine (vitamin B(1)) as cofactor, an accumulation of those deleterious glucose metabolites especially in diabetic patients can be observed.	Thiamine	89-97	transketolase	Homo sapiens	42-55
18384109-3	2008	Owing to a reduced activity of the enzyme transketolase, which requires diphosphorylated thiamine (vitamin B(1)) as cofactor, an accumulation of those deleterious glucose metabolites especially in diabetic patients can be observed.	Thiamine	99-111	transketolase	Homo sapiens	42-55
18317926-0	2008	Translocation of amyloid precursor protein C-terminal fragment(s) to the nucleus precedes neuronal death due to thiamine deficiency-induced mild impairment of oxidative metabolism.	Thiamine	112-120	amyloid beta precursor protein	Homo sapiens	17-42
18236031-3	2008	The proposed hyphenated technique was applied to the simultaneous spectrophotometric determination of thiamine (B(1)), pyridoxine (B(6)) and cyanocobalamin (B(12)) which were taken as model analytes.	Thiamine	102-110	immunoglobulin kappa variable 7-3 (pseudogene)	Homo sapiens	112-116
18028398-0	2008	Involvement of thiaminase II encoded by the THI20 gene in thiamin salvage of Saccharomyces cerevisiae.	Thiamine	15-22	trifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase/thiaminase	Saccharomyces cerevisiae S288C	44-49
18516403-3	2008	OBJECTIVE: We studied the relationship between adding to ACE inhibition further aldosterone suppression with spironolactone and thiamine blood levels (pmol/ml).	Thiamine	128-136	angiotensin I converting enzyme	Homo sapiens	57-60
18332905-0	2008	AtTHIC, a gene involved in thiamine biosynthesis in Arabidopsis thaliana.	Thiamine	27-35	thiaminC	Arabidopsis thaliana	0-6
18332905-4	2008	Here we report the molecular characterization of AtTHIC, which is involved in thiamine biosynthesis in Arabidopsis.	Thiamine	78-86	thiaminC	Arabidopsis thaliana	49-55
18332905-7	2008	Downregulation of AtTHIC expression by T-DNA insertion at its promoter region resulted in a drastic reduction of thiamine content in plants and the knock-down mutant thic1 showed albino (white leaves) and lethal phenotypes under the normal culture conditions.	Thiamine	113-121	thiaminC	Arabidopsis thaliana	18-24
18332905-10	2008	AtTHIC was strongly expressed in leaves, flowers and siliques and the transcription of AtTHIC was downregulated by extrinsic thiamine.	Thiamine	125-133	thiaminC	Arabidopsis thaliana	0-6
18332905-10	2008	AtTHIC was strongly expressed in leaves, flowers and siliques and the transcription of AtTHIC was downregulated by extrinsic thiamine.	Thiamine	125-133	thiaminC	Arabidopsis thaliana	87-93
18332905-11	2008	In conclusion, AtTHIC is a gene involved in pyrimidine synthesis in the thiamine biosynthesis pathway of Arabidopsis, and our results provide some new clues for elucidating the pathway of thiamine biosynthesis in plants.	Thiamine	72-80	thiaminC	Arabidopsis thaliana	15-21
18332905-11	2008	In conclusion, AtTHIC is a gene involved in pyrimidine synthesis in the thiamine biosynthesis pathway of Arabidopsis, and our results provide some new clues for elucidating the pathway of thiamine biosynthesis in plants.	Thiamine	188-196	thiaminC	Arabidopsis thaliana	15-21
18028398-3	2008	On the other hand, the N-terminal domains of THI20 and THI21 encode 2-methyl-4-amino-5-hydroxymethylpyrimidine kinase and 2-methyl-4-amino-5-hydroxymethylpyrimidine phosphate kinase involved in the thiamin synthetic pathway.	Thiamine	198-205	trifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase/thiaminase	Saccharomyces cerevisiae S288C	45-50
18028398-3	2008	On the other hand, the N-terminal domains of THI20 and THI21 encode 2-methyl-4-amino-5-hydroxymethylpyrimidine kinase and 2-methyl-4-amino-5-hydroxymethylpyrimidine phosphate kinase involved in the thiamin synthetic pathway.	Thiamine	198-205	bifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase	Saccharomyces cerevisiae S288C	55-60
18028398-6	2008	It appeared that Thi20p has an affinity for the pyrimidine moiety of thiamin, and HMP produced by the thiaminase II activity is immediately phosphorylated.	Thiamine	69-76	trifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase/thiaminase	Saccharomyces cerevisiae S288C	17-23
18028398-7	2008	Thi20p was found to participate in the formation of thiamin from two synthetic antagonists, pyrithiamin and oxythiamin, by hydrolyzing both antagonists and phosphorylating HMP to give HMP pyrophosphate.	Thiamine	52-59	trifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase/thiaminase	Saccharomyces cerevisiae S288C	0-6
18028398-8	2008	Furthermore, 2-methyl-4-amino-5-aminomethylpyrimidine, a presumed naturally occurring thiamin precursor, was effectively converted to HMP by incubation with Thi20p.	Thiamine	86-93	trifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase/thiaminase	Saccharomyces cerevisiae S288C	157-163
18028398-9	2008	It is proposed that the thiaminase II activity of Thi20p is involved in the thiamin salvage pathway by catalyzing the hydrolysis of HMP precursors in S. cerevisiae.	Thiamine	24-31	trifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase/thiaminase	Saccharomyces cerevisiae S288C	50-56
18182286-1	2008	Inhibition of the thiamine-utilizing enzyme transketolase (TK) has been linked with diminished tumor cell proliferation.	Thiamine	18-26	transketolase	Homo sapiens	59-61
18182286-0	2008	Non-charged thiamine analogs as inhibitors of enzyme transketolase.	Thiamine	12-20	transketolase	Homo sapiens	53-66
18182286-1	2008	Inhibition of the thiamine-utilizing enzyme transketolase (TK) has been linked with diminished tumor cell proliferation.	Thiamine	18-26	transketolase	Homo sapiens	44-57
18083562-0	2008	Prodrug thiamine analogs as inhibitors of the enzyme transketolase.	Thiamine	8-16	transketolase	Homo sapiens	53-66
18182286-2	2008	Most thiamine antagonists have a permanent positive charge on the B-ring, and it has been suggested that this charge is required for diphosphorylation by thiamine pyrophosphokinase (TPPK) and binding to TK.	Thiamine	5-13	transketolase	Homo sapiens	203-205
18048325-0	2007	Vitamin B1 biosynthesis in plants requires the essential iron sulfur cluster protein, THIC.	Thiamine	0-10	thiaminC	Arabidopsis thaliana	86-90
18048325-6	2007	Here, we identify a homolog of THIC in Arabidopsis and demonstrate its essentiality not only for vitamin B1 biosynthesis, but also plant viability.	Thiamine	97-107	thiaminC	Arabidopsis thaliana	31-35
17703232-3	2007	The stalk region preceding the THD of mCD95L conferred secondary aggregation and restored CD95 activation in the absence of cross-linking.	Thiamine	31-34	Fas cell surface death receptor	Homo sapiens	39-43
18048325-9	2007	The results suggest that vitamin B1 biosynthesis in plants is in fact more similar to prokaryotic counterparts and that the THIC protein is likely to be the key regulatory protein in the pathway.	Thiamine	25-35	thiaminC	Arabidopsis thaliana	124-128
17703232-5	2007	Notably, disulfide-bonded fusion proteins of the THD of mTRAIL and mCD95L with a subdomain of the tenascin-C (TNC) oligomerization domain, which still assembled into trimers, efficiently interacted with their cognate cellular receptors and robustly stimulated CD95 and TRAILR2 signaling after secondary cross-linking.	Thiamine	49-52	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	56-62
17703232-5	2007	Notably, disulfide-bonded fusion proteins of the THD of mTRAIL and mCD95L with a subdomain of the tenascin-C (TNC) oligomerization domain, which still assembled into trimers, efficiently interacted with their cognate cellular receptors and robustly stimulated CD95 and TRAILR2 signaling after secondary cross-linking.	Thiamine	49-52	tenascin C	Homo sapiens	98-108
17703232-5	2007	Notably, disulfide-bonded fusion proteins of the THD of mTRAIL and mCD95L with a subdomain of the tenascin-C (TNC) oligomerization domain, which still assembled into trimers, efficiently interacted with their cognate cellular receptors and robustly stimulated CD95 and TRAILR2 signaling after secondary cross-linking.	Thiamine	49-52	tenascin C	Homo sapiens	110-113
17703232-5	2007	Notably, disulfide-bonded fusion proteins of the THD of mTRAIL and mCD95L with a subdomain of the tenascin-C (TNC) oligomerization domain, which still assembled into trimers, efficiently interacted with their cognate cellular receptors and robustly stimulated CD95 and TRAILR2 signaling after secondary cross-linking.	Thiamine	49-52	TNF receptor superfamily member 10b	Homo sapiens	269-276
17703232-6	2007	Introduction of the TNC domain also further enhanced the activity of THD encompassing variants of hTRAIL and hCD95L.	Thiamine	69-72	tenascin C	Homo sapiens	20-23
17703232-6	2007	Introduction of the TNC domain also further enhanced the activity of THD encompassing variants of hTRAIL and hCD95L.	Thiamine	69-72	TNF superfamily member 10	Homo sapiens	98-104
17703232-6	2007	Introduction of the TNC domain also further enhanced the activity of THD encompassing variants of hTRAIL and hCD95L.	Thiamine	69-72	Fas ligand	Homo sapiens	109-115
17963776-1	2007	A rapid and sensitive high-performance liquid chromatography (HPLC) method with coulometric electrochemical and ultraviolet detections for analysis of vitamin B (B(1), B(6) and B(12)) in animal and plant foods has been developed.	Thiamine	151-160	immunoglobulin kappa variable 7-3 (pseudogene)	Homo sapiens	162-166
17445056-1	2007	BACKGROUND: Child malnutrition and thiamine deficiency remain a matter of public concern in Dai children under 5 years old in Southwest areas of China.	Thiamine	35-43	Z-DNA binding protein 1	Homo sapiens	92-95
17914867-0	2007	Strain and near attack conformers in enzymic thiamin catalysis: X-ray crystallographic snapshots of bacterial transketolase in covalent complex with donor ketoses xylulose 5-phosphate and fructose 6-phosphate, and in noncovalent complex with acceptor aldose ribose 5-phosphate.	Thiamine	45-52	transketolase	Homo sapiens	110-123
17331069-1	2007	The micronutrient thiamine is required for normal growth and development of human tissues, and is accumulated into cells through the activity of plasma membrane thiamine transporters, e.g. hTHTR1 (human thiamine transporter 1).	Thiamine	18-26	solute carrier family 19 member 2	Homo sapiens	189-195
17331069-1	2007	The micronutrient thiamine is required for normal growth and development of human tissues, and is accumulated into cells through the activity of plasma membrane thiamine transporters, e.g. hTHTR1 (human thiamine transporter 1).	Thiamine	18-26	solute carrier family 19 member 2	Homo sapiens	203-225
17331069-2	2007	Recent genetic evidence has linked mutations in hTHTR1 with the manifestation of TRMA (thiamine-responsive megaloblastic anaemia), a condition also associated with diabetes mellitus, sensorineural deafness and retinal disorders.	Thiamine	87-95	solute carrier family 19 member 2	Homo sapiens	48-54
17463047-1	2007	Retinal abnormality and visual disturbances occur in thiamine-responsive megaloblastic anaemia (TRMA), an autosomal recessive disorder caused by mutations in the human thiamine transporter-1 (hTHTR-1).	Thiamine	53-61	solute carrier family 19 member 2	Homo sapiens	168-190
17463047-1	2007	Retinal abnormality and visual disturbances occur in thiamine-responsive megaloblastic anaemia (TRMA), an autosomal recessive disorder caused by mutations in the human thiamine transporter-1 (hTHTR-1).	Thiamine	53-61	solute carrier family 19 member 2	Homo sapiens	192-199
17463047-7	2007	Uptake of thiamine was adaptively regulated by extracellular substrate level via transcriptionally mediated mechanisms that involve both hTHTR-1 and hTHTR-2; it was also regulated by an intracellular Ca2+-calmodulin-mediated pathway.	Thiamine	10-18	solute carrier family 19 member 2	Homo sapiens	137-144
17463047-7	2007	Uptake of thiamine was adaptively regulated by extracellular substrate level via transcriptionally mediated mechanisms that involve both hTHTR-1 and hTHTR-2; it was also regulated by an intracellular Ca2+-calmodulin-mediated pathway.	Thiamine	10-18	solute carrier family 19 member 3	Homo sapiens	149-156
17463047-9	2007	These results demonstrate for the first time the existence of a specialized and regulated uptake process for thiamine in a cellular model of human retinal pigment epithelia that involves hTHTR-1 and hTHTR-2.	Thiamine	109-117	solute carrier family 19 member 2	Homo sapiens	187-194
17463047-9	2007	These results demonstrate for the first time the existence of a specialized and regulated uptake process for thiamine in a cellular model of human retinal pigment epithelia that involves hTHTR-1 and hTHTR-2.	Thiamine	109-117	solute carrier family 19 member 3	Homo sapiens	199-206
17963776-0	2007	Reversed-phase high-performance liquid chromatography method with coulometric electrochemical and ultraviolet detection for the quantification of vitamins B(1) (thiamine), B(6) (pyridoxamine, pyridoxal and pyridoxine) and B(12) in animal and plant foods.	Thiamine	161-169	immunoglobulin kappa variable 7-3 (pseudogene)	Homo sapiens	155-159
17686772-7	2007	The potential physiological relevance of AphA and AnsB in contributing to thiamine biosynthesis in vivo is discussed.	Thiamine	74-82	aminoglycoside 3'-phosphotransferase	Escherichia coli	41-45
17659067-3	2007	All children were homozygous, and the parents were heterozygous for a c.196G>T mutation in the SLC19A2 gene on chromosome 1q23.3, which encodes a high-affinity thiamine transporter.	Thiamine	163-171	solute carrier family 19 member 2	Homo sapiens	98-105
17445056-2	2007	The aim of the present study was to understand the status and correlates of malnutrition and thiamine deficiency in Dai children under 18 months old in Yunnan, China, and to explore an effective intervention for improving their nutritional status and decreasing the prevalence of malnutrition and thiamine deficiency in Dai children.	Thiamine	93-101	Z-DNA binding protein 1	Homo sapiens	116-119
17174261-0	2007	Determination of the genetic, molecular, and biochemical basis of the Arabidopsis thaliana thiamin auxotroph th1.	Thiamine	91-98	thiamin biosynthesis protein	Arabidopsis thaliana	109-112
17309261-9	2007	These observations confirm NAD as the substrate for THI4 and elucidate the early steps of this unique biosynthesis of the thiazole moiety of thiamin in eukaryotes.	Thiamine	141-148	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	52-56
17174261-2	2007	A candidate HMPPK/TMPPase gene identified in the Arabidopsis genome complemented the thiamin auxotrophy of the th1 mutant, thus proving that the th1 locus corresponds to the structural gene for the HMPPK/TMPPase.	Thiamine	85-92	thiamin biosynthesis protein	Arabidopsis thaliana	111-114
17174261-2	2007	A candidate HMPPK/TMPPase gene identified in the Arabidopsis genome complemented the thiamin auxotrophy of the th1 mutant, thus proving that the th1 locus corresponds to the structural gene for the HMPPK/TMPPase.	Thiamine	85-92	thiamin biosynthesis protein	Arabidopsis thaliana	145-148
17465256-4	2007	RESULTS: Patients with methylation in p16(INK4a) consumed significantly less folate (p = 0.01), vitamin A (p = 0.01), vitamin B1 (p = 0.007), potassium (p = 0.03) and iron (p = 0.02) than controls.	Thiamine	118-128	cyclin dependent kinase inhibitor 2A	Homo sapiens	38-41
17158583-0	2007	Vitamin B1-induced priming is dependent on hydrogen peroxide and the NPR1 gene in Arabidopsis.	Thiamine	0-10	regulatory protein (NPR1)	Arabidopsis thaliana	69-73
17465256-4	2007	RESULTS: Patients with methylation in p16(INK4a) consumed significantly less folate (p = 0.01), vitamin A (p = 0.01), vitamin B1 (p = 0.007), potassium (p = 0.03) and iron (p = 0.02) than controls.	Thiamine	118-128	cyclin dependent kinase inhibitor 2A	Homo sapiens	42-47
17158583-5	2007	Thiamine treatment and subsequent pathogen invasion triggered hydrogen peroxide accumulation, callose induction, and PR1/PAL1 transcription activation in Arabidopsis mutants insensitive to jasmonic acid (jar1), ethylene (etr1), or abscisic acid (abi3-3), but not in plants expressing bacterial NahG and lacking regulation of SAR (npr1 [nonexpressor of PR genes 1]).	Thiamine	0-8	pathogenesis-related protein 1	Arabidopsis thaliana	117-120
17207784-2	2007	Thiamin (Vitamin B(1)) is an essential coenzyme for transketolase (TK) that is part of the pentose phosphate pathway which helps maintain cellular NADPH levels.	Thiamine	0-7	transketolase	Homo sapiens	52-65
17207784-2	2007	Thiamin (Vitamin B(1)) is an essential coenzyme for transketolase (TK) that is part of the pentose phosphate pathway which helps maintain cellular NADPH levels.	Thiamine	0-7	transketolase	Homo sapiens	67-69
17207784-2	2007	Thiamin (Vitamin B(1)) is an essential coenzyme for transketolase (TK) that is part of the pentose phosphate pathway which helps maintain cellular NADPH levels.	Thiamine	9-18	transketolase	Homo sapiens	52-65
17207784-2	2007	Thiamin (Vitamin B(1)) is an essential coenzyme for transketolase (TK) that is part of the pentose phosphate pathway which helps maintain cellular NADPH levels.	Thiamine	9-18	transketolase	Homo sapiens	67-69
17502925-0	2007	Thiamine deficiency caused by thiamine antagonists triggers upregulation of apoptosis inducing factor gene expression and leads to caspase 3-mediated apoptosis in neuronally differentiated rat PC-12 cells.	Thiamine	0-8	caspase 3	Rattus norvegicus	131-140
17502925-0	2007	Thiamine deficiency caused by thiamine antagonists triggers upregulation of apoptosis inducing factor gene expression and leads to caspase 3-mediated apoptosis in neuronally differentiated rat PC-12 cells.	Thiamine	30-38	caspase 3	Rattus norvegicus	131-140
17502925-3	2007	Here, we report that rat pheochromocytoma PC-12 cells differentiated in the presence of NGF into neurons undergo apoptosis due to thiamine deficiency caused by antagonists of thiamine - amprolium, pyrithiamine and oxythiamine.	Thiamine	130-138	nerve growth factor	Rattus norvegicus	88-91
17502925-4	2007	Confocal laser scanning fluorescence microscopy revealed that annexin V binds to PC-12 cells in presence of thiamine antagonists after 72 h incubation.	Thiamine	108-116	annexin A5	Rattus norvegicus	62-71
17502925-5	2007	Results also show that thiamine antagonists trigger upregulation of gene expression of mitochondrial-derived apoptosis inducing factor, DNA fragmentation, cleavage of caspase 3 and translocation of active product to the nucleus.	Thiamine	23-31	caspase 3	Rattus norvegicus	167-176
17158583-5	2007	Thiamine treatment and subsequent pathogen invasion triggered hydrogen peroxide accumulation, callose induction, and PR1/PAL1 transcription activation in Arabidopsis mutants insensitive to jasmonic acid (jar1), ethylene (etr1), or abscisic acid (abi3-3), but not in plants expressing bacterial NahG and lacking regulation of SAR (npr1 [nonexpressor of PR genes 1]).	Thiamine	0-8	PHE ammonia lyase 1	Arabidopsis thaliana	121-125
17158583-5	2007	Thiamine treatment and subsequent pathogen invasion triggered hydrogen peroxide accumulation, callose induction, and PR1/PAL1 transcription activation in Arabidopsis mutants insensitive to jasmonic acid (jar1), ethylene (etr1), or abscisic acid (abi3-3), but not in plants expressing bacterial NahG and lacking regulation of SAR (npr1 [nonexpressor of PR genes 1]).	Thiamine	0-8	Signal transduction histidine kinase, hybrid-type, ethylene sensor	Arabidopsis thaliana	221-225
17158583-5	2007	Thiamine treatment and subsequent pathogen invasion triggered hydrogen peroxide accumulation, callose induction, and PR1/PAL1 transcription activation in Arabidopsis mutants insensitive to jasmonic acid (jar1), ethylene (etr1), or abscisic acid (abi3-3), but not in plants expressing bacterial NahG and lacking regulation of SAR (npr1 [nonexpressor of PR genes 1]).	Thiamine	0-8	regulatory protein (NPR1)	Arabidopsis thaliana	330-334
16642288-1	2006	Mutations in the gene coding for the high-affinity thiamine transporter Slc19a2 underlie the clinical syndrome known as thiamine-responsive megaloblastic anemia (TRMA) characterized by anemia, diabetes, and sensorineural hearing loss.	Thiamine	51-59	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	72-79
17132746-1	2006	OBJECTIVE: Thiamine-responsive megaloblastic anemia (TRMA) is a rare syndrome characterized by diabetes mellitus (DM), anemia, and sensorineural deafness.	Thiamine	11-19	solute carrier family 19 member 2	Homo sapiens	53-57
17006386-14	2006	Because potential mechanisms exist for thiamine deficiency in diabetes mellitus and institution of insulin and glucose therapy may stress thiamine body stores, thiamine deficiency should be considered in children with diabetic ketoacidosis whose encephalopathy does not improve with improvement of biochemical status.	Thiamine	138-146	insulin	Homo sapiens	99-106
17006386-14	2006	Because potential mechanisms exist for thiamine deficiency in diabetes mellitus and institution of insulin and glucose therapy may stress thiamine body stores, thiamine deficiency should be considered in children with diabetic ketoacidosis whose encephalopathy does not improve with improvement of biochemical status.	Thiamine	138-146	insulin	Homo sapiens	99-106
17043409-0	2006	A Korean female patient with thiamine-responsive pyruvate dehydrogenase complex deficiency due to a novel point mutation (Y161C)in the PDHA1 gene.	Thiamine	29-37	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	135-140
16964967-0	2006	Structural insights into the function of the thiamin biosynthetic enzyme Thi4 from Saccharomyces cerevisiae.	Thiamine	45-52	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	73-77
16790503-0	2006	Biotin-responsive basal ganglia disease-linked mutations inhibit thiamine transport via hTHTR2: biotin is not a substrate for hTHTR2.	Thiamine	65-73	solute carrier family 19 member 3	Homo sapiens	88-94
16790503-2	2006	Thiamine is accumulated into cells through the activity of two cell surface thiamine transporters (hTHTR1 and hTHTR2), which are differentially targeted in polarized tissues.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	99-105
16790503-2	2006	Thiamine is accumulated into cells through the activity of two cell surface thiamine transporters (hTHTR1 and hTHTR2), which are differentially targeted in polarized tissues.	Thiamine	0-8	solute carrier family 19 member 3	Homo sapiens	110-116
16790503-3	2006	Mutational dysfunction of hTHTR1 is associated with the clinical condition of thiamine-responsive megaloblastic anemia: the symptoms of which are alleviated by thiamine supplementation.	Thiamine	78-86	solute carrier family 19 member 2	Homo sapiens	26-32
16790503-3	2006	Mutational dysfunction of hTHTR1 is associated with the clinical condition of thiamine-responsive megaloblastic anemia: the symptoms of which are alleviated by thiamine supplementation.	Thiamine	160-168	solute carrier family 19 member 2	Homo sapiens	26-32
16705148-6	2006	Maintaining the cells in thiamin-deficient medium led to a significant (P < 0.01) and specific upregulation in [(3)H]thiamin uptake, which was associated with an increase in hTHTR-1 and hTHTR-2 protein and mRNA levels as well as promoter activities.	Thiamine	25-32	solute carrier family 19 member 2	Homo sapiens	177-184
16705148-6	2006	Maintaining the cells in thiamin-deficient medium led to a significant (P < 0.01) and specific upregulation in [(3)H]thiamin uptake, which was associated with an increase in hTHTR-1 and hTHTR-2 protein and mRNA levels as well as promoter activities.	Thiamine	25-32	solute carrier family 19 member 3	Homo sapiens	189-196
16705148-6	2006	Maintaining the cells in thiamin-deficient medium led to a significant (P < 0.01) and specific upregulation in [(3)H]thiamin uptake, which was associated with an increase in hTHTR-1 and hTHTR-2 protein and mRNA levels as well as promoter activities.	Thiamine	120-127	solute carrier family 19 member 2	Homo sapiens	177-184
16705148-6	2006	Maintaining the cells in thiamin-deficient medium led to a significant (P < 0.01) and specific upregulation in [(3)H]thiamin uptake, which was associated with an increase in hTHTR-1 and hTHTR-2 protein and mRNA levels as well as promoter activities.	Thiamine	120-127	solute carrier family 19 member 3	Homo sapiens	189-196
16705148-7	2006	Uptake of thiamin by HEK-293 cells also appeared to be under the regulation of an intracellular Ca(2+)/calmodulin-mediated pathway.	Thiamine	10-17	calmodulin 1	Homo sapiens	103-113
16705148-8	2006	These studies demonstrate for the first time that thiamin uptake by HEK-293 cells is mediated via a specific pH-dependent process, which involves both the hTHTR-1 and hTHTR-2.	Thiamine	50-57	solute carrier family 19 member 2	Homo sapiens	155-162
16705148-8	2006	These studies demonstrate for the first time that thiamin uptake by HEK-293 cells is mediated via a specific pH-dependent process, which involves both the hTHTR-1 and hTHTR-2.	Thiamine	50-57	solute carrier family 19 member 3	Homo sapiens	167-174
16705148-9	2006	In addition, the uptake process appears to be under the regulation of an intracellular Ca(2+)/CaM-mediated pathway and also adaptively upregulated in thiamin deficiency via transcriptional regulatory mechanism(s) that involves both the hTHTR-1 and hTHTR-2.	Thiamine	150-157	calmodulin 1	Homo sapiens	94-97
16705148-9	2006	In addition, the uptake process appears to be under the regulation of an intracellular Ca(2+)/CaM-mediated pathway and also adaptively upregulated in thiamin deficiency via transcriptional regulatory mechanism(s) that involves both the hTHTR-1 and hTHTR-2.	Thiamine	150-157	solute carrier family 19 member 2	Homo sapiens	236-243
16705148-9	2006	In addition, the uptake process appears to be under the regulation of an intracellular Ca(2+)/CaM-mediated pathway and also adaptively upregulated in thiamin deficiency via transcriptional regulatory mechanism(s) that involves both the hTHTR-1 and hTHTR-2.	Thiamine	150-157	solute carrier family 19 member 3	Homo sapiens	248-255
16642288-4	2006	When challenged with a low-thiamine diet, Slc19a2-null mice showed 40-60 dB threshold elevations by auditory brainstem response (ABR), but only 10-20 dB elevation by otoacoustic emission (OAE) measures.	Thiamine	27-35	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	42-49
16807400-9	2006	Ammonium chloride-induced intracellular acidification significantly stimulated the hMATE2-K-dependent transport of organic cations such as TEA, MPP, procainamide, metformin, N1-methylnicotinamide, creatinine, guanidine, quinidine, quinine, thiamine, and verapamil.	Thiamine	240-248	solute carrier family 47 member 2	Homo sapiens	83-89
16513100-8	2006	However, simultaneous supplementation of ascorbic acid and thiamine at the highest dose promoted testicular cell apoptosis via increased expressions of TGFbeta1 and caspase-3.	Thiamine	59-67	transforming growth factor, beta 1	Mus musculus	152-160
16513100-8	2006	However, simultaneous supplementation of ascorbic acid and thiamine at the highest dose promoted testicular cell apoptosis via increased expressions of TGFbeta1 and caspase-3.	Thiamine	59-67	caspase 3	Mus musculus	165-174
16850348-6	2006	Using global and gene-specific expression analysis, we show that Pdc2 is required for the upregulation of all genes controlled by thiamine availability.	Thiamine	130-138	Pdc2p	Saccharomyces cerevisiae S288C	65-69
16867079-1	2006	The objective of this study was to investigate the relationship between the thiamine concentration and the fermentation patterns [pH, concentration of short-chain fatty acids (SCFA)] in the free liquid (FRL) and particle-associated liquid (PARL) of the rumen in dairy cows fed with graded concentrate levels in the diet.	Thiamine	76-84	presenilin associated rhomboid like	Bos taurus	240-244
16867079-4	2006	The thiamine concentration in PARL was higher (p < or = 0.05) compared to FRL.	Thiamine	4-12	presenilin associated rhomboid like	Bos taurus	30-34
16889681-4	2006	We conclude that (3)H-thiamine uptake by BeWo cells seems to occur through a process distinct from thiamine transporter-1 (hThTr-1) and thiamine transporter-2 (hThTr-2).	Thiamine	22-30	solute carrier family 19 member 3	Homo sapiens	160-167
16850348-9	2006	While the Thi2, in conjunction with Thi3, seems to control expression of THI genes with respect to thiamine availability, the Pdc2 may link the ThDP demand to carbon source availability.	Thiamine	99-107	Thi2p	Saccharomyces cerevisiae S288C	10-14
16850348-9	2006	While the Thi2, in conjunction with Thi3, seems to control expression of THI genes with respect to thiamine availability, the Pdc2 may link the ThDP demand to carbon source availability.	Thiamine	99-107	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	36-40
16563643-6	2006	Thiamine (6 mM), and dihydrolipoic acid (50 microM), required cofactors for pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase (thiamine as thiamine pyrophosphate), attenuated the reactive oxygen species-induced reductions in these enzyme activities, as well as subsequent loss of mitochondrial transmembrane potential and ATP, and neuronal death.	Thiamine	0-8	oxoglutarate dehydrogenase	Rattus norvegicus	103-136
16563643-6	2006	Thiamine (6 mM), and dihydrolipoic acid (50 microM), required cofactors for pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase (thiamine as thiamine pyrophosphate), attenuated the reactive oxygen species-induced reductions in these enzyme activities, as well as subsequent loss of mitochondrial transmembrane potential and ATP, and neuronal death.	Thiamine	138-146	oxoglutarate dehydrogenase	Rattus norvegicus	103-136
16388576-0	2006	Structure of the Escherichia coli ThiS-ThiF complex, a key component of the sulfur transfer system in thiamin biosynthesis.	Thiamine	102-109	thioredoxin interacting protein	Homo sapiens	39-43
16452468-6	2006	Thiamine and benfotiamine reduce aldose reductase mRNA expression, activity, sorbitol concentrations, and intracellular glucose while increasing the expression and activity of transketolase, for which it is a coenzyme, in human endothelial cells and bovine retinal pericytes cultured in high glucose.	Thiamine	0-8	aldo-keto reductase family 1 member B	Homo sapiens	33-49
16452468-6	2006	Thiamine and benfotiamine reduce aldose reductase mRNA expression, activity, sorbitol concentrations, and intracellular glucose while increasing the expression and activity of transketolase, for which it is a coenzyme, in human endothelial cells and bovine retinal pericytes cultured in high glucose.	Thiamine	0-8	transketolase	Homo sapiens	176-189
16171982-1	2006	The Thi4 protein from Saccharomyces cerevisiae plays a pivotal role in the biosynthesis of thiazole, a precursor of thiamine (vitamin B1).	Thiamine	116-124	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	4-8
16171982-1	2006	The Thi4 protein from Saccharomyces cerevisiae plays a pivotal role in the biosynthesis of thiazole, a precursor of thiamine (vitamin B1).	Thiamine	126-136	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	4-8
16206251-2	2006	Mammals obtain thiamin through intestinal absorption, while in the kidney thiamin is reabsorbed to prevent its loss in the urine, both processes are specialized, carrier-mediated and involve thiamin transporters-1 and 2 (THTR-1 and THTR-2, respectively; products of the SLC19A2 and SLC19A3 genes).	Thiamine	15-22	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	221-227
16206251-2	2006	Mammals obtain thiamin through intestinal absorption, while in the kidney thiamin is reabsorbed to prevent its loss in the urine, both processes are specialized, carrier-mediated and involve thiamin transporters-1 and 2 (THTR-1 and THTR-2, respectively; products of the SLC19A2 and SLC19A3 genes).	Thiamine	74-81	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	221-227
16206251-6	2006	Carrier-mediated thiamin uptake by jejunal and renal brush border membrane vesicles (BBMV) both decreased with maturation (suckling>weanling>adult) and were associated with a reduction in mTHTR-1 and mTHTR-2 protein, mRNA levels, and the activity of human SLC19A2 and SLC19A3 promoter-reporter constructs in the intestines and kidneys of transgenic mice.	Thiamine	17-24	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	194-201
16206251-6	2006	Carrier-mediated thiamin uptake by jejunal and renal brush border membrane vesicles (BBMV) both decreased with maturation (suckling>weanling>adult) and were associated with a reduction in mTHTR-1 and mTHTR-2 protein, mRNA levels, and the activity of human SLC19A2 and SLC19A3 promoter-reporter constructs in the intestines and kidneys of transgenic mice.	Thiamine	17-24	solute carrier family 19, member 3	Mus musculus	206-213
16206251-6	2006	Carrier-mediated thiamin uptake by jejunal and renal brush border membrane vesicles (BBMV) both decreased with maturation (suckling>weanling>adult) and were associated with a reduction in mTHTR-1 and mTHTR-2 protein, mRNA levels, and the activity of human SLC19A2 and SLC19A3 promoter-reporter constructs in the intestines and kidneys of transgenic mice.	Thiamine	17-24	solute carrier family 19 member 2	Homo sapiens	262-269
16206251-6	2006	Carrier-mediated thiamin uptake by jejunal and renal brush border membrane vesicles (BBMV) both decreased with maturation (suckling>weanling>adult) and were associated with a reduction in mTHTR-1 and mTHTR-2 protein, mRNA levels, and the activity of human SLC19A2 and SLC19A3 promoter-reporter constructs in the intestines and kidneys of transgenic mice.	Thiamine	17-24	solute carrier family 19 member 3	Homo sapiens	274-281
16206251-7	2006	These results are the first to demonstrate that intestinal and renal thiamin uptake are developmentally regulated during early stages of life, mediated through mTHTR-1 and mTHTR-2, and suggest the possible involvement of transcriptional regulatory mechanism(s) in this regulation.	Thiamine	69-76	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	160-167
16206251-7	2006	These results are the first to demonstrate that intestinal and renal thiamin uptake are developmentally regulated during early stages of life, mediated through mTHTR-1 and mTHTR-2, and suggest the possible involvement of transcriptional regulatory mechanism(s) in this regulation.	Thiamine	69-76	solute carrier family 19, member 3	Mus musculus	172-179
16388576-2	2006	ThiS and ThiF are bacterial proteins involved in the synthesis of the thiazole moiety of thiamin.	Thiamine	89-96	thioredoxin interacting protein	Homo sapiens	9-13
16194233-3	2005	We found in a DNA microarray analysis that the expression of THI genes increased 10- to 90-fold in response to thiamin deprivation, and likewise, the expression of THI2 and THI3 increased 17-fold and threefold, respectively.	Thiamine	111-118	Thi2p	Saccharomyces cerevisiae S288C	164-168
16373304-1	2006	AIM: Thiamine-responsive megaloblastic anaemia syndrome (TRMA) is the association of diabetes mellitus, anaemia and deafness, due to mutations in SLC19A2, encoding a thiamine transporter protein.	Thiamine	5-13	solute carrier family 19 member 2	Homo sapiens	146-153
16373304-9	2006	CONCLUSION: Diabetes in this syndrome is due to an insulin insufficiency that initially responds to thiamine supplements; however, most patients become fully insulin dependent after puberty.	Thiamine	100-108	insulin	Homo sapiens	51-58
16214141-2	2005	We have demonstrated that reduced dietary thiamin in F344 rats decreased transketolase activity and increased alpha-oxoaldehyde adduct levels.	Thiamine	42-49	transketolase	Rattus norvegicus	73-86
16194233-3	2005	We found in a DNA microarray analysis that the expression of THI genes increased 10- to 90-fold in response to thiamin deprivation, and likewise, the expression of THI2 and THI3 increased 17-fold and threefold, respectively.	Thiamine	111-118	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	173-177
16194233-7	2005	When mutant Thi3p proteins lacking TDP-binding activity were produced in the thi3Delta strain, THI genes were expressed even under thiamin-replete conditions.	Thiamine	131-138	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	12-17
16194233-9	2005	Furthermore, Thi2p and Thi3p were demonstrated to bind each other and this interaction was partially diminished by exogenous thiamin, suggesting that Thi2p and Thi3p stimulate the expression as a complex whose function is disturbed by TDP bound to Thi3p.	Thiamine	125-132	Thi2p	Saccharomyces cerevisiae S288C	13-18
16194233-9	2005	Furthermore, Thi2p and Thi3p were demonstrated to bind each other and this interaction was partially diminished by exogenous thiamin, suggesting that Thi2p and Thi3p stimulate the expression as a complex whose function is disturbed by TDP bound to Thi3p.	Thiamine	125-132	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	23-28
16194233-9	2005	Furthermore, Thi2p and Thi3p were demonstrated to bind each other and this interaction was partially diminished by exogenous thiamin, suggesting that Thi2p and Thi3p stimulate the expression as a complex whose function is disturbed by TDP bound to Thi3p.	Thiamine	125-132	Thi2p	Saccharomyces cerevisiae S288C	150-155
16194233-9	2005	Furthermore, Thi2p and Thi3p were demonstrated to bind each other and this interaction was partially diminished by exogenous thiamin, suggesting that Thi2p and Thi3p stimulate the expression as a complex whose function is disturbed by TDP bound to Thi3p.	Thiamine	125-132	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	160-165
16194233-9	2005	Furthermore, Thi2p and Thi3p were demonstrated to bind each other and this interaction was partially diminished by exogenous thiamin, suggesting that Thi2p and Thi3p stimulate the expression as a complex whose function is disturbed by TDP bound to Thi3p.	Thiamine	125-132	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	160-165
18220605-4	2005	The expression and activity of the thiamine-dependent enzyme, transketolase--the pacemaking enzyme of the reductive pentosephosphate pathway, is consequently decreased.	Thiamine	35-43	transketolase	Homo sapiens	62-75
15967475-0	2005	Thi20, a remarkable enzyme from Saccharomyces cerevisiae with dual thiamin biosynthetic and degradation activities.	Thiamine	67-74	trifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase/thiaminase	Saccharomyces cerevisiae S288C	0-5
15967475-4	2005	This demonstrates that Thi20 is a trifunctional protein with thiamin biosynthetic and degradative activity.	Thiamine	61-68	trifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase/thiaminase	Saccharomyces cerevisiae S288C	23-28
16055442-8	2005	The physiological relevance of in vitro findings with Caco-2 cells was confirmed in wild-type and transgenic mice by demonstrating that thiamin uptake and mRNA levels of the mouse THTR-1 and THTR-2, as well as activity of human SLC19A2 and SLC19A3 promoters expressed in transgenic mice, were all significantly higher in intestinal villus compared with crypt epithelial cells.	Thiamine	136-143	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	180-186
16055442-8	2005	The physiological relevance of in vitro findings with Caco-2 cells was confirmed in wild-type and transgenic mice by demonstrating that thiamin uptake and mRNA levels of the mouse THTR-1 and THTR-2, as well as activity of human SLC19A2 and SLC19A3 promoters expressed in transgenic mice, were all significantly higher in intestinal villus compared with crypt epithelial cells.	Thiamine	136-143	solute carrier family 19, member 3	Mus musculus	191-197
16055442-8	2005	The physiological relevance of in vitro findings with Caco-2 cells was confirmed in wild-type and transgenic mice by demonstrating that thiamin uptake and mRNA levels of the mouse THTR-1 and THTR-2, as well as activity of human SLC19A2 and SLC19A3 promoters expressed in transgenic mice, were all significantly higher in intestinal villus compared with crypt epithelial cells.	Thiamine	136-143	solute carrier family 19 member 2	Homo sapiens	228-235
16055442-8	2005	The physiological relevance of in vitro findings with Caco-2 cells was confirmed in wild-type and transgenic mice by demonstrating that thiamin uptake and mRNA levels of the mouse THTR-1 and THTR-2, as well as activity of human SLC19A2 and SLC19A3 promoters expressed in transgenic mice, were all significantly higher in intestinal villus compared with crypt epithelial cells.	Thiamine	136-143	solute carrier family 19 member 3	Homo sapiens	240-247
16055442-9	2005	These studies demonstrate for the first time that differentiation of intestinal epithelial cells is associated with an up-regulation in thiamin uptake process and that this up-regulation appears to be mediated via transcriptional regulatory mechanisms that involve the SLC19A2 and SLC19A3 genes.	Thiamine	136-143	solute carrier family 19 member 2	Homo sapiens	269-276
16055442-9	2005	These studies demonstrate for the first time that differentiation of intestinal epithelial cells is associated with an up-regulation in thiamin uptake process and that this up-regulation appears to be mediated via transcriptional regulatory mechanisms that involve the SLC19A2 and SLC19A3 genes.	Thiamine	136-143	solute carrier family 19 member 3	Homo sapiens	281-288
15922063-6	2005	The biochemical data revealed that chronic ethanol treatment reduced acetylcholinesterase (AChE) activity in the hippocampus while leaving the neocortex unchanged, whereas thiamine deficiency reduced both cortical and hippocampal AChE activity.	Thiamine	172-180	acetylcholinesterase	Rattus norvegicus	230-234
15871139-6	2005	In this segment, each family displayed one of two different missense mutations that altered the coding sequence of SLC19A3, the gene for a transporter related to the reduced-folate (encoded by SLC19A1) and thiamin (encoded by SLC19A2) transporters.	Thiamine	206-213	solute carrier family 19 member 3	Homo sapiens	115-122
15871139-6	2005	In this segment, each family displayed one of two different missense mutations that altered the coding sequence of SLC19A3, the gene for a transporter related to the reduced-folate (encoded by SLC19A1) and thiamin (encoded by SLC19A2) transporters.	Thiamine	206-213	solute carrier family 19 member 2	Homo sapiens	226-233
15705657-0	2005	Adaptive regulation of intestinal thiamin uptake: molecular mechanism using wild-type and transgenic mice carrying hTHTR-1 and -2 promoters.	Thiamine	34-41	solute carrier family 19 member 2	Homo sapiens	115-129
15980201-9	2005	Treatment of Arabidopsis ecotype Columbia-0 plants with thiamine resulted in the activation of PR-1 but not PDF1.2.	Thiamine	56-64	pathogenesis-related protein 1	Arabidopsis thaliana	95-99
15980201-9	2005	Treatment of Arabidopsis ecotype Columbia-0 plants with thiamine resulted in the activation of PR-1 but not PDF1.2.	Thiamine	56-64	plant defensin 1.2	Arabidopsis thaliana	108-114
15897230-1	2005	The Arabidopsis thaliana THI1 protein is involved in thiamine biosynthesis and is targeted to both chloroplasts and mitochondria by N-terminal control regions.	Thiamine	53-61	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	25-29
15705657-2	2005	The molecular mechanism of the human intestinal thiamin absorption process involves the thiamin transporters-1 (hTHTR-1) and -2 (hTHTR-2), products of the SLC19A2 and SLC19A3 genes.	Thiamine	48-55	solute carrier family 19 member 3	Homo sapiens	129-136
15705657-2	2005	The molecular mechanism of the human intestinal thiamin absorption process involves the thiamin transporters-1 (hTHTR-1) and -2 (hTHTR-2), products of the SLC19A2 and SLC19A3 genes.	Thiamine	48-55	solute carrier family 19 member 2	Homo sapiens	155-162
15705657-2	2005	The molecular mechanism of the human intestinal thiamin absorption process involves the thiamin transporters-1 (hTHTR-1) and -2 (hTHTR-2), products of the SLC19A2 and SLC19A3 genes.	Thiamine	48-55	solute carrier family 19 member 3	Homo sapiens	167-174
15705657-5	2005	We show that, in thiamin deficiency, a significant and specific upregulation in intestinal carrier-mediated thiamin uptake occurs and that this increase is associated with an induction in protein and mRNA levels of mTHTR-2 but not mTHTR-1; in addition, an increase in the activity of the SLC19A3, but not the SLC19A2, promoter was observed in the intestine of transgenic mice.	Thiamine	17-24	solute carrier family 19, member 3	Mus musculus	215-222
15705657-5	2005	We show that, in thiamin deficiency, a significant and specific upregulation in intestinal carrier-mediated thiamin uptake occurs and that this increase is associated with an induction in protein and mRNA levels of mTHTR-2 but not mTHTR-1; in addition, an increase in the activity of the SLC19A3, but not the SLC19A2, promoter was observed in the intestine of transgenic mice.	Thiamine	17-24	solute carrier family 19, member 3	Mus musculus	288-295
15705657-5	2005	We show that, in thiamin deficiency, a significant and specific upregulation in intestinal carrier-mediated thiamin uptake occurs and that this increase is associated with an induction in protein and mRNA levels of mTHTR-2 but not mTHTR-1; in addition, an increase in the activity of the SLC19A3, but not the SLC19A2, promoter was observed in the intestine of transgenic mice.	Thiamine	17-24	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	309-316
15705657-5	2005	We show that, in thiamin deficiency, a significant and specific upregulation in intestinal carrier-mediated thiamin uptake occurs and that this increase is associated with an induction in protein and mRNA levels of mTHTR-2 but not mTHTR-1; in addition, an increase in the activity of the SLC19A3, but not the SLC19A2, promoter was observed in the intestine of transgenic mice.	Thiamine	108-115	solute carrier family 19, member 3	Mus musculus	288-295
15705657-5	2005	We show that, in thiamin deficiency, a significant and specific upregulation in intestinal carrier-mediated thiamin uptake occurs and that this increase is associated with an induction in protein and mRNA levels of mTHTR-2 but not mTHTR-1; in addition, an increase in the activity of the SLC19A3, but not the SLC19A2, promoter was observed in the intestine of transgenic mice.	Thiamine	108-115	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	309-316
15705657-7	2005	We also examined the effect of thiamin deficiency on the level of expression of mTHTR-1 and mTHTR-2 messages and activity of the human promoters in the heart and brain of transgenic mice and found an increase in mTHTR-1 mRNA and a rise in activity of the SLC19A2 promoter in thiamin-deficient mice.	Thiamine	31-38	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	80-87
15705657-7	2005	We also examined the effect of thiamin deficiency on the level of expression of mTHTR-1 and mTHTR-2 messages and activity of the human promoters in the heart and brain of transgenic mice and found an increase in mTHTR-1 mRNA and a rise in activity of the SLC19A2 promoter in thiamin-deficient mice.	Thiamine	31-38	solute carrier family 19, member 3	Mus musculus	92-99
15705657-7	2005	We also examined the effect of thiamin deficiency on the level of expression of mTHTR-1 and mTHTR-2 messages and activity of the human promoters in the heart and brain of transgenic mice and found an increase in mTHTR-1 mRNA and a rise in activity of the SLC19A2 promoter in thiamin-deficient mice.	Thiamine	31-38	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	212-219
15705657-7	2005	We also examined the effect of thiamin deficiency on the level of expression of mTHTR-1 and mTHTR-2 messages and activity of the human promoters in the heart and brain of transgenic mice and found an increase in mTHTR-1 mRNA and a rise in activity of the SLC19A2 promoter in thiamin-deficient mice.	Thiamine	31-38	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	255-262
15705657-8	2005	These results show that the intestinal and renal thiamin uptake processes are adaptively upregulated during dietary thiamin deficiency, that expression of mTHTR-1 and mTHTR-2 is regulated in a tissue-specific manner, and that this upregulation is mediated via transcriptional regulatory mechanism(s).	Thiamine	49-56	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	155-162
15705657-8	2005	These results show that the intestinal and renal thiamin uptake processes are adaptively upregulated during dietary thiamin deficiency, that expression of mTHTR-1 and mTHTR-2 is regulated in a tissue-specific manner, and that this upregulation is mediated via transcriptional regulatory mechanism(s).	Thiamine	49-56	solute carrier family 19, member 3	Mus musculus	167-174
15933030-4	2005	Transcript level analysis revealed that among the five thiamine-pyrophospate-dependent decarboxylases (PDC1, PDC5, PDC6, ARO10, and THI3), only ARO10 was transcriptionally up-regulated when phenylalanine, leucine, or methionine was used as a nitrogen source compared to growth on ammonia, proline, and asparagine.	Thiamine	55-63	indolepyruvate decarboxylase 1	Saccharomyces cerevisiae S288C	103-107
15720653-3	2005	Fission yeast was transformed with plasmids pREP1 and pREP81 with the Arath;CDC25 gene under the control of the thiamine-repressible nmt promoter.	Thiamine	112-120	Rhodanese/Cell cycle control phosphatase superfamily protein	Arabidopsis thaliana	70-81
15933030-4	2005	Transcript level analysis revealed that among the five thiamine-pyrophospate-dependent decarboxylases (PDC1, PDC5, PDC6, ARO10, and THI3), only ARO10 was transcriptionally up-regulated when phenylalanine, leucine, or methionine was used as a nitrogen source compared to growth on ammonia, proline, and asparagine.	Thiamine	55-63	indolepyruvate decarboxylase 5	Saccharomyces cerevisiae S288C	109-113
15933030-4	2005	Transcript level analysis revealed that among the five thiamine-pyrophospate-dependent decarboxylases (PDC1, PDC5, PDC6, ARO10, and THI3), only ARO10 was transcriptionally up-regulated when phenylalanine, leucine, or methionine was used as a nitrogen source compared to growth on ammonia, proline, and asparagine.	Thiamine	55-63	indolepyruvate decarboxylase 6	Saccharomyces cerevisiae S288C	115-119
15933030-4	2005	Transcript level analysis revealed that among the five thiamine-pyrophospate-dependent decarboxylases (PDC1, PDC5, PDC6, ARO10, and THI3), only ARO10 was transcriptionally up-regulated when phenylalanine, leucine, or methionine was used as a nitrogen source compared to growth on ammonia, proline, and asparagine.	Thiamine	55-63	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	132-136
15933030-4	2005	Transcript level analysis revealed that among the five thiamine-pyrophospate-dependent decarboxylases (PDC1, PDC5, PDC6, ARO10, and THI3), only ARO10 was transcriptionally up-regulated when phenylalanine, leucine, or methionine was used as a nitrogen source compared to growth on ammonia, proline, and asparagine.	Thiamine	55-63	phenylpyruvate decarboxylase ARO10	Saccharomyces cerevisiae S288C	144-149
15802905-6	2005	CONCLUSION: Our adult case of hypophosphatasia presented with an absence of intestinal ALP isoenzyme that might result in decreasing the absorption of thiamine in the intestinal tract.	Thiamine	151-159	alkaline phosphatase, placental	Homo sapiens	87-90
16037305-5	2005	We found hydroimidazolone AGE residues derived from glyoxal and methylglyoxal, G-H1 and MG-H1, were increased 115% and 68% in STZ diabetic rats, with respect to normal controls, and were normalized by both thiamine and benfotiamine; whereas N-carboxymethyl-lysine (CML) and N-carboxyethyl-lysine (CEL) residues were increased 74% and 118% in STZ diabetic rats and were normalized by thiamine only.	Thiamine	206-214	growth hormone 1	Rattus norvegicus	79-93
16037305-5	2005	We found hydroimidazolone AGE residues derived from glyoxal and methylglyoxal, G-H1 and MG-H1, were increased 115% and 68% in STZ diabetic rats, with respect to normal controls, and were normalized by both thiamine and benfotiamine; whereas N-carboxymethyl-lysine (CML) and N-carboxyethyl-lysine (CEL) residues were increased 74% and 118% in STZ diabetic rats and were normalized by thiamine only.	Thiamine	383-391	growth hormone 1	Rattus norvegicus	79-93
15614489-1	2005	Two redundant genes, THI20 and THI21, of Saccharomyces cerevisiae encode a 2-methyl-4-amino-5-hydroxymethylpyrimidine monophosphate (HMP-P) kinase required for thiamin biosynthesis.	Thiamine	160-167	trifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase/thiaminase	Saccharomyces cerevisiae S288C	21-26
15614489-1	2005	Two redundant genes, THI20 and THI21, of Saccharomyces cerevisiae encode a 2-methyl-4-amino-5-hydroxymethylpyrimidine monophosphate (HMP-P) kinase required for thiamin biosynthesis.	Thiamine	160-167	bifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase	Saccharomyces cerevisiae S288C	31-36
15614489-4	2005	The thi20 deletion strain grows at the same rate as the parental strain in minimal medium without thiamin, but its ability to synthesize HMP-PP from HMP is significantly decreased.	Thiamine	98-105	trifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase/thiaminase	Saccharomyces cerevisiae S288C	4-9
15715485-3	2005	All compounds of this library were good substrates for recombinant human thymidine kinase 1 (TK1) with phosphorylation rates up to 89% relative to that of Thd.	Thiamine	155-158	thymidine kinase 1	Homo sapiens	73-91
15715485-3	2005	All compounds of this library were good substrates for recombinant human thymidine kinase 1 (TK1) with phosphorylation rates up to 89% relative to that of Thd.	Thiamine	155-158	thymidine kinase 1	Homo sapiens	93-96
15991799-4	2005	In diabetes mellitus patients reduced transketolase enzyme activities have been detected and the lipid-soluble thiamine derivative benfotiamine activates transketolase enzyme reactions, thereby blocking three major pathways of hyperglycemic damage and preventing diabetic retinopathy.	Thiamine	111-119	transketolase	Homo sapiens	154-167
15663478-4	2005	Recently, myeloperoxidase has been identified in the activated microglia of brains from AD patients and thiamine-deficient animals.	Thiamine	104-112	myeloperoxidase	Homo sapiens	10-25
15668660-6	2005	Bivariate analysis showed a significant inverse association between CRP and many nutrients (e.g., carbohydrates, proteins, lipids, thiamine, pyridoxine, tocopherol, and folate), but multiple-regression analysis indicated that only the effect of dietary folate intake was not dependent on other factors.	Thiamine	131-139	C-reactive protein	Homo sapiens	68-71
15337301-5	2004	Non-thiamine-dependent enzymes such as succinate dehydrogenase (SDH), succinate thiokinase (STH) and malate dehydrogenase (MDH) were altered as much or more than thiamine-dependent enzymes such as the alpha-ketoglutarate dehydrogenase complex (KGDHC) (-21.5%) and PDHC (-10.5%).	Thiamine	4-12	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	39-62
15664409-4	2005	As thiamine metabolism deficiencies have been seen in placental infarcts previously, these indicate that PP20/hTPK may have a role in placental diseases.	Thiamine	3-11	thiamin pyrophosphokinase 1	Homo sapiens	105-109
15544818-0	2004	Neurospora crassa CyPBP37: a cytosolic stress protein that is able to replace yeast Thi4p function in the synthesis of vitamin B1.	Thiamine	119-129	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	84-89
15544818-4	2004	Saccharomyces cerevisiae mutants lacking Thi4p (the CyPBP37 ortholog) are auxotrophic for vitamin B1 (thiamine) but can grow in the presence of the thiazole moiety of thiamine, suggesting a role for Thi4p in the biosynthesis of thiazole.	Thiamine	90-100	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	41-46
15544818-4	2004	Saccharomyces cerevisiae mutants lacking Thi4p (the CyPBP37 ortholog) are auxotrophic for vitamin B1 (thiamine) but can grow in the presence of the thiazole moiety of thiamine, suggesting a role for Thi4p in the biosynthesis of thiazole.	Thiamine	102-110	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	41-46
15544818-4	2004	Saccharomyces cerevisiae mutants lacking Thi4p (the CyPBP37 ortholog) are auxotrophic for vitamin B1 (thiamine) but can grow in the presence of the thiazole moiety of thiamine, suggesting a role for Thi4p in the biosynthesis of thiazole.	Thiamine	167-175	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	41-46
15544818-8	2004	The expression of CyPBP37 and Thi4p is repressed by thiamine but not by thiazole in the growth medium.	Thiamine	52-60	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	30-35
15337301-5	2004	Non-thiamine-dependent enzymes such as succinate dehydrogenase (SDH), succinate thiokinase (STH) and malate dehydrogenase (MDH) were altered as much or more than thiamine-dependent enzymes such as the alpha-ketoglutarate dehydrogenase complex (KGDHC) (-21.5%) and PDHC (-10.5%).	Thiamine	4-12	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	64-67
15337301-5	2004	Non-thiamine-dependent enzymes such as succinate dehydrogenase (SDH), succinate thiokinase (STH) and malate dehydrogenase (MDH) were altered as much or more than thiamine-dependent enzymes such as the alpha-ketoglutarate dehydrogenase complex (KGDHC) (-21.5%) and PDHC (-10.5%).	Thiamine	4-12	malic enzyme 1	Homo sapiens	101-121
15337301-5	2004	Non-thiamine-dependent enzymes such as succinate dehydrogenase (SDH), succinate thiokinase (STH) and malate dehydrogenase (MDH) were altered as much or more than thiamine-dependent enzymes such as the alpha-ketoglutarate dehydrogenase complex (KGDHC) (-21.5%) and PDHC (-10.5%).	Thiamine	162-170	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	64-67
15337301-5	2004	Non-thiamine-dependent enzymes such as succinate dehydrogenase (SDH), succinate thiokinase (STH) and malate dehydrogenase (MDH) were altered as much or more than thiamine-dependent enzymes such as the alpha-ketoglutarate dehydrogenase complex (KGDHC) (-21.5%) and PDHC (-10.5%).	Thiamine	162-170	malic enzyme 1	Homo sapiens	101-121
15528987-2	2004	We show here that thiamine has a cytoprotective effect on cultured neonatal rat cardiomyocytes under hypoxic insult, and also protects the cardiomyocytes against hypoxia-induced apoptosis; caspase-3 activation, PARP cleavage and DNA fragmentation are all inhibited.	Thiamine	18-26	caspase 3	Rattus norvegicus	189-198
15656374-0	2004	[The expression of p53, MDM2 and Ref1 gene in cultured retina neurons of SD rats treated with vitamin B1 and/or elevated pressure].	Thiamine	94-104	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	19-22
15656374-0	2004	[The expression of p53, MDM2 and Ref1 gene in cultured retina neurons of SD rats treated with vitamin B1 and/or elevated pressure].	Thiamine	94-104	apurinic/apyrimidinic endodeoxyribonuclease 1	Rattus norvegicus	33-37
15656374-1	2004	PURPOSE: To investigate the expression of p53, MDM2 and Ref1 gene in cultured retina neurons of SD rats treated with Vitamin B1 and (or) elevated pressure.	Thiamine	117-127	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	42-45
15656374-1	2004	PURPOSE: To investigate the expression of p53, MDM2 and Ref1 gene in cultured retina neurons of SD rats treated with Vitamin B1 and (or) elevated pressure.	Thiamine	117-127	apurinic/apyrimidinic endodeoxyribonuclease 1	Rattus norvegicus	56-60
15337749-3	2004	Previous studies showed that deletion of the majority of the central loop domain between TMDs 6 and 7 abolished transport, but this segment could be replaced with mostly non-homologous sequence from the SLC19A2 thiamine transporter to restore transport function.	Thiamine	211-219	solute carrier family 19 member 2	Homo sapiens	203-210
15528987-4	2004	These results suggest that the cytoprotective effect of thiamine in cardiomyocytes under hypoxic stress is due to its ability to induce Hsp70.	Thiamine	56-64	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	136-141
15328374-1	2004	In previous studies, we have shown that RNA levels of the thiamine transporter THTR2 were down-regulated in breast cancer tumors in comparison with normal tissues and that THTR2-mediated increases in thiamine uptake activity contributed to increased apoptosis after exposure to ionizing radiation.	Thiamine	58-66	solute carrier family 19 member 3	Homo sapiens	79-84
15514058-4	2004	We have identified a partial loss-of-function mutation in the Caenorhabditis elegans gene (tpk-1) that encodes thiamine pyrophosphokinase, which forms TPP from thiamine at the expense of ATP inside cells.	Thiamine	111-119	thiamine pyrophosphokinase 1	Caenorhabditis elegans	91-96
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	Thiamine	179-187	tumor protein p53	Homo sapiens	61-64
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	Thiamine	189-201	tumor protein p53	Homo sapiens	61-64
15509798-10	2004	Niacinamide and thiamine affect two p53-regulated cellular responses to ionizing radiation: rereplication and apoptosis.	Thiamine	16-24	tumor protein p53	Homo sapiens	36-39
15509798-11	2004	Thus, niacinamide and thiamine form a novel basis for the development of small molecules that affect p53 function in vivo, and these results suggest that changes in cellular energy metabolism may regulate p53.	Thiamine	22-30	tumor protein p53	Homo sapiens	101-104
15288424-0	2004	Primary cultures of rat astrocytes respond to thiamine deficiency-induced swelling by downregulating aquaporin-4 levels.	Thiamine	46-54	aquaporin 4	Rattus norvegicus	101-112
15328374-5	2004	To determine the role of exogenous thiamine in the expression of these genes, we analyzed THTR2-transfected breast cancer cells grown in thiamine-depleted medium by quantitative reverse transcription-PCR and showed that three of these five genes showed evidence of regulation by exogenous thiamine in a manner concordant with the effects of THTR2 overexpression.	Thiamine	137-145	solute carrier family 19 member 3	Homo sapiens	90-95
15328374-6	2004	One of the genes up-regulated by THTR2 transfection was down-regulated by thiamine depletion (CYP4B1), and two genes with decreased expression in THTR2-transfected breast cancer cells were up-regulated by thiamine depletion (TFF1 and RGDI).	Thiamine	74-82	solute carrier family 19 member 3	Homo sapiens	33-38
15328374-1	2004	In previous studies, we have shown that RNA levels of the thiamine transporter THTR2 were down-regulated in breast cancer tumors in comparison with normal tissues and that THTR2-mediated increases in thiamine uptake activity contributed to increased apoptosis after exposure to ionizing radiation.	Thiamine	58-66	solute carrier family 19 member 3	Homo sapiens	172-177
15328374-6	2004	One of the genes up-regulated by THTR2 transfection was down-regulated by thiamine depletion (CYP4B1), and two genes with decreased expression in THTR2-transfected breast cancer cells were up-regulated by thiamine depletion (TFF1 and RGDI).	Thiamine	74-82	cytochrome P450 family 4 subfamily B member 1	Homo sapiens	94-100
15328374-5	2004	To determine the role of exogenous thiamine in the expression of these genes, we analyzed THTR2-transfected breast cancer cells grown in thiamine-depleted medium by quantitative reverse transcription-PCR and showed that three of these five genes showed evidence of regulation by exogenous thiamine in a manner concordant with the effects of THTR2 overexpression.	Thiamine	35-43	solute carrier family 19 member 3	Homo sapiens	90-95
15328374-6	2004	One of the genes up-regulated by THTR2 transfection was down-regulated by thiamine depletion (CYP4B1), and two genes with decreased expression in THTR2-transfected breast cancer cells were up-regulated by thiamine depletion (TFF1 and RGDI).	Thiamine	74-82	solute carrier family 19 member 3	Homo sapiens	146-151
15328374-5	2004	To determine the role of exogenous thiamine in the expression of these genes, we analyzed THTR2-transfected breast cancer cells grown in thiamine-depleted medium by quantitative reverse transcription-PCR and showed that three of these five genes showed evidence of regulation by exogenous thiamine in a manner concordant with the effects of THTR2 overexpression.	Thiamine	35-43	solute carrier family 19 member 3	Homo sapiens	341-346
15328374-6	2004	One of the genes up-regulated by THTR2 transfection was down-regulated by thiamine depletion (CYP4B1), and two genes with decreased expression in THTR2-transfected breast cancer cells were up-regulated by thiamine depletion (TFF1 and RGDI).	Thiamine	205-213	solute carrier family 19 member 3	Homo sapiens	33-38
15328374-6	2004	One of the genes up-regulated by THTR2 transfection was down-regulated by thiamine depletion (CYP4B1), and two genes with decreased expression in THTR2-transfected breast cancer cells were up-regulated by thiamine depletion (TFF1 and RGDI).	Thiamine	205-213	solute carrier family 19 member 3	Homo sapiens	146-151
15328374-5	2004	To determine the role of exogenous thiamine in the expression of these genes, we analyzed THTR2-transfected breast cancer cells grown in thiamine-depleted medium by quantitative reverse transcription-PCR and showed that three of these five genes showed evidence of regulation by exogenous thiamine in a manner concordant with the effects of THTR2 overexpression.	Thiamine	137-145	solute carrier family 19 member 3	Homo sapiens	90-95
15199756-0	2004	[Thiamine deficiency polyneuropathy after gastrectomy associated with high level of serum vascular endothelial growth factor (VEGF).	Thiamine	1-9	vascular endothelial growth factor A	Homo sapiens	90-124
15328374-6	2004	One of the genes up-regulated by THTR2 transfection was down-regulated by thiamine depletion (CYP4B1), and two genes with decreased expression in THTR2-transfected breast cancer cells were up-regulated by thiamine depletion (TFF1 and RGDI).	Thiamine	205-213	trefoil factor 1	Homo sapiens	225-229
15369988-1	2004	Concentrations of thiamin were determined in pasteurized and UHT-sterilized milks, yoghurt and kefir samples by high-performance liquid chromatography using a reversed-phase C-18 column connected to fluorescence detector.	Thiamine	18-25	Bardet-Biedl syndrome 9	Homo sapiens	174-178
15102695-3	2004	EXPERIMENTAL DESIGN: Potential promiscuous THd from CEA were predicted using available computer algorithms.	Thiamine	43-46	carcinoembryonic antigen gene family	Mus musculus	52-55
14662656-7	2004	The lactic acidosis induced by the NDUFV1 mutations could be partially corrected with the vitamins riboflavin and thiamine or with sodium dichloroacetate, an activator of the pyruvate dehydrogenase complex, resulting in significant increases in animal fitness.	Thiamine	114-122	NADH:ubiquinone oxidoreductase core subunit V1	Homo sapiens	35-41
15230996-5	2004	Thiamin status during this stage of pregnancy was determined by measuring the activation coefficient of erythrocyte transketolase (alpha-ETK).	Thiamine	0-7	BMX non-receptor tyrosine kinase	Homo sapiens	137-140
15230996-9	2004	Subjects with alpha-ETK coefficients >1.25 in the third trimester had significantly lower mature milk thiamin concentration (0.31 (SD 0.10) micromol/l) than did subjects with more satisfactory alpha-ETK levels at this time (0.55 (SD 0.42) micromol/l; P<0.05).	Thiamine	105-112	BMX non-receptor tyrosine kinase	Homo sapiens	20-23
15230996-10	2004	The thiamin status of women can be improved since 25.5% of subjects took less than that recommended and 13.7% showed signs of severe deficiency (alpha-ETK >1.25).	Thiamine	4-11	BMX non-receptor tyrosine kinase	Homo sapiens	151-154
15230996-11	2004	The influence of maternal thiamin intake on alpha-ETK coefficients and on mature breast milk thiamin concentration is confirmed.	Thiamine	26-33	BMX non-receptor tyrosine kinase	Homo sapiens	50-53
15122704-7	2004	Furthermore, liver PDH and KGDH activities were reduced in the Atp7b mouse model of Wilson"s disease prior to liver damage, and were partially restored by oral thiamine supplementation.	Thiamine	160-168	ATPase, Cu++ transporting, beta polypeptide	Mus musculus	63-68
14769791-2	2004	Escherichia coli grown aerobically in LB medium contain no detectable amounts of ThTP, but when they are transferred to M9 minimal medium with a substrate such as glucose or pyruvate, there is a rapid but transient accumulation of relatively high amounts of ThTP (about 20% of total thiamine).	Thiamine	283-291	thiamine triphosphatase	Homo sapiens	258-262
14994241-0	2004	Novel mutation in the SLC19A2 gene in an African-American female with thiamine-responsive megaloblastic anemia syndrome.	Thiamine	70-78	solute carrier family 19 member 2	Homo sapiens	22-29
14994241-11	2004	With oral thiamine therapy, her insulin requirement decreased by 30% over a 20 month period.	Thiamine	10-18	insulin	Homo sapiens	32-39
14615284-0	2004	Expression and functional contribution of hTHTR-2 in thiamin absorption in human intestine.	Thiamine	53-60	solute carrier family 19 member 3	Homo sapiens	42-49
14615284-5	2004	Pretreating Caco-2 cells (which also express the hTHTR-2 at RNA and protein levels) with hTHTR-2 gene-specific small interfering RNA (siRNA) led to a significant (P < 0.01) and specific inhibition (48%) in carrier-mediated thiamin uptake.	Thiamine	226-233	solute carrier family 19 member 3	Homo sapiens	49-56
14615284-5	2004	Pretreating Caco-2 cells (which also express the hTHTR-2 at RNA and protein levels) with hTHTR-2 gene-specific small interfering RNA (siRNA) led to a significant (P < 0.01) and specific inhibition (48%) in carrier-mediated thiamin uptake.	Thiamine	226-233	solute carrier family 19 member 3	Homo sapiens	89-96
14615284-6	2004	Similarly, pretreating Caco-2 cells with siRNA that specifically target hTHTR-1 (which is expressed in Caco-2 cells) also significantly (P < 0.01) and specifically inhibited (by 56%) carrier-mediated thiamin uptake.	Thiamine	203-210	solute carrier family 19 member 2	Homo sapiens	72-79
14615284-7	2004	When Caco-2 cells were pretreated with siRNAs against both hTHTR-2 and hTHTR-1 genes, an almost complete inhibition in carrier-mediated thiamin uptake was observed.	Thiamine	136-143	solute carrier family 19 member 3	Homo sapiens	59-66
14615284-7	2004	When Caco-2 cells were pretreated with siRNAs against both hTHTR-2 and hTHTR-1 genes, an almost complete inhibition in carrier-mediated thiamin uptake was observed.	Thiamine	136-143	solute carrier family 19 member 2	Homo sapiens	71-78
14770311-6	2004	SLC19A2 is expressed ubiquitously and mediates the transport of thiamine, a cation at physiological pH.	Thiamine	64-72	solute carrier family 19 member 2	Homo sapiens	0-7
14770311-7	2004	SLC19A3 is also widely expressed and is capable of transporting thiamine.	Thiamine	64-72	solute carrier family 19 member 3	Homo sapiens	0-7
15199756-0	2004	[Thiamine deficiency polyneuropathy after gastrectomy associated with high level of serum vascular endothelial growth factor (VEGF).	Thiamine	1-9	vascular endothelial growth factor A	Homo sapiens	126-130
15199756-12	2004	Intravenous administration of vitamin B1 (50 mg per day) dramatically improved his symptoms in a few days and the level of VEGF returned to nearly normal.	Thiamine	30-40	vascular endothelial growth factor A	Homo sapiens	123-127
15199756-14	2004	This case suggests that VEGF is involved in the pathogenesis of vitamin B1 deficiency polyneuropathy.	Thiamine	64-74	vascular endothelial growth factor A	Homo sapiens	24-28
13680155-1	2003	The Neurospora crassa homologue of the yeast no message in thiamine ( nmt-1) gene was characterized.	Thiamine	59-67	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	70-75
15359361-6	2004	Using logistic regression analysis, models for predicting the presence of DAT all contained pyridoxal-5-phosphate, and CSF-protein, in combination with either one of variables, age, ascorbic acid, retinol, alpha-tocopherol, homocysteine, thiamin-diphosphate, CSF-thiamin.	Thiamine	238-245	solute carrier family 6 member 3	Homo sapiens	74-77
13680155-4	2003	Unlike other fungi, the N. crassa nmt-1 gene is repressed only 6- to 8-fold by exogenous thiamine concentrations above 0.5 microM; and a high basal level of nmt-1 mRNA persists even at 5 microM thiamine.	Thiamine	89-97	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	34-39
13680155-4	2003	Unlike other fungi, the N. crassa nmt-1 gene is repressed only 6- to 8-fold by exogenous thiamine concentrations above 0.5 microM; and a high basal level of nmt-1 mRNA persists even at 5 microM thiamine.	Thiamine	194-202	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	34-39
13680155-4	2003	Unlike other fungi, the N. crassa nmt-1 gene is repressed only 6- to 8-fold by exogenous thiamine concentrations above 0.5 microM; and a high basal level of nmt-1 mRNA persists even at 5 microM thiamine.	Thiamine	194-202	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	157-162
13680155-7	2003	NMT-1 abundance modulates slowly in response to changes in the concentration of exogenous thiamine, suggesting that N. crassa maintains thiamine reserves in excess of immediate needs.	Thiamine	90-98	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	0-5
13680155-7	2003	NMT-1 abundance modulates slowly in response to changes in the concentration of exogenous thiamine, suggesting that N. crassa maintains thiamine reserves in excess of immediate needs.	Thiamine	136-144	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	0-5
13680155-8	2003	Disruption of the nmt-1 gene demonstrated that it is essential for growth in the absence of exogenous thiamine.	Thiamine	102-110	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	18-23
13680155-9	2003	NMT-1-deficient strains had a growth rate and colony density which was about 70% of the wild type, despite supplementation with a wide range of exogenous thiamine.	Thiamine	154-162	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	0-5
13680155-10	2003	These results suggest that the nmt-1 gene plays some other role in addition to thiamine biosynthesis.	Thiamine	79-87	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	31-36
14568539-0	2003	A novel binding protein for a member of CyP40-type Cyclophilins: N.crassa CyPBP37, a growth and thiamine regulated protein homolog to yeast Thi4p.	Thiamine	96-104	peptidylprolyl isomerase CPR6	Saccharomyces cerevisiae S288C	40-45
14527822-3	2003	The present study investigated a putative modulation of MPP+ intestinal apical uptake and ecto-ALP activity by thiamine (T+) and thiamine pyrophosphate (TPP, a T+ dietary precursor).	Thiamine	111-119	tripartite motif containing 33	Homo sapiens	90-94
14527822-3	2003	The present study investigated a putative modulation of MPP+ intestinal apical uptake and ecto-ALP activity by thiamine (T+) and thiamine pyrophosphate (TPP, a T+ dietary precursor).	Thiamine	111-119	alkaline phosphatase, placental	Homo sapiens	95-98
12893755-4	2003	RNA ribose isolated from TRMA fibroblasts in thiamine-depleted cultures shows a time-dependent decrease in the fraction of ribose derived via transketolase, a thiamine-dependent enzyme in the pentose cycle.	Thiamine	45-53	transketolase	Homo sapiens	142-155
12893755-4	2003	RNA ribose isolated from TRMA fibroblasts in thiamine-depleted cultures shows a time-dependent decrease in the fraction of ribose derived via transketolase, a thiamine-dependent enzyme in the pentose cycle.	Thiamine	159-167	transketolase	Homo sapiens	142-155
12893755-8	2003	We conclude that reduced nucleic acid production through impaired transketolase catalysis is the underlying biochemical disturbance that likely induces cell cycle arrest or apoptosis in bone marrow cells and leads to the TRMA syndrome in patients with defective high-affinity thiamine transport.	Thiamine	276-284	transketolase	Homo sapiens	66-79
14682443-5	2003	RESULTS: Riboflavin and thiamin from food sources, vitamin B12 supplements, and total (food and supplements) folate displayed inverse, dose-responsive associations with high-grade SIL (HSIL).	Thiamine	24-31	STIL centriolar assembly protein	Homo sapiens	180-183
14682443-10	2003	CONCLUSIONS: This investigation provides evidence that thiamin, riboflavin, folate, and vitamin B12 may play a protective role in cervical carcinogenesis.	Thiamine	55-62	NADH:ubiquinone oxidoreductase subunit B3	Homo sapiens	96-99
14622275-6	2003	However, while this mutant THTR1 was targeted to the plasma membrane, it was completely devoid of thiamine transport activity.	Thiamine	98-106	solute carrier family 19 member 2	Homo sapiens	27-32
14568539-0	2003	A novel binding protein for a member of CyP40-type Cyclophilins: N.crassa CyPBP37, a growth and thiamine regulated protein homolog to yeast Thi4p.	Thiamine	96-104	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	140-145
14567833-6	2003	Clinically significant thiamine deficiency in breastfed infants in Lao relates to methods of preparing rice, the food selected by lactating mothers and the family"s socio-economic status.	Thiamine	23-31	interleukin 4 induced 1	Homo sapiens	67-70
12900388-2	2003	Previous studies established that a human thiamin transporter, SLC19A2, plays a role in thiamin uptake in human tissues.	Thiamine	42-49	solute carrier family 19 member 2	Homo sapiens	63-70
14567973-0	2003	Male infertility and thiamine-dependent erythroid hypoplasia in mice lacking thiamine transporter Slc19a2.	Thiamine	21-29	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	98-105
14567973-1	2003	Thiamine-responsive megaloblastic anemia with diabetes and deafness (TRMA) is an autosomal recessive disease caused by mutations in the high-affinity thiamine transporter gene SLC19A2.	Thiamine	0-8	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	69-73
14567973-1	2003	Thiamine-responsive megaloblastic anemia with diabetes and deafness (TRMA) is an autosomal recessive disease caused by mutations in the high-affinity thiamine transporter gene SLC19A2.	Thiamine	0-8	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	176-183
14567973-9	2003	Slc19a2 -/- mice on a pure 129/Sv background develop reticulocytopenia after two weeks on thiamine-depleted chow with a virtual absence of reticulocytes in the peripheral blood (0.12% knockout vs. 2.58% wild type, P=0.0079).	Thiamine	90-98	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	0-7
12923257-4	2003	In analogy to the model of regulation of the riboflavin and thiamin biosynthesis, we suggest Ado-CBL-mediated regulation based on formation of alternative RNA structures including the B12-element.	Thiamine	60-67	Cbl proto-oncogene	Homo sapiens	97-100
14627317-6	2003	Characterization of the metabolic defect of TRMA may shed light on the role of thiamine in common cardiac abnormalities.	Thiamine	79-87	solute carrier family 19 member 2	Homo sapiens	44-48
12838509-0	2003	Thiamine deficiency results in downregulation of the GLAST glutamate transporter in cultured astrocytes.	Thiamine	0-8	solute carrier family 1 member 3	Homo sapiens	53-58
12882930-3	2003	High-dose thiamine and benfotiamine therapy increased transketolase expression in renal glomeruli, increased the conversion of triosephosphates to ribose-5-phosphate, and strongly inhibited the development of microalbuminuria.	Thiamine	10-18	transketolase	Homo sapiens	54-67
12454006-2	2003	The human thiamine transporter hTHTR1 is involved in the cellular accumulation of thiamine (vitamin B1) in many tissues.	Thiamine	10-18	solute carrier family 19 member 2	Homo sapiens	31-37
12861052-5	2003	THTR2-transfected breast cancer cells showed a 2.5-fold increase in specific THTR2 activity and a 3-fold increase in cytotoxicity against a bromoacetyl ester derivative of thiamine.	Thiamine	172-180	solute carrier family 19 member 3	Homo sapiens	0-5
12750353-3	2003	Replacements at positions P-1 and P5 pointing to the TCR in both THd afforded higher levels of IFN-gamma and IL-4 production.	Thiamine	65-68	crystallin gamma F, pseudogene	Homo sapiens	26-36
12750353-3	2003	Replacements at positions P-1 and P5 pointing to the TCR in both THd afforded higher levels of IFN-gamma and IL-4 production.	Thiamine	65-68	interferon gamma	Homo sapiens	95-104
12750353-3	2003	Replacements at positions P-1 and P5 pointing to the TCR in both THd afforded higher levels of IFN-gamma and IL-4 production.	Thiamine	65-68	interleukin 4	Homo sapiens	109-113
12750353-10	2003	Interestingly, IFN-gamma primed by the THd correlated significantly with that induced by the TCd (P < 0.01).	Thiamine	39-42	interferon gamma	Homo sapiens	15-24
12777485-0	2003	The THI5 gene family of Saccharomyces cerevisiae: distribution of homologues among the hemiascomycetes and functional redundancy in the aerobic biosynthesis of thiamin from pyridoxine.	Thiamine	160-167	4-amino-5-hydroxymethyl-2-methylpyrimidine phosphate synthase	Saccharomyces cerevisiae S288C	4-8
12941878-1	2003	A point mutation in the thi1 gene, involved in the synthesis of thiamin, has been identified in a tz-201 mutant line of Arabidopsis thaliana.	Thiamine	64-71	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	24-28
12941878-3	2003	Complementation assays in yeast thi4 mutant confirm that this mutation hinders thiamin synthesis and, thus, is responsible for the tz phenotype.	Thiamine	79-86	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	32-36
12643751-6	2003	Thiamine-coated nanoparticle association with THTR1 and THTR2 cells was significantly greater than that with control breast cancer cells (MTX(R)ZR75 transfected with the empty expression vector pREP4) (p < 0.01; t-test).	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	46-51
12643751-6	2003	Thiamine-coated nanoparticle association with THTR1 and THTR2 cells was significantly greater than that with control breast cancer cells (MTX(R)ZR75 transfected with the empty expression vector pREP4) (p < 0.01; t-test).	Thiamine	0-8	solute carrier family 19 member 3	Homo sapiens	56-61
12454006-2	2003	The human thiamine transporter hTHTR1 is involved in the cellular accumulation of thiamine (vitamin B1) in many tissues.	Thiamine	92-102	solute carrier family 19 member 2	Homo sapiens	31-37
12454006-3	2003	Thiamine deficiency disorders, such as thiamine-responsive megaloblastic anemia (TRMA), which is associated with specific mutations within hTHTR1, likely impairs the functionality and/or intracellular targeting of hTHTR1.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	139-145
12454006-3	2003	Thiamine deficiency disorders, such as thiamine-responsive megaloblastic anemia (TRMA), which is associated with specific mutations within hTHTR1, likely impairs the functionality and/or intracellular targeting of hTHTR1.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	214-220
12454006-3	2003	Thiamine deficiency disorders, such as thiamine-responsive megaloblastic anemia (TRMA), which is associated with specific mutations within hTHTR1, likely impairs the functionality and/or intracellular targeting of hTHTR1.	Thiamine	39-47	solute carrier family 19 member 2	Homo sapiens	139-145
12454006-3	2003	Thiamine deficiency disorders, such as thiamine-responsive megaloblastic anemia (TRMA), which is associated with specific mutations within hTHTR1, likely impairs the functionality and/or intracellular targeting of hTHTR1.	Thiamine	39-47	solute carrier family 19 member 2	Homo sapiens	214-220
12488043-9	2002	In addition, SLC19A2 was found to be the predominant thiamin uptake carrier expressed in these cells and its promoter displays a high level of activity in them.	Thiamine	53-60	solute carrier family 19 member 2	Homo sapiens	13-20
12597176-8	2003	For example, at 250 Hz the BEST has 23 dB higher sensitivity than the B71; the THD is improved from 61% (B71) to 3.3% (BEST) at 40 dB HL (ISO 389-3, 1994).	Thiamine	79-82	CD80 molecule	Homo sapiens	105-108
12454526-7	2002	We conclude that thiamine deficiency was commonly present in the alcoholic patients, and that a subgroup of patients may be predisposed to more severe brain damage as a consequence of abnormalities in the transketolase protein.	Thiamine	17-25	transketolase	Homo sapiens	205-218
15016149-0	2002	TRMA syndrome (thiamine-responsive megaloblastic anemia): a case report and review of the literature.	Thiamine	15-23	solute carrier family 19 member 2	Homo sapiens	0-4
15016149-1	2002	Thiamine-responsive megaloblastic anemia syndrome (TRMA) is an autosomal recessive disorder with features that include megaloblastic anemia, mild thrombocytopenia and leukopenia, sensorineural deafness and diabetes mellitus.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	51-55
12376536-14	2002	Based on analysis of co-occurrence of the thiamin biosynthetic genes in complete genomes, we predict that eubacteria, archaea, and eukaryota have different pathways for the HMP and hydroxyethylthiazole biosynthesis.	Thiamine	42-49	inner membrane mitochondrial protein	Homo sapiens	173-176
12271461-4	2002	We have also found that copies 2 and 3 are activated by the lack of thiamine and that the Snz proteins physically interact with the thiamine biosynthesis Thi5 protein family.	Thiamine	68-76	4-amino-5-hydroxymethyl-2-methylpyrimidine phosphate synthase	Saccharomyces cerevisiae S288C	154-158
12297368-14	2002	Moreover, the study demonstrates that the TK, G6PDH and CYP1A-activities are associated with the thiamine content.	Thiamine	97-105	glucose-6-phosphate 1-dehydrogenase	Salmo salar	46-51
12297368-14	2002	Moreover, the study demonstrates that the TK, G6PDH and CYP1A-activities are associated with the thiamine content.	Thiamine	97-105	cytochrome P450, family 1, subfamily A	Salmo salar	56-61
12393806-4	2002	Erythrocytes from Slc19a2(-/-) mice lacked the high-affinity component of thiamin transport.	Thiamine	74-81	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	18-25
12393806-5	2002	On a thiamin-free diet, Slc19a2(-/-) mice developed diabetes mellitus with reduced insulin secretion and an enhanced response to insulin.	Thiamine	5-12	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	24-31
12393806-7	2002	Auditory-evoked brainstem response thresholds were markedly elevated in Slc19a2(-/-) mice on a thiamin-free diet, but were normal in wild-type mice treated on that diet as well as thiamin-fed Slc19a2(-/-) mice.	Thiamine	95-102	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	72-79
12393806-7	2002	Auditory-evoked brainstem response thresholds were markedly elevated in Slc19a2(-/-) mice on a thiamin-free diet, but were normal in wild-type mice treated on that diet as well as thiamin-fed Slc19a2(-/-) mice.	Thiamine	180-187	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	192-199
12393806-8	2002	Bone marrows from thiamin-deficient Slc19a2(-/-) mice were abnormal, with a megaloblastosis affecting the erythroid, myeloid and megakaryocyte lines.	Thiamine	18-25	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	36-43
12393806-9	2002	Thus, Slc19a2(-/-) mice have provided new insights into the TRMA disease pathogenesis and will provide a tool for studying the role of thiamin homeostasis in diabetes mellitus more broadly.	Thiamine	135-142	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	6-13
12271461-4	2002	We have also found that copies 2 and 3 are activated by the lack of thiamine and that the Snz proteins physically interact with the thiamine biosynthesis Thi5 protein family.	Thiamine	132-140	4-amino-5-hydroxymethyl-2-methylpyrimidine phosphate synthase	Saccharomyces cerevisiae S288C	154-158
12435857-4	2002	The transport activity of the transfected THTR-1 proteins was measured using a [(3) H] thiamine uptake assay.	Thiamine	87-95	solute carrier family 19 member 2	Homo sapiens	42-48
12435857-10	2002	Finally, transfection studies revealed that the mutant G172D THTR-1 failed to transport thiamine.	Thiamine	88-96	solute carrier family 19 member 2	Homo sapiens	61-67
11995411-6	2002	Thiamine deficiency diminishes the mRNA levels of transketolase and pyruvate dehydrogenase.	Thiamine	0-8	transketolase	Rattus norvegicus	50-63
12065289-6	2002	Introducing the clinically relevant mutations (D93H, S143F, G172D) or mutation at the conserved anionic residue (E138A) of SLC19A2 led to a significant (P < 0.01) inhibition of thiamine uptake.	Thiamine	180-188	solute carrier family 19 member 2	Homo sapiens	123-130
11997266-1	2002	Although the reduced folate carrier RFC1 and the thiamine transporters THTR-1 and THTR-2 share approximately 40% of their identity in protein sequence, RFC1 does not transport thiamine and THTR-1 and THTR-2 do not transport folates.	Thiamine	49-57	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	71-77
11997266-1	2002	Although the reduced folate carrier RFC1 and the thiamine transporters THTR-1 and THTR-2 share approximately 40% of their identity in protein sequence, RFC1 does not transport thiamine and THTR-1 and THTR-2 do not transport folates.	Thiamine	49-57	solute carrier family 19, member 3	Mus musculus	82-88
11997266-2	2002	In the present study, we demonstrate that transport of thiamine monophosphate (TMP), an important thiamine metabolite present in plasma and cerebrospinal fluid, is mediated by RFC1 in L1210 murine leukemia cells.	Thiamine	55-63	replication factor C (activator 1) 1	Mus musculus	176-180
11997266-4	2002	At a near-physiological concentration (50 nM), TMP influx mediated by RFC1 in wild-type L1210 cells was approximately 50% of thiamine influx mediated by thiamine transporter(s).	Thiamine	125-133	replication factor C (activator 1) 1	Mus musculus	70-74
11997266-6	2002	These data suggest that RFC1 may be one of the alternative transport routes available for TMP in some tissues when THTR-1 is mutated in the autosomal recessive disorder thiamine-responsive megaloblastic anemia.	Thiamine	169-177	replication factor C (activator 1) 1	Mus musculus	24-28
11997266-6	2002	These data suggest that RFC1 may be one of the alternative transport routes available for TMP in some tissues when THTR-1 is mutated in the autosomal recessive disorder thiamine-responsive megaloblastic anemia.	Thiamine	169-177	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	115-121
11960673-8	2002	Transketolase is dependent on thiamine pyrophosphate as a cofactor, and therefore, the decreased enzyme activity could be the result of an interaction between furazolidone and thiamine metabolism.	Thiamine	30-38	transketolase like 1	Gallus gallus	0-13
11960673-9	2002	Since thiamine residues were not affected by furazolidone and transketolase inhibition in vitro was similar to the inhibition after in ovo exposure, it was concluded that furazolidone interacted with transketolase on the enzymatic level rather than by a depletion of thiamine.	Thiamine	6-14	transketolase like 1	Gallus gallus	200-213
11960673-9	2002	Since thiamine residues were not affected by furazolidone and transketolase inhibition in vitro was similar to the inhibition after in ovo exposure, it was concluded that furazolidone interacted with transketolase on the enzymatic level rather than by a depletion of thiamine.	Thiamine	267-275	transketolase like 1	Gallus gallus	200-213
11997118-14	2002	These findings raise the possibility that SLC19A2 may play a role in the normal intestinal thiamine absorption process.	Thiamine	91-99	solute carrier family 19 member 2	Homo sapiens	42-49
12111441-1	2002	Thiamine is an essential cofactor for several important enzymes involved in brain oxidative metabolism, such as the alpha-ketoglutarate dehydrogenase complex (KGDHC), pyruvate-dehydrogenase complex (PDHC), and transketolase.	Thiamine	0-8	transketolase	Homo sapiens	210-223
11685195-2	2001	This study investigates whether thiamine, an important coenzyme in intracellular glucose metabolism, improves endothelial cell migration and decreases von Willebrand factor secretion under hyperglycemic conditions.	Thiamine	32-40	von Willebrand factor	Bos taurus	151-172
11731220-1	2001	Recently, a new family of facilitative carriers has been cloned consisting of the reduced folate (SLC19A1) and the thiamine (SLC19A2) transporters.	Thiamine	115-123	solute carrier family 19 member 1	Homo sapiens	98-105
11731220-1	2001	Recently, a new family of facilitative carriers has been cloned consisting of the reduced folate (SLC19A1) and the thiamine (SLC19A2) transporters.	Thiamine	115-123	solute carrier family 19 member 2	Homo sapiens	125-132
11731220-5	2001	Uptake of [3H]thiamine, but not of methotrexate nor folic acid, was enhanced in SLC19A3 transfectants relative to vector control.	Thiamine	10-22	solute carrier family 19 member 3	Homo sapiens	80-87
11481326-7	2001	Our findings indicate that p53 may be involved in maintaining thiamine homeostasis through transactivation of THTR-1.	Thiamine	62-70	transformation related protein 53, pseudogene	Mus musculus	27-30
11481326-7	2001	Our findings indicate that p53 may be involved in maintaining thiamine homeostasis through transactivation of THTR-1.	Thiamine	62-70	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	110-116
11488910-3	2001	Thiamine (vitamin B1) is metabolized to thiamine pyrophosphate, the cofactor of transketolase, which is involved in ribose synthesis, necessary for cell replication.	Thiamine	0-8	transketolase	Mus musculus	80-93
11535779-3	2001	The ilv2-thi1 allele encodes a functional AHAS enzyme with an altered dependence for the cofactor TPP resulting in the thiamin auxotrophic phenotype.	Thiamine	119-126	acetolactate synthase catalytic subunit	Saccharomyces cerevisiae S288C	4-8
11535779-3	2001	The ilv2-thi1 allele encodes a functional AHAS enzyme with an altered dependence for the cofactor TPP resulting in the thiamin auxotrophic phenotype.	Thiamine	119-126	acetolactate synthase catalytic subunit	Saccharomyces cerevisiae S288C	9-13
11483659-2	2001	Treatment with pyrithiamine, a central thiamine antagonist, resulted in a 71 and 55% decrease in protein levels of the astrocyte glutamate transporters GLT-1 and GLAST, respectively, by immunoblotting in the medial thalamus of day 14 symptomatic rats at loss of righting reflexes.	Thiamine	19-27	solute carrier family 1 member 2	Rattus norvegicus	152-157
11483659-2	2001	Treatment with pyrithiamine, a central thiamine antagonist, resulted in a 71 and 55% decrease in protein levels of the astrocyte glutamate transporters GLT-1 and GLAST, respectively, by immunoblotting in the medial thalamus of day 14 symptomatic rats at loss of righting reflexes.	Thiamine	19-27	solute carrier family 1 member 3	Rattus norvegicus	162-167
11483659-10	2001	A selective, focal loss of GLT-1 and GLAST transporter proteins provides a rational explanation for the increase in interstitial glutamate levels, and may play a major role in the selective vulnerability of thalamic structures to thiamine deficiency-induced cell death.	Thiamine	230-238	solute carrier family 1 member 2	Rattus norvegicus	27-32
11483659-10	2001	A selective, focal loss of GLT-1 and GLAST transporter proteins provides a rational explanation for the increase in interstitial glutamate levels, and may play a major role in the selective vulnerability of thalamic structures to thiamine deficiency-induced cell death.	Thiamine	230-238	solute carrier family 1 member 3	Rattus norvegicus	37-42
11701192-2	2001	We found that (i) thiamine deficiency induced a significant decrease of the acetylcholinesterase (AChE) activity both in cortex and hippocampus; (ii) chronic ethanol treatment has no effect on cortical AChE activity, but induced a significant decrease of hippocampal enzyme activity; (iii) the reduction in cortical and hippocampal AChE activity induced by chronic ethanol treatment associated with a 1-week thiamine deficiency was also significant and was greater than that induced by ethanol alone.	Thiamine	18-26	acetylcholinesterase	Rattus norvegicus	76-96
11701192-2	2001	We found that (i) thiamine deficiency induced a significant decrease of the acetylcholinesterase (AChE) activity both in cortex and hippocampus; (ii) chronic ethanol treatment has no effect on cortical AChE activity, but induced a significant decrease of hippocampal enzyme activity; (iii) the reduction in cortical and hippocampal AChE activity induced by chronic ethanol treatment associated with a 1-week thiamine deficiency was also significant and was greater than that induced by ethanol alone.	Thiamine	18-26	acetylcholinesterase	Rattus norvegicus	98-102
11701192-2	2001	We found that (i) thiamine deficiency induced a significant decrease of the acetylcholinesterase (AChE) activity both in cortex and hippocampus; (ii) chronic ethanol treatment has no effect on cortical AChE activity, but induced a significant decrease of hippocampal enzyme activity; (iii) the reduction in cortical and hippocampal AChE activity induced by chronic ethanol treatment associated with a 1-week thiamine deficiency was also significant and was greater than that induced by ethanol alone.	Thiamine	408-416	acetylcholinesterase	Rattus norvegicus	98-102
11592824-1	2001	Thiamine-responsive megaloblastic anemia with deafness and diabetes (TRMA) is a rare autosomal recessive disorder of thiamine transport.	Thiamine	0-8	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	69-73
11592824-1	2001	Thiamine-responsive megaloblastic anemia with deafness and diabetes (TRMA) is a rare autosomal recessive disorder of thiamine transport.	Thiamine	117-125	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	69-73
11592824-3	2001	We hypothesize that thiamine transport, mediated by SLC19A2, plays a role in the development and or maintenance of several organ systems, in particular the erythropoietic, auditory, and glucose homeostasis systems.	Thiamine	20-28	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	52-59
11488910-3	2001	Thiamine (vitamin B1) is metabolized to thiamine pyrophosphate, the cofactor of transketolase, which is involved in ribose synthesis, necessary for cell replication.	Thiamine	10-20	transketolase	Mus musculus	80-93
11488910-7	2001	This high control coefficient allows us to predict that in advanced tumours, which are commonly thiamine deficient, supplementation of thiamine could significantly increase tumour growth through transketolase activation.	Thiamine	135-143	transketolase	Mus musculus	195-208
11575719-1	2001	thi1 has been recently isolated from Arabidopsis thaliana and is probably involved in both thiamine biosynthesis and as protection of organellar DNA from damage.	Thiamine	91-99	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	0-4
11575719-2	2001	Studies of thiamine biosynthesis in plants suggests a plastid location for the pathway, which is in agreement with the predicted THI1 N-terminal chloroplastic transit peptide (TP).	Thiamine	11-19	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	129-133
11172768-5	2001	Immunohistochemical detection of Fos proteins was used as a marker to identify neuronal populations in the thiamin-deficient rat brain affected by glucose loading.	Thiamine	107-114	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	33-36
11408266-6	2001	Our results with human-derived colonic epithelial NCM460 cells as a model system showed thiamine uptake to be 1) temperature- and energy dependent, 2) Na(+) independent, 3) increased with increasing buffer pH from 5 to 8 and after cell acidification but inhibited by amiloride, 4) saturable as a function of concentration, 5) inhibited by thiamine structural analogs but not by unrelated organic cations, and 6) inhibited by modulators of a Ca(2+)/calmodulin-mediated pathway.	Thiamine	88-96	calmodulin 1	Homo sapiens	448-458
11408266-8	2001	These results demonstrate for the first time that human NCM460 colonocytes possess a specific carrier-mediated system for thiamine uptake that appears to be under the regulation of an intracellular Ca(2+)/calmodulin-mediated pathway.	Thiamine	122-130	calmodulin 1	Homo sapiens	205-215
11445257-2	2001	Another candidate is the dihydrolipoyl succinyltransferase (DLST) gene, one of three components of thiamine-dependent mitochondrial alpha-ketoglutarate dehydrogenase complex (KGDHC), because KGDHC activity is reported reduced in AD patients.	Thiamine	99-107	dihydrolipoamide S-succinyltransferase	Homo sapiens	25-58
11445257-2	2001	Another candidate is the dihydrolipoyl succinyltransferase (DLST) gene, one of three components of thiamine-dependent mitochondrial alpha-ketoglutarate dehydrogenase complex (KGDHC), because KGDHC activity is reported reduced in AD patients.	Thiamine	99-107	dihydrolipoamide S-succinyltransferase	Homo sapiens	60-64
11380424-0	2001	A novel mutation in the SLC19A2 gene in a Tunisian family with thiamine-responsive megaloblastic anaemia, diabetes and deafness syndrome.	Thiamine	63-71	solute carrier family 19 member 2	Homo sapiens	24-31
11380424-4	2001	These data confirm that the SLC19A2 gene is the high-affinity thiamine carrier and that this novel mutation is responsible for TRMA syndrome.	Thiamine	62-70	solute carrier family 19 member 2	Homo sapiens	28-35
11275553-2	2001	A strategy to counter this is to stimulate the anaerobic pentosephosphate pathway of glycolysis by maximizing transketolase activity by thiamine supplementation, with the consequent consumption of glyceraldehyde-3-phosphate and increased formation of ribose-5-phosphate.	Thiamine	136-144	transketolase	Homo sapiens	110-123
11275553-5	2001	The addition of thiamine (50-500 microM) increased the activity of transketolase, decreased the concentration of the triosephosphate pool, decreased the concentration and metabolic flux of the formation of methylglyoxal, and increased the concentration of total sedoheptulose-7-phosphate and ribose-5-phosphate.	Thiamine	16-24	transketolase	Homo sapiens	67-80
11286512-1	2001	Mutations in the SLC19A2 gene cause thiamine-responsive megaloblastic anemia (TRMA) frequently combined with diabetes mellitus and deafness.	Thiamine	36-44	solute carrier family 19 member 2	Homo sapiens	17-24
11286512-1	2001	Mutations in the SLC19A2 gene cause thiamine-responsive megaloblastic anemia (TRMA) frequently combined with diabetes mellitus and deafness.	Thiamine	36-44	solute carrier family 19 member 2	Homo sapiens	78-82
11172768-6	2001	As thiamin deficiency progressed, the extent and intensity of Fos-like immunoreactivity (FLI) in brain structures typically affected by thiamin deficiency (the thalamus, mammillary bodies, inferior colliculus, vestibular nucleus and inferior olives) were markedly increased when compared to thiamin-replete controls.	Thiamine	3-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
11172768-6	2001	As thiamin deficiency progressed, the extent and intensity of Fos-like immunoreactivity (FLI) in brain structures typically affected by thiamin deficiency (the thalamus, mammillary bodies, inferior colliculus, vestibular nucleus and inferior olives) were markedly increased when compared to thiamin-replete controls.	Thiamine	136-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
11172768-6	2001	As thiamin deficiency progressed, the extent and intensity of Fos-like immunoreactivity (FLI) in brain structures typically affected by thiamin deficiency (the thalamus, mammillary bodies, inferior colliculus, vestibular nucleus and inferior olives) were markedly increased when compared to thiamin-replete controls.	Thiamine	136-143	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-65
11038362-3	2001	However, high level RFC1 expression substantially reduced accumulation of the active thiamin coenzyme, thiamin pyrophosphate (TPP).	Thiamine	85-92	replication factor C (activator 1) 1	Mus musculus	20-24
11342117-6	2001	The availability of the human TPK1 gene will provide another useful tool for studying the role of this enzyme in human thiamin metabolism and deficiency state.	Thiamine	119-126	thiamin pyrophosphokinase 1	Homo sapiens	30-34
11038362-4	2001	This decreased level of TPP, synthesized intracellularly from imported thiamin, resulted from RFC1-mediated efflux of TPP.	Thiamine	71-78	replication factor C (activator 1) 1	Mus musculus	94-98
11038362-10	2001	(v) There was an inverse correlation between thiamin accumulation and RFC1 activity in cells grown at a physiological concentration of thiamin.	Thiamine	45-52	replication factor C (activator 1) 1	Mus musculus	70-74
11038362-10	2001	(v) There was an inverse correlation between thiamin accumulation and RFC1 activity in cells grown at a physiological concentration of thiamin.	Thiamine	135-142	replication factor C (activator 1) 1	Mus musculus	70-74
11038362-11	2001	The modulation of thiamin accumulation by RFC1 in murine leukemia cells suggests that this carrier may play a role in thiamin homeostasis and could serve as a modifying factor in thiamin nutritional deficiency as well as when the high affinity thiamin transporter is mutated.	Thiamine	18-25	replication factor C (activator 1) 1	Mus musculus	42-46
11038362-11	2001	The modulation of thiamin accumulation by RFC1 in murine leukemia cells suggests that this carrier may play a role in thiamin homeostasis and could serve as a modifying factor in thiamin nutritional deficiency as well as when the high affinity thiamin transporter is mutated.	Thiamine	118-125	replication factor C (activator 1) 1	Mus musculus	42-46
11038362-11	2001	The modulation of thiamin accumulation by RFC1 in murine leukemia cells suggests that this carrier may play a role in thiamin homeostasis and could serve as a modifying factor in thiamin nutritional deficiency as well as when the high affinity thiamin transporter is mutated.	Thiamine	118-125	replication factor C (activator 1) 1	Mus musculus	42-46
11113972-11	2000	Taken together, these results imply that DET1, det2, DET12 and DET13 represent new genes encoding negative regulators of thiamine-repressed genes.	Thiamine	121-129	acid phosphatase DET1	Saccharomyces cerevisiae S288C	41-45
11358373-5	2001	The product of the SLC19A2 gene is a membrane protein which transports thiamine (vitamin B1) with sub-micromolar affinity.	Thiamine	71-79	solute carrier family 19 member 2	Homo sapiens	19-26
11358373-5	2001	The product of the SLC19A2 gene is a membrane protein which transports thiamine (vitamin B1) with sub-micromolar affinity.	Thiamine	81-91	solute carrier family 19 member 2	Homo sapiens	19-26
11214358-4	2000	Indeed, cord blood from neonates born to mothers treated with insulin for GDM had significantly higher thiamin concentration than other neonates in the study.	Thiamine	103-110	insulin	Homo sapiens	62-69
11405995-13	2001	Meador 1993a noted that 3/8 on thiamine compared with 6/9 on placebo were worse as measured on the ADAS-Cog at 3 months compared with baseline, but the difference is not statistically significant.	Thiamine	31-39	alkylglycerone phosphate synthase	Homo sapiens	99-103
11135496-0	2000	Thiamine-responsive megaloblastic anemia syndrome (TRMA) with cone-rod dystrophy.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	51-55
11135496-1	2000	Thiamine-responsive megaloblastic anemia (TRMA) is an autosomal recessive disease in which the active thiamine uptake into cells is disturbed.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	42-46
11135496-1	2000	Thiamine-responsive megaloblastic anemia (TRMA) is an autosomal recessive disease in which the active thiamine uptake into cells is disturbed.	Thiamine	102-110	solute carrier family 19 member 2	Homo sapiens	42-46
10869563-1	2000	We have studied the transcript levels of YGR260w and YLR004c, two genes encoding members of the yeast Dal5p subfamily of the major facilitator family, and we show that they increase when extracellular nicotinic acid and thiamine, respectively, are absent.	Thiamine	220-228	allantoate permease	Saccharomyces cerevisiae S288C	102-107
11136357-0	2000	Excitatory effect of thiamin on CA1 pyramidal neurones in rat hippocampal slices in vitro.	Thiamine	21-28	carbonic anhydrase 1	Rattus norvegicus	32-35
10948290-6	2000	In addition, transketolase activity, which was measured as an indicator of thiamine availability in the body, was decreased 25% in brains of 19-day-old embryos.	Thiamine	75-83	transketolase like 1	Gallus gallus	13-26
11049077-0	2000	Effect of dietary thiamin supplementation on milk production by dairy cows.	Thiamine	18-25	Weaning weight-maternal milk	Bos taurus	45-49
11049077-1	2000	We conducted three experiments to determine the effects of dietary thiamin supplementation on milk production by dairy cows.	Thiamine	67-74	Weaning weight-maternal milk	Bos taurus	94-98
11049077-4	2000	Milk yield was 2.7 kg/d higher for thiamin-supplemented cows.	Thiamine	35-42	Weaning weight-maternal milk	Bos taurus	0-4
11049077-5	2000	Yields of milk fat and protein were increased 0.13 and 0.10 kg/d, respectively, by dietary thiamin supplementation.	Thiamine	91-98	Weaning weight-maternal milk	Bos taurus	10-14
11049077-8	2000	Milk and protein yields tended to be 0.7 and 0.04 kg/d higher, respectively, for thiamin-supplemented cows.	Thiamine	81-88	Weaning weight-maternal milk	Bos taurus	0-4
11049077-12	2000	Milk fat percentage tended to be 0.18 percentage units lower and fat yield was 0.08 kg/d lower for thiamin-supplemented cows.	Thiamine	99-106	Weaning weight-maternal milk	Bos taurus	0-4
11049077-13	2000	Thiamin supplementation tended to increase milk and component production when dietary concentrations of neutral and acid detergent fiber were lower and nonfiber carbohydrate was higher than recommended.	Thiamine	0-7	Weaning weight-maternal milk	Bos taurus	43-47
10978358-0	2000	A novel mutation in the thiamine responsive megaloblastic anaemia gene SLC19A2 in a patient with deficiency of respiratory chain complex I.	Thiamine	24-32	solute carrier family 19 member 2	Homo sapiens	71-78
10978358-1	2000	The thiamine transporter gene SLC19A2 was recently found to be mutated in thiamine responsive megaloblastic anaemia with diabetes and deafness (TRMA, Rogers syndrome), an early onset autosomal recessive disorder.	Thiamine	4-12	solute carrier family 19 member 2	Homo sapiens	30-37
10964259-11	2000	The saturable (specific) component is missing in patients of the rare disease known as thiamine-responsive megaloblastic anaemia (TRMA), producing a general disturbance of thiamine transport up to thiamine deficiency.	Thiamine	87-95	solute carrier family 19 member 2	Homo sapiens	130-134
10964259-11	2000	The saturable (specific) component is missing in patients of the rare disease known as thiamine-responsive megaloblastic anaemia (TRMA), producing a general disturbance of thiamine transport up to thiamine deficiency.	Thiamine	172-180	solute carrier family 19 member 2	Homo sapiens	130-134
10964259-11	2000	The saturable (specific) component is missing in patients of the rare disease known as thiamine-responsive megaloblastic anaemia (TRMA), producing a general disturbance of thiamine transport up to thiamine deficiency.	Thiamine	172-180	solute carrier family 19 member 2	Homo sapiens	130-134
11021334-4	2000	Thiamine is essential for glucose oxidation, insulin production by pancreatic beta-cells and cell growth.	Thiamine	0-8	insulin	Homo sapiens	45-52
10861909-4	2000	The pJR vectors differ among them in: (a) the selectable marker (Saccharomyces cerevisiae LEU 2 gene, which complements S. pombe leu1- gene and S. pombe ura4+ and his3+ genes); (b) the thiamine-repressible nmt1 promoter (3X, 41X and 81X with extremely high, moderate or low transcription efficiency, respectively); and (c) the multiple cloning site (two multiple cloning sites, with 12 restriction sites each).	Thiamine	185-193	3-isopropylmalate dehydrogenase	Saccharomyces cerevisiae S288C	90-95
11055941-4	2000	Predicted products of open reading frames with similarity to the thiamine biosynthetic genes thiO, thiG, and thiF; a betT gene coding for choline transport; an msrA gene for the enzyme methionine sulfoxide reductase; a putative methyl-accepting chemotaxis gene; an aldehyde dehydrogenase gene; an hns DNA binding gene; a LysR-type transcriptional regulator; and parA and parB partitioning genes were identified.	Thiamine	65-73	thiF	Erwinia amylovora	109-113
10945258-4	2000	Additionally, the deduced aa sequence has 72% and 63% identity to Fusarium solani sti35 encoding a stress-inducible protein and Saccharomyces cerevisiae THI4 encoding an enzyme involved in thiamine biosynthesis, respectively, indicating that ptrA is a mutated allele of a gene belonging to the THI4 family.	Thiamine	189-197	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	153-157
10945258-4	2000	Additionally, the deduced aa sequence has 72% and 63% identity to Fusarium solani sti35 encoding a stress-inducible protein and Saccharomyces cerevisiae THI4 encoding an enzyme involved in thiamine biosynthesis, respectively, indicating that ptrA is a mutated allele of a gene belonging to the THI4 family.	Thiamine	189-197	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	294-298
10781607-0	2000	The iscS gene in Escherichia coli is required for the biosynthesis of 4-thiouridine, thiamin, and NAD.	Thiamine	85-92	NFS1 cysteine desulfurase	Homo sapiens	4-8
10781607-4	2000	In addition to lacking s(4)U, the iscS(-) strain requires thiamin and nicotinic acid for growth in minimal media.	Thiamine	58-65	NFS1 cysteine desulfurase	Homo sapiens	34-38
10781607-5	2000	The thiamin requirement can be relieved by the addition of the thiamin precursor 5-hydroxyethyl-4-methylthiazole, indicating that iscS is required specifically for thiazole biosynthesis.	Thiamine	4-11	NFS1 cysteine desulfurase	Homo sapiens	130-134
10781607-5	2000	The thiamin requirement can be relieved by the addition of the thiamin precursor 5-hydroxyethyl-4-methylthiazole, indicating that iscS is required specifically for thiazole biosynthesis.	Thiamine	63-70	NFS1 cysteine desulfurase	Homo sapiens	130-134
10781607-7	2000	When the iscS(-) strain is switched from rich to minimal medium containing thiamin and nicotinate, growth is preceded by a considerable lag period relative to the parent strain.	Thiamine	75-82	NFS1 cysteine desulfurase	Homo sapiens	9-13
10781607-14	2000	Thus, IscS plays a significant and specific role at the top of a potentially broad sulfur transfer cascade that is required for the biosynthesis of thiamin, NAD, Fe-S clusters, and thionucleosides.	Thiamine	148-155	NFS1 cysteine desulfurase	Homo sapiens	6-10
10830262-2	2000	Two of them, PIG1 (= THI1) and PIG4 (= THI2), were found to be highly transcribed in haustoria, and are homologous to genes involved in thiamine (vitamin B1) biosynthesis in yeast.	Thiamine	136-144	protein phosphatase regulator PIG1	Saccharomyces cerevisiae S288C	13-17
10822160-0	2000	Immunohistochemical estimation of brain choline acetyltransferase and somatostatin related to the impairment of avoidance learning induced by thiamine deficiency.	Thiamine	142-150	choline O-acetyltransferase	Rattus norvegicus	40-65
10822160-0	2000	Immunohistochemical estimation of brain choline acetyltransferase and somatostatin related to the impairment of avoidance learning induced by thiamine deficiency.	Thiamine	142-150	somatostatin	Rattus norvegicus	70-82
10952481-12	2000	The transketolase activity increased from 3.54+/-0.7 microkat/l initially to 3.84+/-0.6 microkat/l after benfotiamine intake (P = 0.02) and from 3.71+/-0.8 microkat/l to 4.02+/-0.7 microkat/l after thiamine nitrate intake (P = 0.08).	Thiamine	198-214	transketolase	Homo sapiens	4-17
10830262-2	2000	Two of them, PIG1 (= THI1) and PIG4 (= THI2), were found to be highly transcribed in haustoria, and are homologous to genes involved in thiamine (vitamin B1) biosynthesis in yeast.	Thiamine	136-144	acetolactate synthase catalytic subunit	Saccharomyces cerevisiae S288C	21-25
10830262-2	2000	Two of them, PIG1 (= THI1) and PIG4 (= THI2), were found to be highly transcribed in haustoria, and are homologous to genes involved in thiamine (vitamin B1) biosynthesis in yeast.	Thiamine	136-144	Thi2p	Saccharomyces cerevisiae S288C	39-43
10830262-2	2000	Two of them, PIG1 (= THI1) and PIG4 (= THI2), were found to be highly transcribed in haustoria, and are homologous to genes involved in thiamine (vitamin B1) biosynthesis in yeast.	Thiamine	146-156	protein phosphatase regulator PIG1	Saccharomyces cerevisiae S288C	13-17
10830262-2	2000	Two of them, PIG1 (= THI1) and PIG4 (= THI2), were found to be highly transcribed in haustoria, and are homologous to genes involved in thiamine (vitamin B1) biosynthesis in yeast.	Thiamine	146-156	acetolactate synthase catalytic subunit	Saccharomyces cerevisiae S288C	21-25
10830262-2	2000	Two of them, PIG1 (= THI1) and PIG4 (= THI2), were found to be highly transcribed in haustoria, and are homologous to genes involved in thiamine (vitamin B1) biosynthesis in yeast.	Thiamine	146-156	Thi2p	Saccharomyces cerevisiae S288C	39-43
10794826-0	2000	Hepatic activities of thiamine-dependent enzymes, glucose-6-phosphate dehydrogenase and cytochrome P4501A in Baltic salmon (Salmo salar) yolk-sac fry after thiamine treatment.	Thiamine	156-164	glucose-6-phosphate 1-dehydrogenase	Salmo salar	50-83
10794826-3	2000	The aim of this study was to investigate possible relationships between thiamine and hepatic activities of the thiamine-dependent enzymes transketolase (TK) and alpha-ketoglutarate dehydrogenase (alpha-KGDH) in addition to glucose-6-phosphate dehydrogenase (G6PDH) and cytochrome P4501A (CYP1A), measured as 7-ethoxyresorufin O-deethylase (EROD), in Baltic salmon yolk-sac fry after treatment with thiamine.	Thiamine	72-80	glucose-6-phosphate 1-dehydrogenase	Salmo salar	223-256
10794826-3	2000	The aim of this study was to investigate possible relationships between thiamine and hepatic activities of the thiamine-dependent enzymes transketolase (TK) and alpha-ketoglutarate dehydrogenase (alpha-KGDH) in addition to glucose-6-phosphate dehydrogenase (G6PDH) and cytochrome P4501A (CYP1A), measured as 7-ethoxyresorufin O-deethylase (EROD), in Baltic salmon yolk-sac fry after treatment with thiamine.	Thiamine	72-80	glucose-6-phosphate 1-dehydrogenase	Salmo salar	258-263
10794826-3	2000	The aim of this study was to investigate possible relationships between thiamine and hepatic activities of the thiamine-dependent enzymes transketolase (TK) and alpha-ketoglutarate dehydrogenase (alpha-KGDH) in addition to glucose-6-phosphate dehydrogenase (G6PDH) and cytochrome P4501A (CYP1A), measured as 7-ethoxyresorufin O-deethylase (EROD), in Baltic salmon yolk-sac fry after treatment with thiamine.	Thiamine	111-119	glucose-6-phosphate 1-dehydrogenase	Salmo salar	223-256
10794826-3	2000	The aim of this study was to investigate possible relationships between thiamine and hepatic activities of the thiamine-dependent enzymes transketolase (TK) and alpha-ketoglutarate dehydrogenase (alpha-KGDH) in addition to glucose-6-phosphate dehydrogenase (G6PDH) and cytochrome P4501A (CYP1A), measured as 7-ethoxyresorufin O-deethylase (EROD), in Baltic salmon yolk-sac fry after treatment with thiamine.	Thiamine	111-119	glucose-6-phosphate 1-dehydrogenase	Salmo salar	258-263
10794826-3	2000	The aim of this study was to investigate possible relationships between thiamine and hepatic activities of the thiamine-dependent enzymes transketolase (TK) and alpha-ketoglutarate dehydrogenase (alpha-KGDH) in addition to glucose-6-phosphate dehydrogenase (G6PDH) and cytochrome P4501A (CYP1A), measured as 7-ethoxyresorufin O-deethylase (EROD), in Baltic salmon yolk-sac fry after treatment with thiamine.	Thiamine	111-119	glucose-6-phosphate 1-dehydrogenase	Salmo salar	223-256
10794826-3	2000	The aim of this study was to investigate possible relationships between thiamine and hepatic activities of the thiamine-dependent enzymes transketolase (TK) and alpha-ketoglutarate dehydrogenase (alpha-KGDH) in addition to glucose-6-phosphate dehydrogenase (G6PDH) and cytochrome P4501A (CYP1A), measured as 7-ethoxyresorufin O-deethylase (EROD), in Baltic salmon yolk-sac fry after treatment with thiamine.	Thiamine	111-119	glucose-6-phosphate 1-dehydrogenase	Salmo salar	258-263
10713047-7	2000	Urm1 and Uba4 show similarity to prokaryotic proteins essential for molybdopterin and thiamin biosynthesis, although the Urm1 system is not involved in these pathways.	Thiamine	86-93	ubiquitin-related modifier URM1	Saccharomyces cerevisiae S288C	0-4
10827343-0	2000	JNK1 is inactivated during thiamine deficiency-induced apoptosis in human neuroblastoma cells.	Thiamine	27-35	mitogen-activated protein kinase 8	Homo sapiens	0-4
10827343-8	2000	Loss of Jnk1 activity was not found in lymphoblasts, a cell type that did not undergo apoptosis when deprived of thiamine.	Thiamine	113-121	mitogen-activated protein kinase 8	Homo sapiens	8-12
10827343-9	2000	These findings suggest that thiamine deficiency results in a cellular stress that brings about the loss of Jnk1 activity and the loss of its function of protecting cells from programmed cell death.	Thiamine	28-36	mitogen-activated protein kinase 8	Homo sapiens	107-111
10827343-10	2000	We postulate that focal sensitivity to thiamine deficiency results, in part, from specific neuronal cell types being susceptible to the inactivation of Jnk1 in response to depletion of cellular thiamine.	Thiamine	39-47	mitogen-activated protein kinase 8	Homo sapiens	152-156
10827343-10	2000	We postulate that focal sensitivity to thiamine deficiency results, in part, from specific neuronal cell types being susceptible to the inactivation of Jnk1 in response to depletion of cellular thiamine.	Thiamine	194-202	mitogen-activated protein kinase 8	Homo sapiens	152-156
10713047-7	2000	Urm1 and Uba4 show similarity to prokaryotic proteins essential for molybdopterin and thiamin biosynthesis, although the Urm1 system is not involved in these pathways.	Thiamine	86-93	Uba4p	Saccharomyces cerevisiae S288C	9-13
10654580-0	2000	Immunohistochemical estimation of rat brain somatostatin on avoidance learning impairment induced by thiamine deficiency.	Thiamine	101-109	somatostatin	Rattus norvegicus	44-56
10617916-4	2000	In lens, betaAPP and Abeta increase in cultured lenses exposed to oxidative stress, and in areas of lens fiber cell degeneration in thiamine (vitamin B1) deprived mice, a classic model of systemic oxidative stress.	Thiamine	132-140	amyloid beta (A4) precursor protein	Mus musculus	9-16
10617916-4	2000	In lens, betaAPP and Abeta increase in cultured lenses exposed to oxidative stress, and in areas of lens fiber cell degeneration in thiamine (vitamin B1) deprived mice, a classic model of systemic oxidative stress.	Thiamine	142-152	amyloid beta (A4) precursor protein	Mus musculus	9-16
10629262-0	2000	Thiamine (Vitamin B1) protects against glucose- and insulin-mediated proliferation of human infragenicular arterial smooth muscle cells.	Thiamine	0-8	insulin	Homo sapiens	52-59
10629262-0	2000	Thiamine (Vitamin B1) protects against glucose- and insulin-mediated proliferation of human infragenicular arterial smooth muscle cells.	Thiamine	10-20	insulin	Homo sapiens	52-59
10629262-4	2000	The objective of this study is to determine the effect of thiamine on human infragenicular ASMC proliferation induced by high glucose and insulin levels in vitro.	Thiamine	58-66	insulin	Homo sapiens	138-145
10629262-10	2000	The data suggest that thiamine inhibits human infragenicular ASMC proliferation induced by high glucose and insulin.	Thiamine	22-30	insulin	Homo sapiens	108-115
20575821-5	2000	Thiamine deficiency, as revealed by erythrocyte transketolase activation assay, was detected in two moderate drinkers and seven heavy drinkers but was not significantly correlated with electromyographic alterations with the exception of ulnar nerves.	Thiamine	0-8	transketolase	Homo sapiens	48-61
10567383-2	1999	A mouse thiamin pyrophosphokinase cDNA clone (mTPK1) was isolated using a combination of mouse expressed sequence tag database analysis, a two-step polymerase chain reaction procedure, and functional complementation screening with a Saccharomyces cerevisiae thiamin pyrophosphokinase-deficient mutant (thi80).	Thiamine	8-15	thiamine pyrophosphokinase	Mus musculus	46-51
10874303-0	2000	The spectrum of mutations, including four novel ones, in the thiamine-responsive megaloblastic anemia gene SLC19A2 of eight families.	Thiamine	61-69	solute carrier family 19 member 2	Homo sapiens	107-114
10874303-1	2000	Thiamine responsive megaloblastic anemia (TRMA) is an autosomal recessive disorder with a triad of symptoms: megaloblastic anemia, deafness, and non-type 1 diabetes mellitus.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	42-46
10874303-3	2000	Patients with TRMA often respond to treatment with pharmacological doses of thiamine.	Thiamine	76-84	solute carrier family 19 member 2	Homo sapiens	14-18
10890024-1	2000	Metabolic control analysis predicts that stimulators of transketolase enzyme synthesis such as thiamin (vitamin B-1) support a high rate of nucleic acid ribose synthesis necessary for tumor cell survival, chemotherapy resistance, and proliferation.	Thiamine	95-102	transketolase	Homo sapiens	56-69
10890024-1	2000	Metabolic control analysis predicts that stimulators of transketolase enzyme synthesis such as thiamin (vitamin B-1) support a high rate of nucleic acid ribose synthesis necessary for tumor cell survival, chemotherapy resistance, and proliferation.	Thiamine	104-115	transketolase	Homo sapiens	56-69
11109306-2	2000	This role stems from the fact that thiamine acts as the cofactor of transketolase.	Thiamine	35-43	transketolase	Homo sapiens	68-81
10517697-0	1999	Increased "peripheral-type" benzodiazepine receptor sites and mRNA in thalamus of thiamine-deficient rats.	Thiamine	82-90	translocator protein	Rattus norvegicus	11-51
10501001-3	1999	Using complementation screening in the mutants obtained, we isolated a gene that was involved in the thiamine-inducible expression, TIE1, which corresponded to the YDR325w ORF on chromosome IV.	Thiamine	101-109	condensin subunit YCG1	Saccharomyces cerevisiae S288C	132-136
10492392-0	1999	Comparative effects of developmental thiamine deficiencies and ethanol exposure on the morphometry of the CA3 pyramidal cells.	Thiamine	37-45	carbonic anhydrase 3	Rattus norvegicus	106-109
10492392-11	1999	In contrast, comparisons between ethanol-exposed pups and the three patterns of thiamine-deficient pups, exhibited similar intensity in the deficit of CA3 pyramidal cells.	Thiamine	80-88	carbonic anhydrase 3	Rattus norvegicus	151-154
10471207-1	1999	Thiamine is an essential cofactor for several important enzymes involved in brain oxidative metabolism, such as the alpha-ketoglutarate dehydrogenase complex (KGDHC), pyruvate-dehydrogenase complex, and transketolase.	Thiamine	0-8	transketolase	Homo sapiens	203-216
10501001-5	1999	The disruption of the TIE1 gene caused two phenotypes, increase of expression level in thiamine-free medium and ethanol sensitivity.	Thiamine	87-95	condensin subunit YCG1	Saccharomyces cerevisiae S288C	22-26
10501001-6	1999	This increase in thiamine-free medium was also observed in the expression under the control of ENO1 or ADH1 promoter in addition to the GAL10 promoter, suggesting that the TIE1 protein is associated with a similar kind of transcriptional mechanism regulated by thiamine.	Thiamine	17-25	phosphopyruvate hydratase ENO1	Saccharomyces cerevisiae S288C	95-99
10501001-6	1999	This increase in thiamine-free medium was also observed in the expression under the control of ENO1 or ADH1 promoter in addition to the GAL10 promoter, suggesting that the TIE1 protein is associated with a similar kind of transcriptional mechanism regulated by thiamine.	Thiamine	17-25	alcohol dehydrogenase ADH1	Saccharomyces cerevisiae S288C	103-107
10501001-6	1999	This increase in thiamine-free medium was also observed in the expression under the control of ENO1 or ADH1 promoter in addition to the GAL10 promoter, suggesting that the TIE1 protein is associated with a similar kind of transcriptional mechanism regulated by thiamine.	Thiamine	17-25	bifunctional UDP-glucose 4-epimerase/aldose 1-epimerase	Saccharomyces cerevisiae S288C	136-141
10501001-6	1999	This increase in thiamine-free medium was also observed in the expression under the control of ENO1 or ADH1 promoter in addition to the GAL10 promoter, suggesting that the TIE1 protein is associated with a similar kind of transcriptional mechanism regulated by thiamine.	Thiamine	17-25	condensin subunit YCG1	Saccharomyces cerevisiae S288C	172-176
10501001-6	1999	This increase in thiamine-free medium was also observed in the expression under the control of ENO1 or ADH1 promoter in addition to the GAL10 promoter, suggesting that the TIE1 protein is associated with a similar kind of transcriptional mechanism regulated by thiamine.	Thiamine	261-269	condensin subunit YCG1	Saccharomyces cerevisiae S288C	172-176
10391223-9	1999	The sequence homology and predicted structure of SLC19A2, as well as its role in TRMA, suggest that its gene product is a thiamine carrier, the first to be identified in complex eukaryotes.	Thiamine	122-130	solute carrier family 19 member 2	Homo sapiens	81-85
10378477-4	1999	Thiamine contents and transketolase activity, one of the thiamine dependent enzymes in the brain regions were significantly lowered by lead intoxication and thiamine deficiency.	Thiamine	57-65	transketolase	Rattus norvegicus	22-35
10391221-0	1999	Mutations in SLC19A2 cause thiamine-responsive megaloblastic anaemia associated with diabetes mellitus and deafness.	Thiamine	27-35	solute carrier family 19 member 2	Homo sapiens	13-20
10391221-1	1999	Thiamine-responsive megaloblastic anaemia (TRMA), also known as Rogers syndrome, is an early onset, autosomal recessive disorder defined by the occurrence of megaloblastic anaemia, diabetes mellitus and sensorineural deafness, responding in varying degrees to thiamine treatment (MIM 249270).	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	43-47
10391221-1	1999	Thiamine-responsive megaloblastic anaemia (TRMA), also known as Rogers syndrome, is an early onset, autosomal recessive disorder defined by the occurrence of megaloblastic anaemia, diabetes mellitus and sensorineural deafness, responding in varying degrees to thiamine treatment (MIM 249270).	Thiamine	260-268	solute carrier family 19 member 2	Homo sapiens	43-47
10391222-0	1999	The gene mutated in thiamine-responsive anaemia with diabetes and deafness (TRMA) encodes a functional thiamine transporter.	Thiamine	20-28	solute carrier family 19 member 2	Homo sapiens	76-80
10391222-0	1999	The gene mutated in thiamine-responsive anaemia with diabetes and deafness (TRMA) encodes a functional thiamine transporter.	Thiamine	103-111	solute carrier family 19 member 2	Homo sapiens	76-80
10391222-1	1999	Thiamine-responsive megaloblastic anaemia with diabetes and deafness (TRMA; MIM 249270) is an autosomal recessive disease thought to be due to a defect in thiamine (vitamin B1) transport.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	70-74
10391222-1	1999	Thiamine-responsive megaloblastic anaemia with diabetes and deafness (TRMA; MIM 249270) is an autosomal recessive disease thought to be due to a defect in thiamine (vitamin B1) transport.	Thiamine	155-163	solute carrier family 19 member 2	Homo sapiens	70-74
10391222-1	1999	Thiamine-responsive megaloblastic anaemia with diabetes and deafness (TRMA; MIM 249270) is an autosomal recessive disease thought to be due to a defect in thiamine (vitamin B1) transport.	Thiamine	165-175	solute carrier family 19 member 2	Homo sapiens	70-74
10391222-5	1999	We have previously demonstrated that fibroblasts from people with TRMA lack high-affinity thiamine transport.	Thiamine	90-98	solute carrier family 19 member 2	Homo sapiens	66-70
10391222-6	1999	Expression of a gene encoding a known yeast thiamine transporter, THI10 (refs 8-10), in TRMA mutant cells prevents apoptotic cell death in thiamine-depleted medium.	Thiamine	44-52	thiamine transporter THI7	Saccharomyces cerevisiae S288C	66-71
10391222-6	1999	Expression of a gene encoding a known yeast thiamine transporter, THI10 (refs 8-10), in TRMA mutant cells prevents apoptotic cell death in thiamine-depleted medium.	Thiamine	44-52	solute carrier family 19 member 2	Homo sapiens	88-92
10391222-6	1999	Expression of a gene encoding a known yeast thiamine transporter, THI10 (refs 8-10), in TRMA mutant cells prevents apoptotic cell death in thiamine-depleted medium.	Thiamine	139-147	thiamine transporter THI7	Saccharomyces cerevisiae S288C	66-71
10391222-6	1999	Expression of a gene encoding a known yeast thiamine transporter, THI10 (refs 8-10), in TRMA mutant cells prevents apoptotic cell death in thiamine-depleted medium.	Thiamine	139-147	solute carrier family 19 member 2	Homo sapiens	88-92
10391222-7	1999	On the basis of these studies, we hypothesized that a defective thiamine transporter causes TRMA.	Thiamine	64-72	solute carrier family 19 member 2	Homo sapiens	92-96
10391222-9	1999	Here we present evidence that the gene SLC19A2 (for solute carrier family 19 (thiamine transporter), member 2) encodes the first known mammalian thiamine transporter, which we designate thiamine transporter-1 (THTR-1).	Thiamine	78-86	solute carrier family 19 member 2	Homo sapiens	39-46
10391222-9	1999	Here we present evidence that the gene SLC19A2 (for solute carrier family 19 (thiamine transporter), member 2) encodes the first known mammalian thiamine transporter, which we designate thiamine transporter-1 (THTR-1).	Thiamine	78-86	solute carrier family 19 member 2	Homo sapiens	186-208
10391222-9	1999	Here we present evidence that the gene SLC19A2 (for solute carrier family 19 (thiamine transporter), member 2) encodes the first known mammalian thiamine transporter, which we designate thiamine transporter-1 (THTR-1).	Thiamine	78-86	solute carrier family 19 member 2	Homo sapiens	210-216
10391223-1	1999	Thiamine-responsive megaloblastic anaemia syndrome (TRMA; MIM 249270) is an autosomal recessive disorder with features that include megaloblastic anaemia, mild thrombocytopenia and leucopenia, sensorineural deafness and diabetes mellitus.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	52-56
10391223-3	1999	A defect in the plasma membrane transport of thiamine has been demonstrated in erythrocytes and cultured skin fibroblasts from TRMA patients.	Thiamine	45-53	solute carrier family 19 member 2	Homo sapiens	127-131
10391223-9	1999	The sequence homology and predicted structure of SLC19A2, as well as its role in TRMA, suggest that its gene product is a thiamine carrier, the first to be identified in complex eukaryotes.	Thiamine	122-130	solute carrier family 19 member 2	Homo sapiens	49-56
10338141-0	1999	Thiamine repression and pyruvate decarboxylase autoregulation independently control the expression of the Saccharomyces cerevisiae PDC5 gene.	Thiamine	0-8	indolepyruvate decarboxylase 5	Saccharomyces cerevisiae S288C	131-135
10338141-2	1999	In this work we show that expression of PDC5 but not that of PDC1, which encodes the major isoform, is repressed by thiamine.	Thiamine	116-124	indolepyruvate decarboxylase 5	Saccharomyces cerevisiae S288C	40-44
10338141-3	1999	Hence, under thiamine limitation both PDC1 and PDC5 are expressed.	Thiamine	13-21	indolepyruvate decarboxylase 1	Saccharomyces cerevisiae S288C	38-42
10338141-3	1999	Hence, under thiamine limitation both PDC1 and PDC5 are expressed.	Thiamine	13-21	indolepyruvate decarboxylase 5	Saccharomyces cerevisiae S288C	47-51
10338141-5	1999	Two-dimensional gel electrophoresis of whole protein extracts shows that thiamine limitation stimulates the production of THI gene products and of Pdc5p.	Thiamine	73-81	indolepyruvate decarboxylase 5	Saccharomyces cerevisiae S288C	147-152
10378477-4	1999	Thiamine contents and transketolase activity, one of the thiamine dependent enzymes in the brain regions were significantly lowered by lead intoxication and thiamine deficiency.	Thiamine	157-165	transketolase	Rattus norvegicus	22-35
10082768-8	1999	Varying dietary thiamin had marked but opposite effects on the activities of alpha-ketoglutarate dehydrogenase (alpha-KGDH) and BCKDH.	Thiamine	16-23	oxoglutarate dehydrogenase	Rattus norvegicus	77-110
10074490-9	1999	At 30 nM thiamine, the rate of uptake of thiamine by TRMA fibroblasts was 10-fold less than that of wild-type, and cells from obligate heterozygotes had an intermediate phenotype.	Thiamine	41-49	solute carrier family 19 member 2	Homo sapiens	53-57
10074490-10	1999	Transfection of TRMA fibroblasts with the yeast thiamine transporter gene THI10 prevented cell death when cells were grown in the absence of supplemental thiamine.	Thiamine	48-56	solute carrier family 19 member 2	Homo sapiens	16-20
10074490-10	1999	Transfection of TRMA fibroblasts with the yeast thiamine transporter gene THI10 prevented cell death when cells were grown in the absence of supplemental thiamine.	Thiamine	48-56	thiamine transporter THI7	Saccharomyces cerevisiae S288C	74-79
10074490-11	1999	We therefore propose that the primary abnormality in TRMA is absence of a high-affinity thiamine transporter and that low intracellular thiamine concentrations in the mutant cells cause biochemical abnormalities that lead to apoptotic cell death.	Thiamine	88-96	solute carrier family 19 member 2	Homo sapiens	53-57
10450194-3	1999	Vitamin-dependent activities--aspartate aminotransferase (AST) for pyridoxine, glutathione reductase (GTR) for riboflavin, transketolase (TK) for thiamine--were measured in erythrocyte haemolysates before and after in-vitro addition of the relevant vitamin.	Thiamine	146-154	solute carrier family 17 member 5	Homo sapiens	58-61
10450194-3	1999	Vitamin-dependent activities--aspartate aminotransferase (AST) for pyridoxine, glutathione reductase (GTR) for riboflavin, transketolase (TK) for thiamine--were measured in erythrocyte haemolysates before and after in-vitro addition of the relevant vitamin.	Thiamine	146-154	glutathione-disulfide reductase	Homo sapiens	102-105
10450194-3	1999	Vitamin-dependent activities--aspartate aminotransferase (AST) for pyridoxine, glutathione reductase (GTR) for riboflavin, transketolase (TK) for thiamine--were measured in erythrocyte haemolysates before and after in-vitro addition of the relevant vitamin.	Thiamine	146-154	transketolase	Homo sapiens	123-136
10450194-3	1999	Vitamin-dependent activities--aspartate aminotransferase (AST) for pyridoxine, glutathione reductase (GTR) for riboflavin, transketolase (TK) for thiamine--were measured in erythrocyte haemolysates before and after in-vitro addition of the relevant vitamin.	Thiamine	146-154	transketolase	Homo sapiens	138-140
10074490-1	1999	We have investigated the cellular pathology of the syndrome called thiamine-responsive megaloblastic anemia (TRMA) with diabetes and deafness.	Thiamine	67-75	solute carrier family 19 member 2	Homo sapiens	109-113
10074490-4	1999	TRMA fibroblasts were rescued from death with 10-30 nM thiamine (in the range of normal plasma thiamine concentrations).	Thiamine	55-63	solute carrier family 19 member 2	Homo sapiens	0-4
10074490-4	1999	TRMA fibroblasts were rescued from death with 10-30 nM thiamine (in the range of normal plasma thiamine concentrations).	Thiamine	95-103	solute carrier family 19 member 2	Homo sapiens	0-4
10074490-9	1999	At 30 nM thiamine, the rate of uptake of thiamine by TRMA fibroblasts was 10-fold less than that of wild-type, and cells from obligate heterozygotes had an intermediate phenotype.	Thiamine	9-17	solute carrier family 19 member 2	Homo sapiens	53-57
10082768-8	1999	Varying dietary thiamin had marked but opposite effects on the activities of alpha-ketoglutarate dehydrogenase (alpha-KGDH) and BCKDH.	Thiamine	16-23	oxoglutarate dehydrogenase	Rattus norvegicus	112-122
10082768-9	1999	Thiamin deficiency decreased alpha-KGDH activity, increased BCKDH activity, and increased the proportion of BCKDH in the active, dephosphorylated, state.	Thiamine	0-7	oxoglutarate dehydrogenase	Rattus norvegicus	29-39
10230710-2	1999	In this study the effects of a therapeutic combination of amantadine, thiamine and L-tryptophan on the serotonin (5-HT) innervation was assessed in Lurcher mice by autoradiography, using [3H]citalopram to label 5-HT transporters.	Thiamine	70-78	glutamate receptor, ionotropic, delta 2	Mus musculus	148-155
10066388-1	1999	Thiamine-responsive megaloblastic anemia (TRMA) is a rare autosomal recessive syndrome characterized by megaloblastic anemia, deafness, and diabetes mellitus.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	42-46
9924800-11	1998	However, a modification of transketolase is a marker for Alzheimer"s disease, and transketolase activity in erythrocytes is a measure of thiamin nutrition.	Thiamine	137-144	transketolase	Homo sapiens	82-95
9933732-5	1999	The effect of exogenous thiamine pyrophosphate (TPP) addition on the blood transketolase (TK) activity (TPP TK effect) served to estimate thiamine deficiency.	Thiamine	24-32	transketolase	Homo sapiens	75-88
9933732-5	1999	The effect of exogenous thiamine pyrophosphate (TPP) addition on the blood transketolase (TK) activity (TPP TK effect) served to estimate thiamine deficiency.	Thiamine	24-32	transketolase	Homo sapiens	90-92
9972506-7	1999	Microspheres with a different polymer matrix, Eudragit RS PO, were also prepared by a similar technique, and these particles prolonged the release of thiamin for over 6 h, under simulated GI conditions.	Thiamine	150-157	R-spondin 1	Homo sapiens	55-60
9862430-1	1998	Here we summarize evidence for non-equivalence of two structurally similar active sites in transketolase and other thiamine-dependent enzymes.	Thiamine	115-123	transketolase	Homo sapiens	91-104
9435271-4	1998	At the same gradient, the Km and Jmax values of the saturable component of the thiamine uptake curve after a 6 sec incubation time were 6.2 +/- 1.4 microM and 14.9 +/- 3 pmol.mg-1 protein.6 sec-1 respectively.	Thiamine	79-87	secretory blood group 1	Rattus norvegicus	190-195
9521628-0	1998	Thiamine deficiency decreases steady-state transketolase and pyruvate dehydrogenase but not alpha-ketoglutarate dehydrogenase mRNA levels in three human cell types.	Thiamine	0-8	transketolase	Homo sapiens	43-56
9521628-4	1998	In all three cell types, the mRNA levels of transketolase and the E1beta subunit of pyruvate dehydrogenase complex were lower in thiamine-deficient cultures.	Thiamine	129-137	transketolase	Homo sapiens	44-57
9856490-1	1998	Thiamine-responsive megaloblastic anemia (TRMA, also known as Rogers syndrome, OMIM 249270) is a rare autosomal recessive disorder characterized by a triad of megaloblastic anemia, diabetes mellitus, and sensorineural deafness.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	42-46
9856490-7	1998	The multi-system manifestations of TRMA suggest that thiamine has a pivotal role in a multiplicity of physiological processes.	Thiamine	53-61	solute carrier family 19 member 2	Homo sapiens	35-39
9856490-8	1998	Mapping the TRMA gene and understanding the molecular basis of the disease might, thus, shed light on the role of thiamine in common disorders such as deafness, anemia, and diabetes.	Thiamine	114-122	solute carrier family 19 member 2	Homo sapiens	12-16
9655943-0	1998	Crystallography and mutagenesis of transketolase: mechanistic implications for enzymatic thiamin catalysis.	Thiamine	89-96	transketolase	Homo sapiens	35-48
9655943-1	1998	The ThDP dependent enzyme transketolase is a convenient model system to study enzymatic thiamin catalysis.	Thiamine	88-95	transketolase	Homo sapiens	26-39
9568183-1	1998	The objectives of this review are to (a) explain the mechanism by which thiamine (vitamin B1) promotes nucleic acid ribose synthesis and tumor cell proliferation via the nonoxidative transketolase (TK) pathway; (b) estimate the thiamine intake of cancer patients and (c) provide background information and to develop guidelines for alternative treatments with antithiamine transketolase inhibitors in the clinical setting.	Thiamine	72-80	transketolase	Homo sapiens	183-196
9568183-1	1998	The objectives of this review are to (a) explain the mechanism by which thiamine (vitamin B1) promotes nucleic acid ribose synthesis and tumor cell proliferation via the nonoxidative transketolase (TK) pathway; (b) estimate the thiamine intake of cancer patients and (c) provide background information and to develop guidelines for alternative treatments with antithiamine transketolase inhibitors in the clinical setting.	Thiamine	72-80	transketolase	Homo sapiens	198-200
9568183-1	1998	The objectives of this review are to (a) explain the mechanism by which thiamine (vitamin B1) promotes nucleic acid ribose synthesis and tumor cell proliferation via the nonoxidative transketolase (TK) pathway; (b) estimate the thiamine intake of cancer patients and (c) provide background information and to develop guidelines for alternative treatments with antithiamine transketolase inhibitors in the clinical setting.	Thiamine	72-80	transketolase	Homo sapiens	373-386
9568183-1	1998	The objectives of this review are to (a) explain the mechanism by which thiamine (vitamin B1) promotes nucleic acid ribose synthesis and tumor cell proliferation via the nonoxidative transketolase (TK) pathway; (b) estimate the thiamine intake of cancer patients and (c) provide background information and to develop guidelines for alternative treatments with antithiamine transketolase inhibitors in the clinical setting.	Thiamine	82-92	transketolase	Homo sapiens	183-196
9568183-1	1998	The objectives of this review are to (a) explain the mechanism by which thiamine (vitamin B1) promotes nucleic acid ribose synthesis and tumor cell proliferation via the nonoxidative transketolase (TK) pathway; (b) estimate the thiamine intake of cancer patients and (c) provide background information and to develop guidelines for alternative treatments with antithiamine transketolase inhibitors in the clinical setting.	Thiamine	82-92	transketolase	Homo sapiens	198-200
9568183-1	1998	The objectives of this review are to (a) explain the mechanism by which thiamine (vitamin B1) promotes nucleic acid ribose synthesis and tumor cell proliferation via the nonoxidative transketolase (TK) pathway; (b) estimate the thiamine intake of cancer patients and (c) provide background information and to develop guidelines for alternative treatments with antithiamine transketolase inhibitors in the clinical setting.	Thiamine	82-92	transketolase	Homo sapiens	373-386
9568183-3	1998	Analysis of RNA ribose indicates that glucose carbons contribute to over 90% of ribose synthesis in cultured cervix und pancreatic carcinoma cells and that ribose is synthesized primarily through the thiamine dependent TK pathway (> 70%).	Thiamine	200-208	transketolase	Homo sapiens	219-221
9568183-5	1998	The medical literature reveals little information regarding the role of the thiamine dependent TK reaction in tumor cell ribose production which is a central process in de novo nucleic acid synthesis and the salvage pathways for purines.	Thiamine	76-84	transketolase	Homo sapiens	95-97
9568183-7	1998	The thiamine dependent TK pathway is the central avenue which supplies ribose phosphate for nucleic acids in tumors and excessive thiamine supplementation maybe responsible for failed therapeutic attempts to terminate cancer cell proliferation.	Thiamine	4-12	transketolase	Homo sapiens	23-25
9568183-7	1998	The thiamine dependent TK pathway is the central avenue which supplies ribose phosphate for nucleic acids in tumors and excessive thiamine supplementation maybe responsible for failed therapeutic attempts to terminate cancer cell proliferation.	Thiamine	130-138	transketolase	Homo sapiens	23-25
9399900-1	1997	Thiamine-responsive megaloblastic anemia, also known as "TRMA" or "Rogers syndrome," is an early-onset autosomal recessive disorder defined by the occurrence of megaloblastic anemia, diabetes mellitus, and sensorineural deafness, responding in varying degrees to thiamine treatment.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	56-62
9706499-9	1998	Thiamin saturation of transketolase was greater in fetal than in maternal erythrocytes (p < 0.005); severe thiamin deficiency was not observed.	Thiamine	0-7	transketolase	Homo sapiens	22-35
9706499-12	1998	Transketolase activities suggest that thiamin status is sufficient even in late pregnancy.	Thiamine	38-45	transketolase	Homo sapiens	0-13
9399900-1	1997	Thiamine-responsive megaloblastic anemia, also known as "TRMA" or "Rogers syndrome," is an early-onset autosomal recessive disorder defined by the occurrence of megaloblastic anemia, diabetes mellitus, and sensorineural deafness, responding in varying degrees to thiamine treatment.	Thiamine	263-271	solute carrier family 19 member 2	Homo sapiens	56-62
9399900-7	1997	Characterization of the metabolic defect of TRMA may shed light on the role of thiamine deficiency in such common diseases.	Thiamine	79-87	solute carrier family 19 member 2	Homo sapiens	44-48
9358046-5	1997	Conditional thiamine biosynthesis was generated by cloning THI4, a thiamine biosynthetic gene, into a URA3 containing plasmid and transforming a strain disrupted in THI4.	Thiamine	12-20	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	59-63
9513273-4	1997	The mutant strain constitutively produced PHO3 mRNA encoding T-rAPase in medium supplemented with thiamine.	Thiamine	98-106	acid phosphatase PHO3	Saccharomyces cerevisiae S288C	42-46
9367751-0	1997	Dual role for the yeast THI4 gene in thiamine biosynthesis and DNA damage tolerance.	Thiamine	37-45	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	24-28
9367751-1	1997	The THI4 gene of Saccharomyces cerevisiae encodes an enzyme of the thiamine biosynthetic pathway.	Thiamine	67-75	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	4-8
9367751-2	1997	The plant homolog thi1, from Arabidopsis thaliana, is also involved in thiamine biosynthesis; but was originally cloned due to its capacity to complement DNA repair deficient phenotypes in Escherichia coli.	Thiamine	71-79	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	18-22
9367751-8	1997	Thus, Thi4 and its plant homolog appear to be dual functional proteins with roles in thiamine biosynthesis and mitochondrial DNA damage tolerance.	Thiamine	85-93	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	6-10
9358046-5	1997	Conditional thiamine biosynthesis was generated by cloning THI4, a thiamine biosynthetic gene, into a URA3 containing plasmid and transforming a strain disrupted in THI4.	Thiamine	12-20	orotidine-5'-phosphate decarboxylase	Saccharomyces cerevisiae S288C	102-106
9358046-5	1997	Conditional thiamine biosynthesis was generated by cloning THI4, a thiamine biosynthetic gene, into a URA3 containing plasmid and transforming a strain disrupted in THI4.	Thiamine	12-20	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	165-169
9358046-5	1997	Conditional thiamine biosynthesis was generated by cloning THI4, a thiamine biosynthetic gene, into a URA3 containing plasmid and transforming a strain disrupted in THI4.	Thiamine	67-75	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	59-63
9246733-6	1997	Lactating rat dams fed a thiamin-free diet and their offspring were classified as thiamin-deficient on the basis of growth retardation and a lower activity of transketolase in blood, liver and brain.	Thiamine	82-89	transketolase	Rattus norvegicus	159-172
9346467-4	1997	Glutamic acid decarboxylase (GAD), an enzyme mainly confined to the central nervous system, protects most regions of the brain from glutamate that accumulates when the activity of alpha-ketoglutarate dehydrogenase, a thiamine-dependent enzyme complex, is reduced.	Thiamine	217-225	glutamate decarboxylase 1	Homo sapiens	0-27
9346467-4	1997	Glutamic acid decarboxylase (GAD), an enzyme mainly confined to the central nervous system, protects most regions of the brain from glutamate that accumulates when the activity of alpha-ketoglutarate dehydrogenase, a thiamine-dependent enzyme complex, is reduced.	Thiamine	217-225	glutamate decarboxylase 1	Homo sapiens	29-32
9346467-5	1997	During severe thiamine deficiency, glutamate accumulates in GAD-free peripheral tissues and reaches a concentration in blood at which it passes through circumventricular organs into the cerebral ventricles or contiguous brain and finally diffuses into the extracellular space of proximate diencephalic and brain stem tissues.	Thiamine	14-22	glutamate decarboxylase 1	Homo sapiens	60-63
9235906-1	1997	We isolated a thiamin transporter gene, THI10, from a genomic library of Saccharomyces cerevisiae by the complementation of a yeast mutant defective in thiamin transport activity.	Thiamine	14-21	thiamine transporter THI7	Saccharomyces cerevisiae S288C	40-45
9235906-6	1997	Gene disruption of the THI10 locus completely abolished the thiamin transport activity and thiamin binding activity in yeast plasma membrane fraction.	Thiamine	60-67	thiamine transporter THI7	Saccharomyces cerevisiae S288C	23-28
9235906-6	1997	Gene disruption of the THI10 locus completely abolished the thiamin transport activity and thiamin binding activity in yeast plasma membrane fraction.	Thiamine	91-98	thiamine transporter THI7	Saccharomyces cerevisiae S288C	23-28
9235906-7	1997	Both the transport and thiamin binding activities were restored in the disrupted cells when the THI10 open reading frame was expressed by yeast GAL1 promoter, suggesting that the THI10 gene encodes for the thiamin transport carrier protein.	Thiamine	23-30	thiamine transporter THI7	Saccharomyces cerevisiae S288C	96-101
9235906-7	1997	Both the transport and thiamin binding activities were restored in the disrupted cells when the THI10 open reading frame was expressed by yeast GAL1 promoter, suggesting that the THI10 gene encodes for the thiamin transport carrier protein.	Thiamine	23-30	galactokinase	Saccharomyces cerevisiae S288C	144-148
9235906-7	1997	Both the transport and thiamin binding activities were restored in the disrupted cells when the THI10 open reading frame was expressed by yeast GAL1 promoter, suggesting that the THI10 gene encodes for the thiamin transport carrier protein.	Thiamine	23-30	thiamine transporter THI7	Saccharomyces cerevisiae S288C	179-184
9235906-7	1997	Both the transport and thiamin binding activities were restored in the disrupted cells when the THI10 open reading frame was expressed by yeast GAL1 promoter, suggesting that the THI10 gene encodes for the thiamin transport carrier protein.	Thiamine	206-213	thiamine transporter THI7	Saccharomyces cerevisiae S288C	96-101
9235906-7	1997	Both the transport and thiamin binding activities were restored in the disrupted cells when the THI10 open reading frame was expressed by yeast GAL1 promoter, suggesting that the THI10 gene encodes for the thiamin transport carrier protein.	Thiamine	206-213	galactokinase	Saccharomyces cerevisiae S288C	144-148
9235906-7	1997	Both the transport and thiamin binding activities were restored in the disrupted cells when the THI10 open reading frame was expressed by yeast GAL1 promoter, suggesting that the THI10 gene encodes for the thiamin transport carrier protein.	Thiamine	206-213	thiamine transporter THI7	Saccharomyces cerevisiae S288C	179-184
9246733-7	1997	Within these variables transketolase in blood has been shown to be most sensitive, and reached a plateau feeding 6 mg/kg thiamin.	Thiamine	121-128	transketolase	Rattus norvegicus	23-36
9196356-5	1997	A decreased fat intake was associated with an increased sugar intake, but also with increased nutrient densities of thiamin, niacin, folate, vitamin C, magnesium, and iron, reflecting an increased intake of fruit, vegetables, and grains.	Thiamine	116-123	FAT atypical cadherin 1	Homo sapiens	12-15
9211578-6	1997	Thiamine was found to significantly improve recognition accuracy and P300 amplitude, at the midline parietal (Pz) electrode.	Thiamine	0-8	E1A binding protein p300	Homo sapiens	69-73
9115179-1	1997	Members of the transketolase group of thiamine-diphosphate-dependent enzymes from 17 different organisms including mammals, yeast, bacteria, and plants have been used for phylogenetic reconstruction.	Thiamine	38-46	transketolase	Homo sapiens	15-28
9196834-1	1997	In late 1995 and early 1996, Sydney vet Dr Bob Steel reported first-hand experience with a cat dying from thiamine deficiency.	Thiamine	106-114	G protein-coupled receptor 15	Homo sapiens	43-46
9387133-0	1997	Comparison of the thiamine level in blood and erythrocyte transketolase activity in hemodialyzed and nondialyzed patients during recombinant human erythropoietin therapy.	Thiamine	18-26	erythropoietin	Homo sapiens	147-161
9285254-3	1997	Rat dams receiving inadequate thiamin during gestation and their offspring were thiamin-deficient on the basis of reduced activity of transketolase in blood and erythrocytes, which did not reach completely the control level even two weeks postpartum.	Thiamine	30-37	transketolase	Rattus norvegicus	134-147
9285254-3	1997	Rat dams receiving inadequate thiamin during gestation and their offspring were thiamin-deficient on the basis of reduced activity of transketolase in blood and erythrocytes, which did not reach completely the control level even two weeks postpartum.	Thiamine	80-87	transketolase	Rattus norvegicus	134-147
8946985-8	1996	Thiamine status was assessed by assaying thiamine pyrophosphate, transketolase activity, and blood thiamine levels.	Thiamine	0-8	transketolase	Homo sapiens	65-78
31195509-1	1996	The effect of the application of CO2 for extending the storage life of raw cow"s milk on the retention of some vitamins-all-trans-retinol, 13-cis-retinol, beta-carotene, alpha tocopherol, gamma tocopherol, thiamin and riboflavin-and on the growth of psychrotrophic spoilage bacteria has been studied.	Thiamine	206-213	Weaning weight-maternal milk	Bos taurus	81-85
8974135-3	1996	The vitamin B1 level was determined as thiamine pyrophosphate effect on transketolase activity in red blood cell lysates.	Thiamine	4-14	transketolase	Homo sapiens	72-85
8905932-1	1996	A recessive mutation leading to complete loss of thiamine uptake in Saccharomyces cerevisiae was mapped on the left arm of chromosome VII, approximately 56 cM centromere-distal to trp5.	Thiamine	49-57	tryptophan synthase TRP5	Saccharomyces cerevisiae S288C	180-184
8930410-3	1996	Thiamin-dependent enzymes were studied in brain mitochondria: alpha-ketoglutarate dehydrogenase activity exhibited 40% reduction, whereas pyruvate dehydrogenase did not change significantly.	Thiamine	0-7	oxoglutarate dehydrogenase	Rattus norvegicus	62-95
8780408-0	1996	Novel neuritic clusters with accumulations of amyloid precursor protein and amyloid precursor-like protein 2 immunoreactivity in brain regions damaged by thiamine deficiency.	Thiamine	154-162	amyloid beta precursor protein	Rattus norvegicus	46-71
8949966-1	1996	Thiamine deficiency may be assessed clinically by an abnormally low specific erythrocyte transketolase activity and/or by abnormally large activation by thiamine diphosphate in vitro (or "TPP effect").	Thiamine	0-8	transketolase	Homo sapiens	89-102
8949966-3	1996	A new age-dependent parameter was used to improve the reliability of transketolase activity as an indicator of marginal thiamine deficiency.	Thiamine	120-128	transketolase	Homo sapiens	69-82
8949966-11	1996	We conclude that our findings confirm previous reports and that this modified transketolase activation test improves its reliability as an indicator of marginal thiamine deficiency.	Thiamine	161-169	transketolase	Homo sapiens	78-91
8764596-0	1996	Regional reductions of transketolase in thiamine-deficient rat brain.	Thiamine	40-48	transketolase	Rattus norvegicus	23-36
8896289-0	1996	Can megadoses of thiamine prevent ethanol-induced damages of rat hippocampal CA1 pyramidal neurones?	Thiamine	17-25	carbonic anhydrase 1	Rattus norvegicus	77-80
8896289-1	1996	The specific aim of this study was to evaluate whether high doses of thiamine can compensate or prevent alcohol-induced damages of rat hippocampus CA1 pyramids.	Thiamine	69-77	carbonic anhydrase 1	Rattus norvegicus	147-150
8764596-3	1996	To assess the role of TK, we have delineated the regional/cellular distribution of TK protein and mRNA in adult rat brain in pyrithiamine-induced thiamine deficiency.	Thiamine	129-137	transketolase	Rattus norvegicus	83-85
8764596-7	1996	In contrast to the pronounced, general decline of TK protein, in situ hybridization revealed a regional decrease of 0-25% of TK mRNA in thiamine deficiency.	Thiamine	136-144	transketolase	Rattus norvegicus	125-127
8764596-8	1996	Northern blots indicated a similar level of TK mRNA in whole brain in thiamine deficiency.	Thiamine	70-78	transketolase	Rattus norvegicus	44-46
8879292-1	1996	It was found that the activity of the marker thiamine-dependent enzyme, transketolase (TK), was decreased (down to 61-79% of control) in blood, liver and brain of inbred rats following a 6-month consumption of 15% ethanol as their only source of drinking fluid.	Thiamine	45-53	transketolase	Rattus norvegicus	72-85
8879292-1	1996	It was found that the activity of the marker thiamine-dependent enzyme, transketolase (TK), was decreased (down to 61-79% of control) in blood, liver and brain of inbred rats following a 6-month consumption of 15% ethanol as their only source of drinking fluid.	Thiamine	45-53	transketolase	Rattus norvegicus	87-89
8813226-4	1996	However, a nonsignificant trend was observed for slightly reduced levels of TDP and total thiamine in cerebellar cortex of the SCA1 patients, a finding that might be related to the severe neuronal damage in this brain area.	Thiamine	90-98	ataxin 1	Homo sapiens	127-131
8683340-3	1996	Activities of both transketolase and alpha-ketoglutarate dehydrogenase (alpha-KGDH) decreased at the same rate and to roughly the same levels in response to thiamine deficiency within a given cell line.	Thiamine	157-165	transketolase	Homo sapiens	19-32
8683340-7	1996	For transketolase, the non-recoverable activity was due mainly to a decrease in the synthesis rate of the protein during thiamine deficiency, suggesting that thiamine has a direct effect on the expression of the transketolase gene and/or protein.	Thiamine	121-129	transketolase	Homo sapiens	4-17
8683340-7	1996	For transketolase, the non-recoverable activity was due mainly to a decrease in the synthesis rate of the protein during thiamine deficiency, suggesting that thiamine has a direct effect on the expression of the transketolase gene and/or protein.	Thiamine	158-166	transketolase	Homo sapiens	4-17
8683340-7	1996	For transketolase, the non-recoverable activity was due mainly to a decrease in the synthesis rate of the protein during thiamine deficiency, suggesting that thiamine has a direct effect on the expression of the transketolase gene and/or protein.	Thiamine	158-166	transketolase	Homo sapiens	212-225
8533474-0	1995	An 8.2 kb DNA segment from chromosome XIV carries the RPD3 and PAS8 genes as well as the Saccharomyces cerevisiae homologue of the thiamine-repressed nmt1 gene and a chromosome III-duplicated gene for a putative aryl-alcohol dehydrogenase.	Thiamine	131-139	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	150-154
8662211-0	1996	Molecular cloning of thi-4, a gene necessary for the biosynthesis of thiamine in Neurospora crassa.	Thiamine	69-77	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	21-26
8662211-1	1996	The thiamine-4 (thi-4) gene was cloned by functional complementation of a thi-4 mutant of Neurospora crassa.	Thiamine	4-12	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	16-21
8662211-1	1996	The thiamine-4 (thi-4) gene was cloned by functional complementation of a thi-4 mutant of Neurospora crassa.	Thiamine	4-12	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	74-79
8790291-0	1996	Thi1, a thiamine biosynthetic gene in Arabidopsis thaliana, complements bacterial defects in DNA repair.	Thiamine	8-16	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	0-4
8790291-6	1996	This cDNA presents a high homology to a stress related gene from two species of Fusarium (sti35) and to genes whose products participate in the thiamine biosynthesis pathway, THI4, from Saccharomyces cerevisiae and nmt2 from Schizosaccharomyces pombe.	Thiamine	144-152	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	175-179
8790291-8	1996	The auxotrophy for thiamine in the yeast thi4::URA3 disruption strain is complemented by the Arabidopsis gene.	Thiamine	19-27	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	41-45
8790291-9	1996	Thus, the cloned gene, named thi1, is likely to function in the biosynthesis of thiamine in plants.	Thiamine	80-88	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	29-33
8838793-3	1996	Comparison with known transketolases (TK) demonstrated a TKR-specific deletion mutating one thiamine binding site.	Thiamine	92-100	transketolase like 1	Homo sapiens	57-60
8815392-2	1996	Studies in autopsied brain tissue from neuropathologically proven AD patients reveal significantly reduced activities of the thiamine phosphate dephosphorylating enzymes thiamine diphosphatase (TDPase) and thiamine monophosphatase (TMPase) as well as the thiamine diphosphate-dependent enzymes, pyruvate dehydrogenase complex, alpha-ketoglutarate dehydrogenase (alpha KGDH) and transketolase.	Thiamine	125-133	acid phosphatase 3	Homo sapiens	206-230
8815392-2	1996	Studies in autopsied brain tissue from neuropathologically proven AD patients reveal significantly reduced activities of the thiamine phosphate dephosphorylating enzymes thiamine diphosphatase (TDPase) and thiamine monophosphatase (TMPase) as well as the thiamine diphosphate-dependent enzymes, pyruvate dehydrogenase complex, alpha-ketoglutarate dehydrogenase (alpha KGDH) and transketolase.	Thiamine	125-133	acid phosphatase 3	Homo sapiens	232-238
8541506-4	1995	Here we report the cloning and characterization of two cDNAs representing members of the maize thi1 gene family encoding an enzyme of the thiamine biosynthetic pathway.	Thiamine	138-146	thiamine thiazole synthase 1, chloroplastic	Zea mays	95-99
8541506-7	1995	RNA gel blot analysis of various tissues and developmental stages indicated thi1 expression was differentially regulated in a manner consistent with what is known about thiamine synthesis in plants.	Thiamine	169-177	acetolactate synthase catalytic subunit	Saccharomyces cerevisiae S288C	76-80
8540828-2	1995	They comment on the importance of physiological aspects of thiamine as a co-enzyme of transketolase and pyruvate-decarboxilase in the metabolic pathway for ATP production and the possibility of existing an interaction between genetical and environmental factors in the onset the symptoms.	Thiamine	59-67	transketolase	Homo sapiens	86-99
7485819-7	1995	The generalized reductions of transketolase activity undoubtedly result from thiamine deficiency.	Thiamine	77-85	transketolase	Homo sapiens	30-43
8533474-2	1995	The ORF N0295 is highly similar to the Aspergillus parasiticus and Schizosaccharomyces pombe nmt1 gene products, which are involved in thiamine biosynthesis and are strongly repressed by thiamine.	Thiamine	135-143	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	93-97
8533474-2	1995	The ORF N0295 is highly similar to the Aspergillus parasiticus and Schizosaccharomyces pombe nmt1 gene products, which are involved in thiamine biosynthesis and are strongly repressed by thiamine.	Thiamine	187-195	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	93-97
7548453-1	1995	The indirect estimation of thiamine levels in human blood by measuring thiamine pyrophosphate effect on erythrocyte transketolase activity is the method of choice in most clinical laboratories.	Thiamine	27-35	transketolase	Homo sapiens	116-129
8574774-0	1995	Intestinal alkaline phosphatase can transphosphorylate thiamin to thiamin monophosphate during intestinal transport in the rat.	Thiamine	55-62	intestinal-type alkaline phosphatase	Bos taurus	0-31
7722187-6	1995	MAIN OUTCOME MEASURES: Thiamin status was assessed biochemically by in vitro erythrocyte transketolase activity assay.	Thiamine	23-30	transketolase	Homo sapiens	89-102
7606469-4	1995	In the current study, we examined APP and A beta immunoreactivity in the brains of thiamine-deficient rats.	Thiamine	83-91	amyloid beta precursor protein	Rattus norvegicus	42-48
8574774-1	1995	Intestinal alkaline phosphatase (IAP) purified from calf intestine and IAP present in the brush border membrane of rat small intestine effectively transphosphorylated thiamin (T) to thiamin monophosphate (TMP) using Na2-beta-glycerophosphate or Na2-creatine phosphate as phosphate donors at pH 8.5.	Thiamine	167-174	intestinal-type alkaline phosphatase	Bos taurus	0-31
8574774-1	1995	Intestinal alkaline phosphatase (IAP) purified from calf intestine and IAP present in the brush border membrane of rat small intestine effectively transphosphorylated thiamin (T) to thiamin monophosphate (TMP) using Na2-beta-glycerophosphate or Na2-creatine phosphate as phosphate donors at pH 8.5.	Thiamine	167-174	intestinal-type alkaline phosphatase	Bos taurus	33-36
8574774-1	1995	Intestinal alkaline phosphatase (IAP) purified from calf intestine and IAP present in the brush border membrane of rat small intestine effectively transphosphorylated thiamin (T) to thiamin monophosphate (TMP) using Na2-beta-glycerophosphate or Na2-creatine phosphate as phosphate donors at pH 8.5.	Thiamine	167-174	intestinal-type alkaline phosphatase	Bos taurus	71-74
7614549-6	1995	Upon de-repression of the nmt1 promoter by removing thiamine from the medium, the rate of appearance of Leu- was increased.	Thiamine	52-60	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	26-30
7861245-0	1995	The thiamine-dependent hysteretic behavior of human transketolase: implications for thiamine deficiency.	Thiamine	4-12	transketolase	Homo sapiens	52-65
7861245-0	1995	The thiamine-dependent hysteretic behavior of human transketolase: implications for thiamine deficiency.	Thiamine	84-92	transketolase	Homo sapiens	52-65
7861245-6	1995	Moreover, at low levels of thiamine, the rate of the transition was different between fibroblast- and lymphoblast-derived transketolase.	Thiamine	27-35	transketolase	Homo sapiens	122-135
7861245-7	1995	The substantial lag in formation of active holoenzyme and the findings of interindividual variation and cell type variation in the lag period suggest mechanisms for the loss of transketolase activity during thiamine deficiency and may explain, at least in part, the differential sensitivity to deficiency demonstrated by tissues and individuals.	Thiamine	207-215	transketolase	Homo sapiens	177-190
7674851-0	1995	MRI demonstration of impairment of the blood-CSF barrier by glucose administration to the thiamin-deficient rat brain.	Thiamine	90-97	colony stimulating factor 2	Rattus norvegicus	45-48
7674851-2	1995	The period of the onset of this blood-CSF or blood-brain barrier dysfunction coincides with our previous observations of accumulation of glutamate or glutamate derivatives following an equivalent glucose load under identical conditions of thiamin deficiency, consistent with a relationship between these two observations.	Thiamine	239-246	colony stimulating factor 2	Rattus norvegicus	38-41
7917868-3	1994	Thiamine and riboflavin were assessed by the activation of erythrocyte transketolase and erythrocyte glutathione reductase, respectively.	Thiamine	0-8	transketolase	Homo sapiens	71-84
7982968-7	1994	Gene disruption demonstrated that the thi6 null strain is auxotrophic for thiamin, indicating that the THI6 protein is essential for thiamin synthesis in yeast.	Thiamine	74-81	bifunctional hydroxyethylthiazole kinase/thiamine-phosphate diphosphorylase	Saccharomyces cerevisiae S288C	38-42
7982968-7	1994	Gene disruption demonstrated that the thi6 null strain is auxotrophic for thiamin, indicating that the THI6 protein is essential for thiamin synthesis in yeast.	Thiamine	74-81	bifunctional hydroxyethylthiazole kinase/thiamine-phosphate diphosphorylase	Saccharomyces cerevisiae S288C	103-107
7982968-7	1994	Gene disruption demonstrated that the thi6 null strain is auxotrophic for thiamin, indicating that the THI6 protein is essential for thiamin synthesis in yeast.	Thiamine	133-140	bifunctional hydroxyethylthiazole kinase/thiamine-phosphate diphosphorylase	Saccharomyces cerevisiae S288C	38-42
7982968-7	1994	Gene disruption demonstrated that the thi6 null strain is auxotrophic for thiamin, indicating that the THI6 protein is essential for thiamin synthesis in yeast.	Thiamine	133-140	bifunctional hydroxyethylthiazole kinase/thiamine-phosphate diphosphorylase	Saccharomyces cerevisiae S288C	103-107
7982968-8	1994	A recently isolated thi6 mutant, thi6-3, bearing a replacement of Glu370 by Lys370, showed a decrease in only Th-kinase activity, proving that the THI6 gene of S. cerevisiae encodes a structural gene of the thiamin biosynthetic bifunctional enzyme.	Thiamine	207-214	bifunctional hydroxyethylthiazole kinase/thiamine-phosphate diphosphorylase	Saccharomyces cerevisiae S288C	20-24
7982968-8	1994	A recently isolated thi6 mutant, thi6-3, bearing a replacement of Glu370 by Lys370, showed a decrease in only Th-kinase activity, proving that the THI6 gene of S. cerevisiae encodes a structural gene of the thiamin biosynthetic bifunctional enzyme.	Thiamine	207-214	bifunctional hydroxyethylthiazole kinase/thiamine-phosphate diphosphorylase	Saccharomyces cerevisiae S288C	33-37
7982968-8	1994	A recently isolated thi6 mutant, thi6-3, bearing a replacement of Glu370 by Lys370, showed a decrease in only Th-kinase activity, proving that the THI6 gene of S. cerevisiae encodes a structural gene of the thiamin biosynthetic bifunctional enzyme.	Thiamine	207-214	bifunctional hydroxyethylthiazole kinase/thiamine-phosphate diphosphorylase	Saccharomyces cerevisiae S288C	147-151
7982968-11	1994	Northern blot analysis demonstrated that THI6 gene expression is regulated at the mRNA level by intracellular thiamin pyrophosphate, a coenzyme form of thiamin, and that it requires the positive regulatory factors encoded by the THI2 and THI3 genes.	Thiamine	110-117	bifunctional hydroxyethylthiazole kinase/thiamine-phosphate diphosphorylase	Saccharomyces cerevisiae S288C	41-45
8088540-1	1994	Our previous genetic data indicate that the product of the Schizosaccharomyces pombe thi1 gene acts as an activator of several thiamine-repressible genes which are involved in the control of thiamine metabolism [Schweingruber et al., Genetics 130 (1992) 445-449; Zurlinden and Schweingruber, Gene 117 (1992) 141-143].	Thiamine	127-135	acetolactate synthase catalytic subunit	Saccharomyces cerevisiae S288C	85-89
8088540-1	1994	Our previous genetic data indicate that the product of the Schizosaccharomyces pombe thi1 gene acts as an activator of several thiamine-repressible genes which are involved in the control of thiamine metabolism [Schweingruber et al., Genetics 130 (1992) 445-449; Zurlinden and Schweingruber, Gene 117 (1992) 141-143].	Thiamine	191-199	acetolactate synthase catalytic subunit	Saccharomyces cerevisiae S288C	85-89
8088540-3	1994	We, therefore, suggest that the thi1-encoded protein binds to upstream activator sequences of thiamine-repressible genes.	Thiamine	94-102	acetolactate synthase catalytic subunit	Saccharomyces cerevisiae S288C	32-36
7917868-3	1994	Thiamine and riboflavin were assessed by the activation of erythrocyte transketolase and erythrocyte glutathione reductase, respectively.	Thiamine	0-8	glutathione-disulfide reductase	Homo sapiens	101-122
8054263-0	1994	Effects of magnesium, high energy phosphates, piracetam and thiamin on erythrocyte transketolase.	Thiamine	60-67	transketolase	Homo sapiens	83-96
8163491-1	1994	The nmt1+ gene of the fission yeast Schizosaccharomyces pombe is subject to transcriptional repression mediated by thiamine.	Thiamine	115-123	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	4-8
7941734-0	1994	Regulation of THI4 (MOL1), a thiamine-biosynthetic gene of Saccharomyces cerevisiae.	Thiamine	29-37	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	14-18
7941734-0	1994	Regulation of THI4 (MOL1), a thiamine-biosynthetic gene of Saccharomyces cerevisiae.	Thiamine	29-37	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	20-24
7941734-1	1994	THI4, a Saccharomyces cerevisiae gene originally identified as a result of transient expression in molasses medium and named MOL1 is regulated by thiamine.	Thiamine	146-154	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	0-4
7941734-1	1994	THI4, a Saccharomyces cerevisiae gene originally identified as a result of transient expression in molasses medium and named MOL1 is regulated by thiamine.	Thiamine	146-154	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	125-129
7941734-2	1994	Using a THI4 promoter-lacZ fusion on a centromeric yeast vector, we have shown that the THI4 is completely repressed throughout batch culture by thiamine at a concentration around 1 microM, but shows high level constitutive expression in thiamine-free medium.	Thiamine	145-153	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	8-12
7941734-2	1994	Using a THI4 promoter-lacZ fusion on a centromeric yeast vector, we have shown that the THI4 is completely repressed throughout batch culture by thiamine at a concentration around 1 microM, but shows high level constitutive expression in thiamine-free medium.	Thiamine	145-153	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	88-92
7941734-2	1994	Using a THI4 promoter-lacZ fusion on a centromeric yeast vector, we have shown that the THI4 is completely repressed throughout batch culture by thiamine at a concentration around 1 microM, but shows high level constitutive expression in thiamine-free medium.	Thiamine	238-246	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	88-92
7941734-7	1994	After transfer from repressing to non-repressing medium, THI4 becomes induced when the intracellular concentration of thiamine falls to 20 pmol/10(7) cells.	Thiamine	118-126	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	57-61
7941734-8	1994	A thi4::URA3 disruption strain is auxotrophic for thiamine, but can grow in the presence of hydroxyethyl thiazole, indicating that the gene product is involved in the biosynthetic pathway leading to the formation of the thiazole precursor of thiamine.	Thiamine	50-58	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	2-6
7941734-8	1994	A thi4::URA3 disruption strain is auxotrophic for thiamine, but can grow in the presence of hydroxyethyl thiazole, indicating that the gene product is involved in the biosynthetic pathway leading to the formation of the thiazole precursor of thiamine.	Thiamine	242-250	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	2-6
8974347-3	1994	We have investigated the interactions of the thiamine-utilizing enzyme transketolase [Tk], derived from human fibroblasts, lymphoblasts, and various brain regions, with its cofactor, thiamine pyrophosphate [TPP], in an attempt to elucidate the molecular basis of selective brain damage in alcoholism-associated thiamine deficiency.	Thiamine	45-53	transketolase	Homo sapiens	71-84
8974347-3	1994	We have investigated the interactions of the thiamine-utilizing enzyme transketolase [Tk], derived from human fibroblasts, lymphoblasts, and various brain regions, with its cofactor, thiamine pyrophosphate [TPP], in an attempt to elucidate the molecular basis of selective brain damage in alcoholism-associated thiamine deficiency.	Thiamine	45-53	transketolase	Homo sapiens	86-88
8974347-3	1994	We have investigated the interactions of the thiamine-utilizing enzyme transketolase [Tk], derived from human fibroblasts, lymphoblasts, and various brain regions, with its cofactor, thiamine pyrophosphate [TPP], in an attempt to elucidate the molecular basis of selective brain damage in alcoholism-associated thiamine deficiency.	Thiamine	183-191	transketolase	Homo sapiens	71-84
8974347-3	1994	We have investigated the interactions of the thiamine-utilizing enzyme transketolase [Tk], derived from human fibroblasts, lymphoblasts, and various brain regions, with its cofactor, thiamine pyrophosphate [TPP], in an attempt to elucidate the molecular basis of selective brain damage in alcoholism-associated thiamine deficiency.	Thiamine	183-191	transketolase	Homo sapiens	86-88
8192530-0	1994	Recombinant human erythropoietin administration improves thiamine content in blood and erythrocytes transketolase activity in pre-dialyzed patients.	Thiamine	57-65	erythropoietin	Homo sapiens	18-32
8394635-5	1993	After thiamine therapy was ceased an increase in insulin requirement was observed and macrocytic anemia developed again.	Thiamine	6-14	insulin	Homo sapiens	49-56
8263044-1	1994	Quantitative receptor autoradiography was used to evaluate the density of high-affinity binding sites for the "peripheral-type" benzodiazepine receptor (PTBR) ligand [3H]PK11195 in brain regions of the rat at different stages of pyrithiamine-induced thiamine deficiency encephalopathy, an experimental model of the Wernicke-Korsakoff syndrome (WKS).	Thiamine	233-241	translocator protein	Rattus norvegicus	153-157
8263044-6	1994	Increased densities of binding sites for the PTBR ligand probably reflect glial proliferation and are consistent with an excitotoxic mechanism in the pathogenesis of neuronal cell loss in thiamine deficiency encephalopathy.	Thiamine	188-196	translocator protein	Rattus norvegicus	45-49
7903547-3	1993	The results are consistent with a metabolic block at the reaction catalyzed by the thiamin dependent enzyme alpha-keto glutarate dehydrogenase soon after the onset of neurological symptoms of thiamin deficiency, and a further block at pyruvate dehydrogenase arising late in the course of thiamin deficiency.	Thiamine	83-90	oxoglutarate dehydrogenase	Rattus norvegicus	108-142
7903547-3	1993	The results are consistent with a metabolic block at the reaction catalyzed by the thiamin dependent enzyme alpha-keto glutarate dehydrogenase soon after the onset of neurological symptoms of thiamin deficiency, and a further block at pyruvate dehydrogenase arising late in the course of thiamin deficiency.	Thiamine	192-199	oxoglutarate dehydrogenase	Rattus norvegicus	108-142
8263044-0	1994	Increased densities of binding sites for the "peripheral-type" benzodiazepine receptor ligand [3H]PK11195 in vulnerable regions of the rat brain in thiamine deficiency encephalopathy.	Thiamine	148-156	translocator protein	Rattus norvegicus	45-86
7903021-6	1993	The highest levels of total intake (from food and supplements) of vitamins C and B1 and niacin were associated with a significantly decreased progression rate to AIDS: vitamin C (relative hazard (RH) = 0.55, 95% confidence interval (CI) 0.34-0.91), vitamin B1 (RH = 0.60, 95% CI 0.36-0.98), and niacin (RH = 0.52, 95% CI 0.31-0.86).	Thiamine	249-259	membrane spanning 4-domains A1	Homo sapiens	75-83
8229066-0	1993	Proto-oncogene c-fos induction in thiamine-deficient encephalopathy.	Thiamine	34-42	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-20
8229066-3	1993	Induction of proto-oncogene c-fos expression, often related to seizure activity, has been detected in the brains of thiamine-deficient rats by means of Northern blot analysis and in situ hybridization.	Thiamine	116-124	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-33
8394343-4	1993	We have isolated a DNA fragment carrying the THI80 gene from a yeast genomic library by its ability to complement constitutive synthesis of the thiamin-repressible acid phosphatase, encoded by the PHO3 gene, of thi80 mutant cells.	Thiamine	144-151	thiamine diphosphokinase	Saccharomyces cerevisiae S288C	45-50
8394343-4	1993	We have isolated a DNA fragment carrying the THI80 gene from a yeast genomic library by its ability to complement constitutive synthesis of the thiamin-repressible acid phosphatase, encoded by the PHO3 gene, of thi80 mutant cells.	Thiamine	144-151	acid phosphatase PHO3	Saccharomyces cerevisiae S288C	197-201
8394343-4	1993	We have isolated a DNA fragment carrying the THI80 gene from a yeast genomic library by its ability to complement constitutive synthesis of the thiamin-repressible acid phosphatase, encoded by the PHO3 gene, of thi80 mutant cells.	Thiamine	144-151	thiamine diphosphokinase	Saccharomyces cerevisiae S288C	211-216
8419340-2	1993	Since the syndrome has been shown to be directly related to thiamine deficiency, it has been hypothesized that such transketolase variants may represent a genetic predisposition to the development of this syndrome.	Thiamine	60-68	transketolase	Homo sapiens	116-129
8315945-6	1993	The activity of the thiamine-dependent enzyme transketolase in erythrocytes (ETKo) was insufficient in 35% and marginal in 21% of the patients, while whole blood thiamine determined simultaneously in 10 of the ETKo-deficient patients was within the normal range.	Thiamine	20-28	transketolase	Homo sapiens	46-59
1332781-7	1992	After incubation of the purified TPK and AK1 with 20 microM thiamin in the presence of ATP, ADP and Mg2+ at 37 degrees C for 48 h, the amounts of TDP and TTP synthesized were 465 and 54.0 pmol/250 microliters reaction mixture, respectively.	Thiamine	60-67	adenylate kinase 1	Homo sapiens	41-44
1332781-9	1992	These results indicate that thiamin is converted to TDP by TPK and, subsequently, to TTP by AK1 in human RBC.	Thiamine	28-35	adenylate kinase 1	Homo sapiens	92-95
1624458-4	1992	These results suggest that thiamine metabolism in S. cerevisiae is subject to two positive regulatory genes, THI2 (PHO6) and THI3.	Thiamine	27-35	Thi2p	Saccharomyces cerevisiae S288C	109-113
1452946-1	1992	In 20 patients, we investigated the effect of interleukin-2 (IL-2) treatment during adoptive immunotherapy for various cancers on circulating levels of: thiamin; biotin; folate; pantothenate; riboflavin; nicotinate; vitamins A, B6, B12 and E; carotenes; free and total cholines; inositol; and free and total carnitines.	Thiamine	153-160	interleukin 2	Homo sapiens	46-59
1452946-1	1992	In 20 patients, we investigated the effect of interleukin-2 (IL-2) treatment during adoptive immunotherapy for various cancers on circulating levels of: thiamin; biotin; folate; pantothenate; riboflavin; nicotinate; vitamins A, B6, B12 and E; carotenes; free and total cholines; inositol; and free and total carnitines.	Thiamine	153-160	interleukin 2	Homo sapiens	61-65
1624458-0	1992	A positive regulatory gene, THI3, is required for thiamine metabolism in Saccharomyces cerevisiae.	Thiamine	50-58	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	28-32
1624458-1	1992	We have isolated a thiamine auxotrophic mutant carrying a recessive mutation which lacks the positive regulatory gene, THI3, which differs in the regulation of thiamine transport from the THI2 (PHO6) gene described previously (Y. Kawasaki, K. Nosaka, Y. Kaneko, H. Nishimura, and A. Iwashima, J. Bacteriol.	Thiamine	19-27	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	119-123
1624458-1	1992	We have isolated a thiamine auxotrophic mutant carrying a recessive mutation which lacks the positive regulatory gene, THI3, which differs in the regulation of thiamine transport from the THI2 (PHO6) gene described previously (Y. Kawasaki, K. Nosaka, Y. Kaneko, H. Nishimura, and A. Iwashima, J. Bacteriol.	Thiamine	19-27	Thi2p	Saccharomyces cerevisiae S288C	188-192
1624458-1	1992	We have isolated a thiamine auxotrophic mutant carrying a recessive mutation which lacks the positive regulatory gene, THI3, which differs in the regulation of thiamine transport from the THI2 (PHO6) gene described previously (Y. Kawasaki, K. Nosaka, Y. Kaneko, H. Nishimura, and A. Iwashima, J. Bacteriol.	Thiamine	19-27	Thi2p	Saccharomyces cerevisiae S288C	194-198
1624458-1	1992	We have isolated a thiamine auxotrophic mutant carrying a recessive mutation which lacks the positive regulatory gene, THI3, which differs in the regulation of thiamine transport from the THI2 (PHO6) gene described previously (Y. Kawasaki, K. Nosaka, Y. Kaneko, H. Nishimura, and A. Iwashima, J. Bacteriol.	Thiamine	160-168	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	119-123
1624458-1	1992	We have isolated a thiamine auxotrophic mutant carrying a recessive mutation which lacks the positive regulatory gene, THI3, which differs in the regulation of thiamine transport from the THI2 (PHO6) gene described previously (Y. Kawasaki, K. Nosaka, Y. Kaneko, H. Nishimura, and A. Iwashima, J. Bacteriol.	Thiamine	160-168	Thi2p	Saccharomyces cerevisiae S288C	188-192
1624458-1	1992	We have isolated a thiamine auxotrophic mutant carrying a recessive mutation which lacks the positive regulatory gene, THI3, which differs in the regulation of thiamine transport from the THI2 (PHO6) gene described previously (Y. Kawasaki, K. Nosaka, Y. Kaneko, H. Nishimura, and A. Iwashima, J. Bacteriol.	Thiamine	160-168	Thi2p	Saccharomyces cerevisiae S288C	194-198
1624458-3	1992	The mutant (thi3) had a markedly reduced thiamine transport system as well as reduced activity of thiamine-repressible acid phosphatase and of several enzymes for thiamine synthesis from 2-methyl-4-amino-5-hydroxymethylpyrimidine and 4-methyl-5-beta-hydroxyethylthiazole.	Thiamine	41-49	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	12-16
1624458-3	1992	The mutant (thi3) had a markedly reduced thiamine transport system as well as reduced activity of thiamine-repressible acid phosphatase and of several enzymes for thiamine synthesis from 2-methyl-4-amino-5-hydroxymethylpyrimidine and 4-methyl-5-beta-hydroxyethylthiazole.	Thiamine	98-106	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	12-16
1624458-3	1992	The mutant (thi3) had a markedly reduced thiamine transport system as well as reduced activity of thiamine-repressible acid phosphatase and of several enzymes for thiamine synthesis from 2-methyl-4-amino-5-hydroxymethylpyrimidine and 4-methyl-5-beta-hydroxyethylthiazole.	Thiamine	98-106	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	12-16
1624458-4	1992	These results suggest that thiamine metabolism in S. cerevisiae is subject to two positive regulatory genes, THI2 (PHO6) and THI3.	Thiamine	27-35	Thi2p	Saccharomyces cerevisiae S288C	115-119
1624458-4	1992	These results suggest that thiamine metabolism in S. cerevisiae is subject to two positive regulatory genes, THI2 (PHO6) and THI3.	Thiamine	27-35	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	125-129
1624458-5	1992	We have also isolated a hybrid plasmid, pTTR1, containing a 6.2-kb DNA fragment from an S. cerevisiae genomic library which complements thiamine auxotrophy in the thi3 mutant.	Thiamine	136-144	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	163-167
1624458-7	1992	Complementation of the activities for thiamine metabolism in the thi3 mutant transformed by some plasmids with the THI3 gene was also examined.	Thiamine	38-46	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	65-69
1624458-7	1992	Complementation of the activities for thiamine metabolism in the thi3 mutant transformed by some plasmids with the THI3 gene was also examined.	Thiamine	38-46	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	115-119
1550204-2	1992	EGF induced dose-dependent [3H]Thd uptake (P less than 0.001); after 10(-9) M EGF, DNA synthesis rate peaked at 24 h, averaging 77% of the response to 10% FCS, and then declined steeply with nadir at 48-60 h. Unexpectedly, EGF failed to induce cell proliferation in the first 4 days, leaving this initial burst of DNA synthesis (12-60 h) uncoupled from cell division.	Thiamine	31-34	epidermal growth factor	Homo sapiens	0-3
1551422-1	1992	A thi2(pho6) mutant of Saccharomyces cerevisiae, defective in the expression of structural genes for thiamin-repressible acid phosphatase and enzymes involved in thiamin biosynthesis, was found to retain sufficient thiamin transport activity.	Thiamine	162-169	Thi2p	Saccharomyces cerevisiae S288C	2-6
1551422-1	1992	A thi2(pho6) mutant of Saccharomyces cerevisiae, defective in the expression of structural genes for thiamin-repressible acid phosphatase and enzymes involved in thiamin biosynthesis, was found to retain sufficient thiamin transport activity.	Thiamine	162-169	Thi2p	Saccharomyces cerevisiae S288C	7-11
1551422-0	1992	Cloning and characteristics of a positive regulatory gene, THI2 (PHO6), of thiamin biosynthesis in Saccharomyces cerevisiae.	Thiamine	75-82	Thi2p	Saccharomyces cerevisiae S288C	59-63
1551422-1	1992	A thi2(pho6) mutant of Saccharomyces cerevisiae, defective in the expression of structural genes for thiamin-repressible acid phosphatase and enzymes involved in thiamin biosynthesis, was found to retain sufficient thiamin transport activity.	Thiamine	162-169	Thi2p	Saccharomyces cerevisiae S288C	2-6
1551422-0	1992	Cloning and characteristics of a positive regulatory gene, THI2 (PHO6), of thiamin biosynthesis in Saccharomyces cerevisiae.	Thiamine	75-82	Thi2p	Saccharomyces cerevisiae S288C	65-69
1551422-1	1992	A thi2(pho6) mutant of Saccharomyces cerevisiae, defective in the expression of structural genes for thiamin-repressible acid phosphatase and enzymes involved in thiamin biosynthesis, was found to retain sufficient thiamin transport activity.	Thiamine	162-169	Thi2p	Saccharomyces cerevisiae S288C	7-11
1551422-1	1992	A thi2(pho6) mutant of Saccharomyces cerevisiae, defective in the expression of structural genes for thiamin-repressible acid phosphatase and enzymes involved in thiamin biosynthesis, was found to retain sufficient thiamin transport activity.	Thiamine	101-108	Thi2p	Saccharomyces cerevisiae S288C	2-6
1551422-1	1992	A thi2(pho6) mutant of Saccharomyces cerevisiae, defective in the expression of structural genes for thiamin-repressible acid phosphatase and enzymes involved in thiamin biosynthesis, was found to retain sufficient thiamin transport activity.	Thiamine	101-108	Thi2p	Saccharomyces cerevisiae S288C	7-11
1551422-5	1992	Complementation of the enzyme activities for thiamin metabolism in the thi2(pho6) mutant transformed by some plasmids with the TH12(PHO6) gene was also examined.	Thiamine	45-52	Thi2p	Saccharomyces cerevisiae S288C	71-75
1551422-5	1992	Complementation of the enzyme activities for thiamin metabolism in the thi2(pho6) mutant transformed by some plasmids with the TH12(PHO6) gene was also examined.	Thiamine	45-52	Thi2p	Saccharomyces cerevisiae S288C	76-80
1551422-5	1992	Complementation of the enzyme activities for thiamin metabolism in the thi2(pho6) mutant transformed by some plasmids with the TH12(PHO6) gene was also examined.	Thiamine	45-52	Thi2p	Saccharomyces cerevisiae S288C	132-136
1297775-8	1992	Further studies of thiamin-dependent mechanisms in DAT seem justified.	Thiamine	19-26	solute carrier family 6 member 3	Homo sapiens	51-54
1341235-4	1992	H322a, H226b, H460a, and H596b cells showed stimulated [3H]thymidine (Thd) uptake in response to TGF-alpha.	Thiamine	70-73	transforming growth factor alpha	Homo sapiens	97-106
1341235-8	1992	The anti-TGF-alpha monoclonal antibody AB-3 inhibited the uptake of [3H]Thd by proliferating H322a and H226b cells but not H460a and H596b cells.	Thiamine	72-75	transforming growth factor alpha	Homo sapiens	9-18
8577140-3	1991	Vitamin B1 deficiency (hydroxy thiamine in drinking water at a dose of 2 mg/kg body weight for 15 days) led to a substantial decrease of TK in blood, AlAT and AsAT in the spleen; it diminished AsAT and increased AlAT in the thymus.	Thiamine	0-10	transketolase	Rattus norvegicus	137-139
1807869-0	1991	In thiamine deficiency, activation of erythrocyte transketolase by thiamine in vivo exceeds activation by cofactor in vitro.	Thiamine	3-11	transketolase	Homo sapiens	50-63
1807869-0	1991	In thiamine deficiency, activation of erythrocyte transketolase by thiamine in vivo exceeds activation by cofactor in vitro.	Thiamine	67-75	transketolase	Homo sapiens	50-63
1807869-1	1991	In 60 thiamine deficient patients, the mean erythrocyte transketolase activity after activation by thiamine diphosphate cofactor in vitro, representing the apparent sum of holoenzyme and apoenzyme activities, was 0.609 (SD 0.166) U/g Hb before thiamine therapy and rose to 0.772 (SD 0.152) U/g Hb immediately after the administration of thiamine to the patients.	Thiamine	6-14	transketolase	Homo sapiens	56-69
1807869-1	1991	In 60 thiamine deficient patients, the mean erythrocyte transketolase activity after activation by thiamine diphosphate cofactor in vitro, representing the apparent sum of holoenzyme and apoenzyme activities, was 0.609 (SD 0.166) U/g Hb before thiamine therapy and rose to 0.772 (SD 0.152) U/g Hb immediately after the administration of thiamine to the patients.	Thiamine	99-107	transketolase	Homo sapiens	56-69
1807869-1	1991	In 60 thiamine deficient patients, the mean erythrocyte transketolase activity after activation by thiamine diphosphate cofactor in vitro, representing the apparent sum of holoenzyme and apoenzyme activities, was 0.609 (SD 0.166) U/g Hb before thiamine therapy and rose to 0.772 (SD 0.152) U/g Hb immediately after the administration of thiamine to the patients.	Thiamine	99-107	transketolase	Homo sapiens	56-69
1807869-2	1991	The difference between these values, 0.163 (SD 0.130) U/g, is the mean activity of transketolase protein which can be activated by thiamine in vivo but not by thiamine diphosphate in vitro.	Thiamine	131-139	transketolase	Homo sapiens	83-96
8577140-3	1991	Vitamin B1 deficiency (hydroxy thiamine in drinking water at a dose of 2 mg/kg body weight for 15 days) led to a substantial decrease of TK in blood, AlAT and AsAT in the spleen; it diminished AsAT and increased AlAT in the thymus.	Thiamine	0-10	glutamic--pyruvic transaminase	Rattus norvegicus	150-154
8577140-3	1991	Vitamin B1 deficiency (hydroxy thiamine in drinking water at a dose of 2 mg/kg body weight for 15 days) led to a substantial decrease of TK in blood, AlAT and AsAT in the spleen; it diminished AsAT and increased AlAT in the thymus.	Thiamine	0-10	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	159-163
8577140-3	1991	Vitamin B1 deficiency (hydroxy thiamine in drinking water at a dose of 2 mg/kg body weight for 15 days) led to a substantial decrease of TK in blood, AlAT and AsAT in the spleen; it diminished AsAT and increased AlAT in the thymus.	Thiamine	0-10	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	193-197
8577140-3	1991	Vitamin B1 deficiency (hydroxy thiamine in drinking water at a dose of 2 mg/kg body weight for 15 days) led to a substantial decrease of TK in blood, AlAT and AsAT in the spleen; it diminished AsAT and increased AlAT in the thymus.	Thiamine	0-10	glutamic--pyruvic transaminase	Rattus norvegicus	212-216
8577140-4	1991	Combined exposure to hypokinesia and vitamin B1 deficiency caused a more marked decrease of the weight of lymph organs, a significant loss of body weight, an increase of DNA in the thymus and spleen, and an increase of TK, met-tRNA-synthetase and AlAT in the thymus.	Thiamine	37-47	transketolase	Rattus norvegicus	219-221
8577140-4	1991	Combined exposure to hypokinesia and vitamin B1 deficiency caused a more marked decrease of the weight of lymph organs, a significant loss of body weight, an increase of DNA in the thymus and spleen, and an increase of TK, met-tRNA-synthetase and AlAT in the thymus.	Thiamine	37-47	glutamic--pyruvic transaminase	Rattus norvegicus	247-251
2070293-1	1991	Thiamine status was evaluated using the erythrocyte transketolase activation assay in 20 alcoholic patients admitted on a voluntary basis to a Detoxification Unit.	Thiamine	0-8	transketolase	Homo sapiens	52-65
1685763-4	1991	Possible explanations for the decreased "neurotransmitter pool" of glutamate in thiamine-deficient rat brain include decreased synthesis of glutamate as a result of decreased activities of the thiamine-dependent enzyme alpha-ketoglutarate dehydrogenase or increased release of glutamate per se.	Thiamine	80-88	oxoglutarate dehydrogenase	Rattus norvegicus	219-252
1685763-4	1991	Possible explanations for the decreased "neurotransmitter pool" of glutamate in thiamine-deficient rat brain include decreased synthesis of glutamate as a result of decreased activities of the thiamine-dependent enzyme alpha-ketoglutarate dehydrogenase or increased release of glutamate per se.	Thiamine	193-201	oxoglutarate dehydrogenase	Rattus norvegicus	219-252
1778246-1	1991	Metabolites have been studied for their effect (sodium succinate, thiamine, riboflavin) on the pentosophosphate pathways and glutathione reductase.	Thiamine	66-74	glutathione-disulfide reductase	Homo sapiens	125-146
1855320-1	1991	We report the case of a patient with terminal renal disease on chronic hemodialysis who developed acute thiamine deficiency as confirmed by erythrocyte transketolase determinations.	Thiamine	104-112	transketolase	Homo sapiens	152-165
1833883-3	1991	Use of alpha-tocopherol and thiamine normalizes LPO level and induces elevation of GR activity.	Thiamine	28-36	glutathione-disulfide reductase	Rattus norvegicus	83-85
1849514-0	1991	A constitutive thiamine metabolism mutation, thi80, causing reduced thiamine pyrophosphokinase activity in Saccharomyces cerevisiae.	Thiamine	15-23	thiamine diphosphokinase	Saccharomyces cerevisiae S288C	45-50
1849514-1	1991	We identified a strain carrying a recessive constitutive mutation (thi80-1) with an altered thiamine transport system, thiamine-repressible acid phosphatase, and several enzymes of thiamine synthesis from 2-methyl-4-amino-5-hydroxymethylpyrimidine and 4-methyl-5-beta-hydroxyethylthiazole.	Thiamine	92-100	thiamine diphosphokinase	Saccharomyces cerevisiae S288C	67-72
1849514-1	1991	We identified a strain carrying a recessive constitutive mutation (thi80-1) with an altered thiamine transport system, thiamine-repressible acid phosphatase, and several enzymes of thiamine synthesis from 2-methyl-4-amino-5-hydroxymethylpyrimidine and 4-methyl-5-beta-hydroxyethylthiazole.	Thiamine	119-127	thiamine diphosphokinase	Saccharomyces cerevisiae S288C	67-72
1849514-1	1991	We identified a strain carrying a recessive constitutive mutation (thi80-1) with an altered thiamine transport system, thiamine-repressible acid phosphatase, and several enzymes of thiamine synthesis from 2-methyl-4-amino-5-hydroxymethylpyrimidine and 4-methyl-5-beta-hydroxyethylthiazole.	Thiamine	119-127	thiamine diphosphokinase	Saccharomyces cerevisiae S288C	67-72
1705463-2	1991	Alterations in CSF amine metabolite levels were related primarily to PHT intoxication, and low CSF folate and thiamine levels, but not to length of treatment or CNS atrophy.	Thiamine	110-118	colony stimulating factor 2	Homo sapiens	15-18
1705463-2	1991	Alterations in CSF amine metabolite levels were related primarily to PHT intoxication, and low CSF folate and thiamine levels, but not to length of treatment or CNS atrophy.	Thiamine	110-118	colony stimulating factor 2	Homo sapiens	95-98
1705463-4	1991	Low folate levels were associated with decreased CSF 5HIAA and homovanillic acid, while low thiamine levels were associated with decreased CSF 5HIAA and 3-methyoxy-4-hydroxyphenylethylene glycol.	Thiamine	92-100	colony stimulating factor 2	Homo sapiens	139-142
2087217-1	1990	Activities of thiamine-dependent enzymes [pyruvate dehydrogenase (PDHC), alpha-ketoglutarate dehydrogenase (alpha KGDH), and transketolase (TK)] were measured in autopsied samples of temporal cortex from six patients with Alzheimer"s disease and from eight age-matched control subjects who were free from neurological or psychiatric diseases.	Thiamine	14-22	transketolase	Homo sapiens	140-142
1650797-5	1991	Thalamic beta-endorphin in controls was inversely correlated with thiamin in frontal white matter, frontal cortex, parietal white matter and parietal cortex, while beta-endorphin in the hypothalamus of patients was inversely correlated with thiamin in frontal cortex, parietal white matter, thalamus and brainstem.	Thiamine	66-73	proopiomelanocortin	Homo sapiens	9-23
1650797-5	1991	Thalamic beta-endorphin in controls was inversely correlated with thiamin in frontal white matter, frontal cortex, parietal white matter and parietal cortex, while beta-endorphin in the hypothalamus of patients was inversely correlated with thiamin in frontal cortex, parietal white matter, thalamus and brainstem.	Thiamine	241-248	proopiomelanocortin	Homo sapiens	164-178
1851363-1	1991	In an effort to clarify the mechanism of pain accompanying thiamine deficiency, thiamine monophosphatase (TMPase) activity was demonstrated, by means of electron microscopic cytochemistry, in small ganglion cells in pyrithiamine-treated thiamine-deficient rats.	Thiamine	59-67	acid phosphatase 3	Rattus norvegicus	80-104
1851363-1	1991	In an effort to clarify the mechanism of pain accompanying thiamine deficiency, thiamine monophosphatase (TMPase) activity was demonstrated, by means of electron microscopic cytochemistry, in small ganglion cells in pyrithiamine-treated thiamine-deficient rats.	Thiamine	59-67	acid phosphatase 3	Rattus norvegicus	106-112
1851363-1	1991	In an effort to clarify the mechanism of pain accompanying thiamine deficiency, thiamine monophosphatase (TMPase) activity was demonstrated, by means of electron microscopic cytochemistry, in small ganglion cells in pyrithiamine-treated thiamine-deficient rats.	Thiamine	80-88	acid phosphatase 3	Rattus norvegicus	106-112
1851363-4	1991	These results indicate that thiamine deficiency causes a disturbance in the transportation and/or production of TMPase, which is an integral part of the synaptic transmission of the nociception impulses.	Thiamine	28-36	acid phosphatase 3	Rattus norvegicus	112-118
1813718-7	1991	As part of the pyruvate-dehydrogenase (PDH) complex, thiamine was capable of improving the life-threatening situation.	Thiamine	53-61	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	15-37
1813718-7	1991	As part of the pyruvate-dehydrogenase (PDH) complex, thiamine was capable of improving the life-threatening situation.	Thiamine	53-61	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	39-42
1984333-3	1991	On the contrary, transketolase activity in the liver correlated positively with concentration, and both transketolase activity and concentration were decreased in the thiamin-deficient groups.	Thiamine	167-174	transketolase	Rattus norvegicus	104-117
2406589-1	1990	Incubation of Escherichia coli AB1157 in a thiamine-deficient medium causes a large, time-dependent increase in resistance to UV-radiation (254 nm) and a fall in its UV-induced mutation frequency to histidine prototrophy which are abolished in its uvrA mutant, but only delayed in lon- and recA- cells.	Thiamine	43-51	putative ATP-dependent Lon protease	Escherichia coli	281-284
2170344-1	1990	A pho6 mutant of Saccharomyces cerevisiae, lacking a regulatory gene for the synthesis of periplasmic thiamine-repressible acid phosphatase activity, was found to be auxotrophic for thiamine.	Thiamine	102-110	Thi2p	Saccharomyces cerevisiae S288C	2-6
2170344-1	1990	A pho6 mutant of Saccharomyces cerevisiae, lacking a regulatory gene for the synthesis of periplasmic thiamine-repressible acid phosphatase activity, was found to be auxotrophic for thiamine.	Thiamine	182-190	Thi2p	Saccharomyces cerevisiae S288C	2-6
2170344-4	1990	These results suggest that thiamine synthesis in S. cerevisiae is subject to a positive regulatory gene, PHO6, whereas it is controlled negatively by the intracellular thiamine level.	Thiamine	27-35	Thi2p	Saccharomyces cerevisiae S288C	105-109
2385216-3	1990	In order to study the basis of this susceptibility, activities of the three thiamine-dependent enzymes [pyruvate dehydrogenase complex (PDHC), alpha-ketoglutarate dehydrogenase (alpha KGDH), and transketolase (TK)] were measured in homogenates of brain tissue from thiamine-deficient female rats and their offspring.	Thiamine	76-84	oxoglutarate dehydrogenase	Rattus norvegicus	143-176
2407294-1	1990	The enzymatic properties of acid phosphatase (orthophosphoric-monoester phosphohydrolase, EC 3.1.3.2) encoded by PHO3 gene in Saccharomyces cerevisiae, which is repressed by thiamin and has thiamin-binding activity at pH 5.0, were investigated to study physiological functions.	Thiamine	174-181	acid phosphatase PHO3	Saccharomyces cerevisiae S288C	113-117
2407294-1	1990	The enzymatic properties of acid phosphatase (orthophosphoric-monoester phosphohydrolase, EC 3.1.3.2) encoded by PHO3 gene in Saccharomyces cerevisiae, which is repressed by thiamin and has thiamin-binding activity at pH 5.0, were investigated to study physiological functions.	Thiamine	190-197	acid phosphatase PHO3	Saccharomyces cerevisiae S288C	113-117
2316528-5	1990	The deduced amino acid sequence of this subunit in the patients was identical to that in normal controls, suggesting that in the patients the thiamine-binding site is abnormal because of a mutation in the E1 beta subunit.	Thiamine	142-150	branched chain keto acid dehydrogenase E1 subunit beta	Homo sapiens	205-220
33146542-2	2021	Pancreatic acinar cells (PACs) import thiamin from circulation via specific carrier-mediated uptake that involves thiamin transporters-1 & -2 (THTR-1 & -2; products of SLC19A2 and SLC19A3, respectively).	Thiamine	38-45	solute carrier family 19 member 2	Homo sapiens	143-154
2369074-5	1990	Vitamin B1 deficiency of 4 weeks" duration could augment the activity of glycolate oxidase only, with no alterations in the glycolate dehydrogenase and lactate dehydrogenase levels.	Thiamine	0-10	hydroxyacid oxidase 1	Rattus norvegicus	73-90
33816400-1	2021	Background: Thiamine-responsive megaloblastic anemia syndrome (TRMA) is a rare autosomal recessive hereditary disease due to mutations in SLC19A2.	Thiamine	12-20	solute carrier family 19 member 2	Homo sapiens	138-145
2318357-8	1990	Thiamine status was assessed by determining red cell transketolase activity and, in a blinded manner, by recording the development of clinical signs known to be associated with thiamine deficiency.	Thiamine	0-8	transketolase	Rattus norvegicus	53-66
2318357-11	1990	Coadministration of thiamine substantially reduced evidence of thiamine deficiency and normalized transketolase activity.	Thiamine	20-28	transketolase	Rattus norvegicus	98-111
2318357-15	1990	We conclude that stimulation by DCA of thiamine-requiring enzymes may lead to depletion of total body thiamine stores and to both a fall in transketolase activity and an increase in oxalate accumulation in vivo.	Thiamine	39-47	transketolase	Rattus norvegicus	140-153
33146542-2	2021	Pancreatic acinar cells (PACs) import thiamin from circulation via specific carrier-mediated uptake that involves thiamin transporters-1 & -2 (THTR-1 & -2; products of SLC19A2 and SLC19A3, respectively).	Thiamine	38-45	solute carrier family 19 member 2	Homo sapiens	168-175
33146542-2	2021	Pancreatic acinar cells (PACs) import thiamin from circulation via specific carrier-mediated uptake that involves thiamin transporters-1 & -2 (THTR-1 & -2; products of SLC19A2 and SLC19A3, respectively).	Thiamine	38-45	solute carrier family 19 member 3	Homo sapiens	180-187
33146542-2	2021	Pancreatic acinar cells (PACs) import thiamin from circulation via specific carrier-mediated uptake that involves thiamin transporters-1 & -2 (THTR-1 & -2; products of SLC19A2 and SLC19A3, respectively).	Thiamine	114-121	solute carrier family 19 member 2	Homo sapiens	143-154
33146542-2	2021	Pancreatic acinar cells (PACs) import thiamin from circulation via specific carrier-mediated uptake that involves thiamin transporters-1 & -2 (THTR-1 & -2; products of SLC19A2 and SLC19A3, respectively).	Thiamine	114-121	solute carrier family 19 member 2	Homo sapiens	168-175
33146542-6	2021	Exposing hPACs and PAC 266-6 to pro-inflammatory cytokines (hyper IL-6, TNF-alpha, and IL-1beta) was found to lead to a significant inhibition in thiamin uptake.	Thiamine	146-153	interleukin 6	Homo sapiens	66-70
33146542-6	2021	Exposing hPACs and PAC 266-6 to pro-inflammatory cytokines (hyper IL-6, TNF-alpha, and IL-1beta) was found to lead to a significant inhibition in thiamin uptake.	Thiamine	146-153	tumor necrosis factor	Homo sapiens	72-81
33146542-6	2021	Exposing hPACs and PAC 266-6 to pro-inflammatory cytokines (hyper IL-6, TNF-alpha, and IL-1beta) was found to lead to a significant inhibition in thiamin uptake.	Thiamine	146-153	interleukin 1 alpha	Homo sapiens	87-95
33146542-7	2021	Focusing on hyper-IL-6 (which also inhibited thiamin uptake by primary mouse PACs), the inhibition in thiamin uptake was found to be associated with significant reduction in THTR-1 & -2 proteins and mRNAs expression as well as in activity of the SLC19A2 and SLC19A3 promoters; it was also associated with reduction in level of expression of the transcription factor Sp1 (which is required for activity of these promoters).	Thiamine	45-52	interleukin 6	Mus musculus	18-22
33146542-7	2021	Focusing on hyper-IL-6 (which also inhibited thiamin uptake by primary mouse PACs), the inhibition in thiamin uptake was found to be associated with significant reduction in THTR-1 & -2 proteins and mRNAs expression as well as in activity of the SLC19A2 and SLC19A3 promoters; it was also associated with reduction in level of expression of the transcription factor Sp1 (which is required for activity of these promoters).	Thiamine	102-109	interleukin 6	Mus musculus	18-22
33146542-7	2021	Focusing on hyper-IL-6 (which also inhibited thiamin uptake by primary mouse PACs), the inhibition in thiamin uptake was found to be associated with significant reduction in THTR-1 & -2 proteins and mRNAs expression as well as in activity of the SLC19A2 and SLC19A3 promoters; it was also associated with reduction in level of expression of the transcription factor Sp1 (which is required for activity of these promoters).	Thiamine	102-109	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	174-185
33146542-7	2021	Focusing on hyper-IL-6 (which also inhibited thiamin uptake by primary mouse PACs), the inhibition in thiamin uptake was found to be associated with significant reduction in THTR-1 & -2 proteins and mRNAs expression as well as in activity of the SLC19A2 and SLC19A3 promoters; it was also associated with reduction in level of expression of the transcription factor Sp1 (which is required for activity of these promoters).	Thiamine	102-109	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	246-253
33146542-7	2021	Focusing on hyper-IL-6 (which also inhibited thiamin uptake by primary mouse PACs), the inhibition in thiamin uptake was found to be associated with significant reduction in THTR-1 & -2 proteins and mRNAs expression as well as in activity of the SLC19A2 and SLC19A3 promoters; it was also associated with reduction in level of expression of the transcription factor Sp1 (which is required for activity of these promoters).	Thiamine	102-109	solute carrier family 19, member 3	Mus musculus	258-265
33146542-8	2021	Finally, blocking the intracellular Stat3 signaling pathway was found to lead to a significant reversal in the inhibitory effect of hyper IL-6 on thiamin uptake by PAC 266-6.	Thiamine	146-153	signal transducer and activator of transcription 3	Homo sapiens	36-41
33146542-8	2021	Finally, blocking the intracellular Stat3 signaling pathway was found to lead to a significant reversal in the inhibitory effect of hyper IL-6 on thiamin uptake by PAC 266-6.	Thiamine	146-153	interleukin 6	Mus musculus	138-142
19460453-6	2009	Furthermore, the thiamine-repressible S. cerevisiae THI13 promoter was established to regulate gene expression in A. gossypii.	Thiamine	17-25	4-amino-5-hydroxymethyl-2-methylpyrimidine phosphate synthase	Saccharomyces cerevisiae S288C	52-57
34662241-2	2022	The Thi5-dependent pathway(s) for synthesis of the pyrimidine moiety of thiamine from Saccharomyces cerevisiae and Legionella pneumophila functioned differently when incorporated into the metabolic network of Salmonella enterica.	Thiamine	72-80	4-amino-5-hydroxymethyl-2-methylpyrimidine phosphate synthase	Saccharomyces cerevisiae S288C	4-8
34942318-1	2022	BACKGROUND: Thiamine diphosphate (ThDP), an indispensable cofactor for oxidative energy metabolism, is synthesized through the reaction thiamine + ATP   ThDP + AMP, catalyzed by thiamine pyrophosphokinase 1 (TPK1), a cytosolic dimeric enzyme.	Thiamine	136-144	thiamin pyrophosphokinase 1	Homo sapiens	178-206
34942318-1	2022	BACKGROUND: Thiamine diphosphate (ThDP), an indispensable cofactor for oxidative energy metabolism, is synthesized through the reaction thiamine + ATP   ThDP + AMP, catalyzed by thiamine pyrophosphokinase 1 (TPK1), a cytosolic dimeric enzyme.	Thiamine	136-144	thiamin pyrophosphokinase 1	Homo sapiens	208-212
34942318-9	2022	GENERAL SIGNIFICANCE: Inhibition of TPK1 by ThDP explains why intracellular ThDP levels remain low after administration of even very high doses of thiamine.	Thiamine	147-155	thiamine pyrophosphokinase	Mus musculus	36-40
19631047-3	2009	A cross-sectional study recently reported that approximately one third of hospitalized patients with heart failure had tissue levels suggestive of thiamin deficiency (vitamin B-1).	Thiamine	147-154	immunoglobulin kappa variable 7-3 (pseudogene)	Homo sapiens	175-178
34821467-1	2022	Thiamine-responsive megaloblastic anemia syndrome (TRMA) is an autosomal recessive disorder, inherited by the defective SLC19A2 gene that encodes a high-affinity thiamine transporter (THTR-1).	Thiamine	162-170	solute carrier family 19 member 2	Homo sapiens	184-190
34970882-0	2021	(Clinical observation on treatment of functional dyspepsia by injection of vitamin B1 into Zusanli (ST36) and Hegu (LI4)).	Thiamine	75-85	lipase family member N	Homo sapiens	116-119
34970882-1	2021	OBJECTIVE: To observe the effect and safety of injection of vitamin B1 into Zusanli (ST36) and Hegu (LI4) in the treatment of functional dyspepsia (FD).	Thiamine	60-70	lipase family member N	Homo sapiens	101-104
34970882-8	2021	CONCLUSION: Injection of vitamin B1 into ST36 and LI4 is effective in improving symptoms of PD patients, which may be related to its functions in regulating the levels of GAS and MTL in blood, and facilitating gastrointestinal motility.	Thiamine	25-35	lipase family member N	Homo sapiens	50-53
34970882-8	2021	CONCLUSION: Injection of vitamin B1 into ST36 and LI4 is effective in improving symptoms of PD patients, which may be related to its functions in regulating the levels of GAS and MTL in blood, and facilitating gastrointestinal motility.	Thiamine	25-35	motilin	Homo sapiens	179-182
34821467-1	2022	Thiamine-responsive megaloblastic anemia syndrome (TRMA) is an autosomal recessive disorder, inherited by the defective SLC19A2 gene that encodes a high-affinity thiamine transporter (THTR-1).	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	120-127
34821467-1	2022	Thiamine-responsive megaloblastic anemia syndrome (TRMA) is an autosomal recessive disorder, inherited by the defective SLC19A2 gene that encodes a high-affinity thiamine transporter (THTR-1).	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	184-190
34821467-1	2022	Thiamine-responsive megaloblastic anemia syndrome (TRMA) is an autosomal recessive disorder, inherited by the defective SLC19A2 gene that encodes a high-affinity thiamine transporter (THTR-1).	Thiamine	162-170	solute carrier family 19 member 2	Homo sapiens	120-127
34390792-2	2021	The aim of this study is to understand how alimentary TD, accompanied by OS, affects the expression and level of two thiamine metabolism proteins in rat brain, namely, thiamine transporter 1 (THTR1) and thiamine pyrophosphokinase (TPK1), and what factors are responsible for the observed changes.	Thiamine	117-125	solute carrier family 19 member 2	Rattus norvegicus	168-190
34390792-2	2021	The aim of this study is to understand how alimentary TD, accompanied by OS, affects the expression and level of two thiamine metabolism proteins in rat brain, namely, thiamine transporter 1 (THTR1) and thiamine pyrophosphokinase (TPK1), and what factors are responsible for the observed changes.	Thiamine	117-125	solute carrier family 19 member 2	Rattus norvegicus	192-197
34390792-2	2021	The aim of this study is to understand how alimentary TD, accompanied by OS, affects the expression and level of two thiamine metabolism proteins in rat brain, namely, thiamine transporter 1 (THTR1) and thiamine pyrophosphokinase (TPK1), and what factors are responsible for the observed changes.	Thiamine	117-125	thiamin pyrophosphokinase 1	Rattus norvegicus	231-235
34390792-9	2021	A single high-dose thiamine administration to TD animals had no effect on THTR1 expression, partly raised TPK1 mRNA and protein levels, but is unable to normalize TPK1 enzyme activity.	Thiamine	19-27	thiamin pyrophosphokinase 1	Rattus norvegicus	106-110
34468817-10	2021	Interestingly, after recurrent TD and recovery, ERK1/2 phosphorylation remained high only in the deficient mice treated with thiamine and/or Trolox or thiamine with DMSO.	Thiamine	125-133	mitogen-activated protein kinase 3	Mus musculus	48-54
34468817-10	2021	Interestingly, after recurrent TD and recovery, ERK1/2 phosphorylation remained high only in the deficient mice treated with thiamine and/or Trolox or thiamine with DMSO.	Thiamine	151-159	mitogen-activated protein kinase 3	Mus musculus	48-54
34390104-3	2021	For this we use the Cytolysin A nanopore and equip it with an engineered periplasmic thiamine binding protein (TbpA).	Thiamine	85-93	transthyretin	Homo sapiens	111-115
34461161-0	2021	Thiamine increases resident endoglin positive cardiac progenitor cells and atrial contractile force in humans: A randomised controlled trial.	Thiamine	0-8	endoglin	Homo sapiens	28-36
34461161-9	2021	In exploratory analyses, isolated CPCs in the thiamine group showed an increase in the proportion of CD34-/CD105+ (endoglin) cells, but no difference in CD34-/CD90+ or CD34+ cells.	Thiamine	46-54	CD34 molecule	Homo sapiens	101-105
34461161-9	2021	In exploratory analyses, isolated CPCs in the thiamine group showed an increase in the proportion of CD34-/CD105+ (endoglin) cells, but no difference in CD34-/CD90+ or CD34+ cells.	Thiamine	46-54	endoglin	Homo sapiens	115-123
34461161-11	2021	CONCLUSION: Thiamine does not improve proliferation ability of CPC in patients undergoing CABG, but increases the proportion of CD34-/CD105+ cells.	Thiamine	12-20	CD34 molecule	Homo sapiens	128-132
34390104-4	2021	To allow fast measurements we tuned the affinity of TbpA for thiamine by redesigning the pi-pi stacking interactions between the thiazole group of thiamine and TbpA.	Thiamine	61-69	transthyretin	Homo sapiens	52-56
34390104-4	2021	To allow fast measurements we tuned the affinity of TbpA for thiamine by redesigning the pi-pi stacking interactions between the thiazole group of thiamine and TbpA.	Thiamine	61-69	transthyretin	Homo sapiens	160-164
34390104-4	2021	To allow fast measurements we tuned the affinity of TbpA for thiamine by redesigning the pi-pi stacking interactions between the thiazole group of thiamine and TbpA.	Thiamine	147-155	transthyretin	Homo sapiens	52-56
34390104-4	2021	To allow fast measurements we tuned the affinity of TbpA for thiamine by redesigning the pi-pi stacking interactions between the thiazole group of thiamine and TbpA.	Thiamine	147-155	transthyretin	Homo sapiens	160-164
34631424-1	2021	Background: Biotin-thiamine-responsive basal ganglia disease (BTBGD) is an autosomal recessive neurometabolic disorder associated with pathogenic variants in SLC19A3 gene.	Thiamine	19-27	solute carrier family 19 member 3	Homo sapiens	158-165
34587972-0	2021	Identification and functional analysis of novel SLC25A19 variants causing thiamine metabolism dysfunction syndrome 4.	Thiamine	74-82	solute carrier family 25 member 19	Homo sapiens	48-56
34587972-1	2021	BACKGROUND: Thiamine metabolism dysfunction syndrome 4 (THMD4, OMIM #613710) is an autosomal recessive inherited disease caused by the deficiency of SLC25A19 that encodes the mitochondrial thiamine pyrophosphate (TPP) transporter.	Thiamine	12-20	solute carrier family 25 member 19	Homo sapiens	56-61
34587972-1	2021	BACKGROUND: Thiamine metabolism dysfunction syndrome 4 (THMD4, OMIM #613710) is an autosomal recessive inherited disease caused by the deficiency of SLC25A19 that encodes the mitochondrial thiamine pyrophosphate (TPP) transporter.	Thiamine	12-20	solute carrier family 25 member 19	Homo sapiens	149-157
34232130-4	2021	In this study, we found that NLRP3 inflammasomes were significantly activated in the microglia of thiamine deficiency mice model.	Thiamine	98-106	NLR family, pyrin domain containing 3	Mus musculus	29-34
34587972-1	2021	BACKGROUND: Thiamine metabolism dysfunction syndrome 4 (THMD4, OMIM #613710) is an autosomal recessive inherited disease caused by the deficiency of SLC25A19 that encodes the mitochondrial thiamine pyrophosphate (TPP) transporter.	Thiamine	12-20	solute carrier family 44 member 4	Homo sapiens	189-229
34839858-2	2021	METHODS: Databases including CNKI, Sino Med, VIP, Wanfang, PubMed, the Cochrane Library, and Embase were searched from inception to January 2021 for the randomized controlled trial (RCT) about hydrocortisone combined with vitamin C and vitamin B1 to treat sepsis or septic shock.	Thiamine	236-246	vasoactive intestinal peptide	Homo sapiens	45-48
34384471-6	2021	Thiamine was significantly more stable in pH 3 than in pH 6 solutions.	Thiamine	0-8	phenylalanine hydroxylase	Homo sapiens	42-44
34384471-6	2021	Thiamine was significantly more stable in pH 3 than in pH 6 solutions.	Thiamine	0-8	phenylalanine hydroxylase	Homo sapiens	55-57
34232130-6	2021	These data identify an important role of thiamine metabolism in NLRP3 inflammasome activation, and correcting thiamine metabolism through benfotiamine provides a new therapeutic strategy for NLRP3 inflammasome related neurological, metabolic, and inflammatory diseases.	Thiamine	41-49	NLR family, pyrin domain containing 3	Mus musculus	64-69
34232130-0	2021	The impact of thiamine deficiency and benfotiamine treatment on Nod-like receptor protein-3 inflammasome in microglia.	Thiamine	14-22	NLR family, pyrin domain containing 3	Mus musculus	64-91
34303375-13	2021	Furthermore, CMap (Connectivity map) analysis has identified three potential bioactive small molecule inhibitors (NU-1025, thiamine, vinburnine) for HOXB7 targeted therapy in HNSCC.	Thiamine	123-131	homeobox B7	Homo sapiens	149-154
34337137-6	2021	Thiamine deficiency has many consequences including hypometabolism, mitochondrial depression, oxidative stress, lactic acidosis and cerebral acidosis, amyloid deposition, tau deposition, synaptic dysfunction and abnormal neuro-transmission, astrocyte function, and blood brain barrier integrity, all of which are features of AD.	Thiamine	0-8	microtubule associated protein tau	Homo sapiens	171-174
34337137-8	2021	Providing a thiamine supplement to elderly persons who still have normal cognition but who have deposition of either amyloid or tau, may prevent subsequent cognitive loss and eventual dementia.	Thiamine	12-20	microtubule associated protein tau	Homo sapiens	128-131
34421975-4	2021	Here, we show that the classical thiamin-requiring 3 (th3) mutant is a point mutation in plastid localized 5-deoxyxylulose synthase 1 (DXS1), a key regulated enzyme in the methylerythritol 4-phosphate (MEP) isoprene biosynthesis pathway.	Thiamine	33-40	Deoxyxylulose-5-phosphate synthase	Arabidopsis thaliana	107-133
34421975-4	2021	Here, we show that the classical thiamin-requiring 3 (th3) mutant is a point mutation in plastid localized 5-deoxyxylulose synthase 1 (DXS1), a key regulated enzyme in the methylerythritol 4-phosphate (MEP) isoprene biosynthesis pathway.	Thiamine	33-40	Deoxyxylulose-5-phosphate synthase	Arabidopsis thaliana	135-139
34095275-12	2021	The results show that dietary thiamine supplementation improves the rumen epithelial barrier function by regulating Nrf2-NFkappaB signaling pathways during high-concentrate-diet feeding.	Thiamine	30-38	nuclear factor erythroid 2-related factor 2	Capra hircus	116-120
34360775-6	2021	Morning administration of thiamine significantly downregulates both the PDH phosphorylation at Ser293 and SIRT3 protein level, the effects not observed upon the evening administration.	Thiamine	26-34	sirtuin 3	Rattus norvegicus	106-111
34360775-10	2021	Simultaneously, thiamine heightens interplay between the expression of PDHC components and total acetylation or SIRT2 protein level.	Thiamine	16-24	sirtuin 2	Rattus norvegicus	112-117
34360775-12	2021	The changes are exemplified by the thiamine enhancement of the SIRT2 correlations with metabolic enzymes and proteins of thiol-disulfide metabolism.	Thiamine	35-43	sirtuin 2	Rattus norvegicus	63-68
34360775-14	2021	The daytime-dependent action of thiamine on PDHC and SIRT3 may be of therapeutic significance in correcting perturbed diurnal regulation.	Thiamine	32-40	sirtuin 3	Rattus norvegicus	53-58
34276785-1	2021	Thiamine metabolism dysfunction syndrome 2 (THMD2) is a rare metabolic disorder caused by SLC19A3 mutations, inherited in autosomal recessive pattern.	Thiamine	0-8	solute carrier family 19 member 3	Homo sapiens	44-49
34276785-1	2021	Thiamine metabolism dysfunction syndrome 2 (THMD2) is a rare metabolic disorder caused by SLC19A3 mutations, inherited in autosomal recessive pattern.	Thiamine	0-8	solute carrier family 19 member 3	Homo sapiens	90-97
34276785-10	2021	Thiamine supplementation is indispensable in the treatment of THMD2, whereas combination of biotin and thiamine is not superior to thiamine alone.	Thiamine	0-8	solute carrier family 19 member 3	Homo sapiens	62-67
35512554-1	2022	The thiamine transporters, SLC19A2 and SLC19A3, have recently been shown to transport pyridoxine in addition to thiamine, the originally identified substrate, in our study on human orthologs.	Thiamine	4-12	solute carrier family 19 member 2	Homo sapiens	27-34
34220059-1	2021	Biotin-thiamine-responsive basal ganglia disease is a rare, autosomal recessive, treatable, neurometabolic disorder associated with biallelic pathogenic variations in the SLC19A3 gene.	Thiamine	7-15	solute carrier family 19 member 3	Homo sapiens	171-178
34470947-8	2021	Thiamine also significantly decreased the levels of MDA, while increasing SOD and CAT levels.	Thiamine	0-8	superoxide dismutase 1	Homo sapiens	74-77
34470947-8	2021	Thiamine also significantly decreased the levels of MDA, while increasing SOD and CAT levels.	Thiamine	0-8	catalase	Homo sapiens	82-85
35102031-1	2022	Thiamine metabolism dysfunction syndrome-4 (THMD-4) is an autosomal recessive inherited rare disease (OMIM #613710) characterized by febrile illness associated episodic encephalopathy, leading to transient neurological dysfunction and progressive polyneuropathy.	Thiamine	0-8	solute carrier family 25 member 19	Homo sapiens	44-50
35512554-1	2022	The thiamine transporters, SLC19A2 and SLC19A3, have recently been shown to transport pyridoxine in addition to thiamine, the originally identified substrate, in our study on human orthologs.	Thiamine	4-12	solute carrier family 19 member 3	Homo sapiens	39-46
35512554-1	2022	The thiamine transporters, SLC19A2 and SLC19A3, have recently been shown to transport pyridoxine in addition to thiamine, the originally identified substrate, in our study on human orthologs.	Thiamine	112-120	solute carrier family 19 member 2	Homo sapiens	27-34
35512554-1	2022	The thiamine transporters, SLC19A2 and SLC19A3, have recently been shown to transport pyridoxine in addition to thiamine, the originally identified substrate, in our study on human orthologs.	Thiamine	112-120	solute carrier family 19 member 3	Homo sapiens	39-46
35512554-4	2022	However, all SLC19A2/3 orthologs were capable of thiamine transport.	Thiamine	49-57	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	13-22
35277069-0	2022	Effects of Thiamin Restriction on Exercise-Associated Glycogen Metabolism and AMPK Activation Level in Skeletal Muscle.	Thiamine	11-18	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	78-82
35512554-6	2022	This is supported by the finding that rat Slc19a3, for which the human ortholog operates for the intestinal uptake of both pyridoxine and thiamine, lacks the pyridoxine transport function.	Thiamine	138-146	solute carrier family 19 member 3	Rattus norvegicus	42-49
35465832-5	2022	The erythrocyte thiamine transketolase levels were found to be 13 u/L.	Thiamine	16-24	transketolase	Homo sapiens	25-38
35050500-0	2022	Thiamine-dependent regulation of mammalian brain pyridoxal kinase in vitro and in vivo.	Thiamine	0-8	pyridoxal kinase	Homo sapiens	49-65
35050500-2	2022	Here, the non-coenzyme action of thiamine on the major mammalian producers of pyridoxal-5"-phosphate (PLP), such as pyridoxal kinase (PdxK) and pyridoxine 5"-phosphate oxidase (PNPO), is characterized.	Thiamine	33-41	pyridoxal phosphatase	Homo sapiens	102-105
35050500-2	2022	Here, the non-coenzyme action of thiamine on the major mammalian producers of pyridoxal-5"-phosphate (PLP), such as pyridoxal kinase (PdxK) and pyridoxine 5"-phosphate oxidase (PNPO), is characterized.	Thiamine	33-41	pyridoxal kinase	Homo sapiens	116-132
35532649-1	2022	Background and Aims: Biotin-thiamine-responsive basal ganglia disease (BTBGD) is an autosomal recessive disorder due to mutations in the SLC19A3-gene, typically seen in early childhood.	Thiamine	28-36	solute carrier family 19 member 3	Homo sapiens	137-144
35090865-6	2022	AG835, thiamine and paroxetine specifically inhibited PMAT-, THTR2- and SERT-mediated uptake of metformin, respectively.	Thiamine	7-15	solute carrier family 29 member 4	Homo sapiens	54-58
35090865-6	2022	AG835, thiamine and paroxetine specifically inhibited PMAT-, THTR2- and SERT-mediated uptake of metformin, respectively.	Thiamine	7-15	solute carrier family 19 member 3	Homo sapiens	61-66
35090865-6	2022	AG835, thiamine and paroxetine specifically inhibited PMAT-, THTR2- and SERT-mediated uptake of metformin, respectively.	Thiamine	7-15	solute carrier family 6 member 4	Homo sapiens	72-76
35484175-0	2022	Randomised trial of intravenous thiamine and/or magnesium sulphate administration on erythrocyte transketolase activity, lactate concentrations and alcohol withdrawal scores.	Thiamine	32-40	transketolase	Homo sapiens	97-110
35050500-2	2022	Here, the non-coenzyme action of thiamine on the major mammalian producers of pyridoxal-5"-phosphate (PLP), such as pyridoxal kinase (PdxK) and pyridoxine 5"-phosphate oxidase (PNPO), is characterized.	Thiamine	33-41	pyridoxal kinase	Homo sapiens	134-138
35050500-2	2022	Here, the non-coenzyme action of thiamine on the major mammalian producers of pyridoxal-5"-phosphate (PLP), such as pyridoxal kinase (PdxK) and pyridoxine 5"-phosphate oxidase (PNPO), is characterized.	Thiamine	33-41	pyridoxamine 5'-phosphate oxidase	Homo sapiens	144-175
35050500-2	2022	Here, the non-coenzyme action of thiamine on the major mammalian producers of pyridoxal-5"-phosphate (PLP), such as pyridoxal kinase (PdxK) and pyridoxine 5"-phosphate oxidase (PNPO), is characterized.	Thiamine	33-41	pyridoxamine 5'-phosphate oxidase	Homo sapiens	177-181
35050500-3	2022	Among the natural thiamine compounds, thiamine triphosphate (ThTP) is the best effector of recombinant human PdxK (hPdxK) in vitro, inhibiting hPdxK in the presence of Mg2+ , but activating the Zn2+ -dependent reaction.	Thiamine	18-26	pyridoxal kinase	Homo sapiens	109-113
35050500-3	2022	Among the natural thiamine compounds, thiamine triphosphate (ThTP) is the best effector of recombinant human PdxK (hPdxK) in vitro, inhibiting hPdxK in the presence of Mg2+ , but activating the Zn2+ -dependent reaction.	Thiamine	18-26	pyridoxal kinase	Homo sapiens	115-120
35050500-3	2022	Among the natural thiamine compounds, thiamine triphosphate (ThTP) is the best effector of recombinant human PdxK (hPdxK) in vitro, inhibiting hPdxK in the presence of Mg2+ , but activating the Zn2+ -dependent reaction.	Thiamine	18-26	pyridoxal kinase	Homo sapiens	143-148
35050500-4	2022	Inhibition of hPdxK by thiamine antagonists decreases from amprolium to pyrithiamine to oxythiamine, highlighting possible dysregulation of both the B1 - and B6 -dependent metabolism in the chemical models of thiamine deficiency.	Thiamine	23-31	pyridoxal kinase	Homo sapiens	14-19
35050500-4	2022	Inhibition of hPdxK by thiamine antagonists decreases from amprolium to pyrithiamine to oxythiamine, highlighting possible dysregulation of both the B1 - and B6 -dependent metabolism in the chemical models of thiamine deficiency.	Thiamine	209-217	pyridoxal kinase	Homo sapiens	14-19
35050500-5	2022	Compared to the canonical hPdxK, the D87H and V128I variants show a 2-fold increase in Kapp of thiamine inhibition, and the V128I and H246Q variants show a 4-fold and a 2-fold decreased Kapp of ThDP, respectively.	Thiamine	95-103	pyridoxal kinase	Homo sapiens	26-31
35050500-6	2022	Thiamine administration changes diurnal regulation of PdxK activity and phosphorylation at Ser213 and Ser285, expression of the PdxK-related circadian kinases / phosphatases in the rat brain, and ECG.	Thiamine	0-8	pyridoxal kinase	Rattus norvegicus	54-58
35050500-6	2022	Thiamine administration changes diurnal regulation of PdxK activity and phosphorylation at Ser213 and Ser285, expression of the PdxK-related circadian kinases / phosphatases in the rat brain, and ECG.	Thiamine	0-8	pyridoxal kinase	Homo sapiens	128-132
35050500-11	2022	Diurnal effects of thiamine administration on the metabolically linked ThDP- and PLP-dependent enzymes may support the brain homeostatic mechanisms and physiological fitness.	Thiamine	19-27	pyridoxal phosphatase	Homo sapiens	81-84
35277069-1	2022	This study aimed to investigate the direct influence of a decrease in the cellular thiamin level, before the onset of anorexia (one of the symptoms of thiamin deficiency) on glycogen metabolism and the AMP-activated protein kinase (AMPK) activation levels in skeletal muscle at rest and in response to exercise.	Thiamine	83-90	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	202-230
35277069-1	2022	This study aimed to investigate the direct influence of a decrease in the cellular thiamin level, before the onset of anorexia (one of the symptoms of thiamin deficiency) on glycogen metabolism and the AMP-activated protein kinase (AMPK) activation levels in skeletal muscle at rest and in response to exercise.	Thiamine	83-90	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	232-236
34998824-0	2022	Hypoxia inhibits colonic uptake of the microbiota-generated forms of vitamin B1 via HIF-1alpha-mediated transcriptional regulation of their transporters.	Thiamine	69-79	hypoxia inducible factor 1 subunit alpha	Homo sapiens	84-94
34998824-5	2022	Knocking down HIF-1alpha using gene-specific siRNAs in NCM460 cells maintained under hypoxic conditions, on the other hand, led to a significant reversal in the inhibitory effect of hypoxia on TPP and free thiamin uptake, as well as on the expression of their transporters.	Thiamine	206-213	hypoxia inducible factor 1 subunit alpha	Homo sapiens	14-24
34998824-7	2022	In summary, hypoxia causes severe inhibition in colonic TPP and free thiamin uptake that is mediated at least in part via HIF-1alpha-mediated transcriptional mechanisms affecting their respective transporters.	Thiamine	69-76	hypoxia inducible factor 1 subunit alpha	Homo sapiens	122-132
2750771-3	1989	Low serum transketolase (thiamin; p less than 0.055), red blood cell (RBC) folate (p less than 0.06), and serum vitamin B-12 (p less than 0.05) levels occurred more often in SDAT patients than in CN subjects.	Thiamine	25-32	transketolase	Homo sapiens	10-23
35079241-8	2022	Furthermore, thiamine, biotin, and tocopherol are viewed as satisfying inhibitors to Mpro, but pyridoxine was observed as the weakest inhibitor.	Thiamine	13-21	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	85-89
2799573-4	1989	The transketolase response to thiamine pyrophosphate (TPP effect) suggested thiamine deficiency in 32.4%, of whom 13.2% were classified as severely deficient.	Thiamine	30-38	transketolase	Homo sapiens	4-17
2621527-5	1989	White adolescents had significantly higher total whole blood thiamine values than black adolescents, and white parents had significantly higher thiamine values than black parents by both total whole blood assay and level of transketolase activity.	Thiamine	144-152	transketolase	Homo sapiens	224-237
3418348-4	1988	Activities of the thiamine-dependent enzyme alpha-ketoglutarate dehydrogenase (alpha KGDH) were reduced in parallel with the GABA changes.	Thiamine	18-26	oxoglutarate dehydrogenase	Rattus norvegicus	44-77
2676709-0	1989	A possible role for acid phosphatase with thiamin-binding activity encoded by PHO3 in yeast.	Thiamine	42-49	acid phosphatase PHO3	Saccharomyces cerevisiae S288C	78-82
2676709-9	1989	The pho3 mutant cells of S. cerevisiae in contrast to the parent cells have markedly reduced activity of the uptake of [14C]thiamin phosphates, suggesting that thiamin repressible acid phosphatase plays a role in the hydrolysis of thiamin phosphates in the periplasmic space prior to the uptake of their thiamin moieties by S. cerevisiae.	Thiamine	124-131	acid phosphatase PHO3	Saccharomyces cerevisiae S288C	4-8
2815713-1	1989	The authors have studied activity of thiamine-dependent enzymes: transketolase, pyruvate- and alpha-ketoglutarate dehydrogenases, the content of thiamine diphosphate in the tissue of the liver and musculus gastrocnemius, activity of transketolase of the whole blood hemolysates and different age populations of red blood cells under 15-day hypokinesia with B1-deficiency induced by enteral administration of oxythiamine.	Thiamine	37-45	transketolase	Homo sapiens	65-78
2665563-2	1989	Previously induced thiamine deficiency was associated with about a 50% reduction of BECs and a significant increase in liver alcohol dehydrogenase (ADH) activity suggesting a persistent acceleration of ethanol metabolism.	Thiamine	19-27	aldo-keto reductase family 1 member A1	Rattus norvegicus	148-151
2564421-4	1989	Activities of the thiamine-dependent enzyme alpha-ketoglutarate dehydrogenase (alpha KGDH) were decreased in parallel with the aspartate decreases; pyruvate dehydrogenase complex activities were unchanged in all brain regions.	Thiamine	18-26	oxoglutarate dehydrogenase	Rattus norvegicus	44-77
2537896-3	1989	A month after institution of treatment with thiamine, the hematologic findings had returned to normal and the insulin requirements had decreased.	Thiamine	44-52	insulin	Homo sapiens	110-117
2537896-4	1989	Withdrawal of thiamine repeatedly induced relapse of the anemia and an increase in insulin requirements.	Thiamine	14-22	insulin	Homo sapiens	83-90
2707476-2	1989	Simultaneous dietary supplementation with thiamine plus zinc was found to be the most effective way of reducing the lead-induced inhibition of delta-aminolevulinic acid dehydratase activity in blood, urinary, excretion of delta-aminolevulinic acid and accumulation of lead in blood, liver and kidney.	Thiamine	42-50	aminolevulinate dehydratase	Rattus norvegicus	143-180
3240094-3	1988	Ascorbic acid or its combination with thiamine enhanced the urinary elimination of Pb, reduced the hepatic and renal burden of Pb, and reversed the Pb-induced inhibition of the activity of blood delta-aminolevulinic acid dehydratase (delta-ALA-D).	Thiamine	38-46	aminolevulinate dehydratase	Rattus norvegicus	195-232
3240094-3	1988	Ascorbic acid or its combination with thiamine enhanced the urinary elimination of Pb, reduced the hepatic and renal burden of Pb, and reversed the Pb-induced inhibition of the activity of blood delta-aminolevulinic acid dehydratase (delta-ALA-D).	Thiamine	38-46	aminolevulinate dehydratase	Rattus norvegicus	234-245
2834878-5	1988	Thiamine deficiency led to lowered G-6-P and F-D-P activities in the liver and kidneys and PEPCK in the liver of the test animals as compared to the control.	Thiamine	0-8	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	35-40
2834878-5	1988	Thiamine deficiency led to lowered G-6-P and F-D-P activities in the liver and kidneys and PEPCK in the liver of the test animals as compared to the control.	Thiamine	0-8	fructose-bisphosphatase 1	Rattus norvegicus	45-50
2834878-5	1988	Thiamine deficiency led to lowered G-6-P and F-D-P activities in the liver and kidneys and PEPCK in the liver of the test animals as compared to the control.	Thiamine	0-8	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	91-96
3683723-7	1987	Although the activity of the thiamin dependent enzyme transketolase (TK) was affected similarly at all ages, the activity of KGDH in the aged brain was more sensitive to thiamin deficiency than in the young; KGDH activity declined 41%, 57% or 74% at 3, 10, or 30 months, respectively.	Thiamine	29-36	transketolase	Mus musculus	54-67
3439087-1	1987	Investigation of diphosphothiamine content in the mouse tissues, associated with transketolase activity in the dynamic dependence on the body provision with vitamin B1, has proved the organ-specificity of deposition and elimination of diphosphothiamine under conditions of developing thiamine deficiency.	Thiamine	157-167	transketolase	Mus musculus	81-94
3439087-1	1987	Investigation of diphosphothiamine content in the mouse tissues, associated with transketolase activity in the dynamic dependence on the body provision with vitamin B1, has proved the organ-specificity of deposition and elimination of diphosphothiamine under conditions of developing thiamine deficiency.	Thiamine	26-34	transketolase	Mus musculus	81-94
3683723-7	1987	Although the activity of the thiamin dependent enzyme transketolase (TK) was affected similarly at all ages, the activity of KGDH in the aged brain was more sensitive to thiamin deficiency than in the young; KGDH activity declined 41%, 57% or 74% at 3, 10, or 30 months, respectively.	Thiamine	29-36	transketolase	Mus musculus	69-71
3436636-0	1987	Purification of rat liver alcohol dehydrogenase and studies on kinetic characteristics of thiamine, thiazole and NAD+ by the purified enzyme.	Thiamine	90-98	aldo-keto reductase family 1 member A1	Rattus norvegicus	26-47
3675411-3	1987	Decreased erythrocyte transketolase activity indicated thiamine insufficiency in lambs with high thiaminase activity.	Thiamine	55-63	transketolase	Ovis aries	22-35
3603737-0	1987	[Effect of thiamine and its derivatives on acetylcholinesterase activity of the blood and brain of albino mice].	Thiamine	11-19	acetylcholinesterase	Mus musculus	43-63
3602224-0	1987	The activation of red blood cell transketolase in groups of patients especially at risk from thiamin deficiency.	Thiamine	93-100	transketolase	Homo sapiens	33-46
3603737-1	1987	Thiamine, thiaminepyrophosphate and 4-methyl-5-beta-oxyethylthiazole are studied for their effect on the acetylcholinesterase activity in the brain, blood plasma and cells.	Thiamine	0-8	acetylcholinesterase	Mus musculus	105-125
3602224-4	1987	The modified transketolase activation test may warn not only of marginal thiamin deficiency but also independently, of susceptibility to brain damage in patients at risk.	Thiamine	73-80	transketolase	Homo sapiens	13-26
3630045-3	1987	It was also shown that the cellulose thiamine derivative had a prolonged effect in the body, which was manifested in a slower increase in the activities of transketolase, pyruvate dehydrogenase and in the amount of thiamine diphosphate in tissues of vitamin B1-deficient animals, as compared to the effect of thiamine.	Thiamine	37-45	transketolase	Mus musculus	156-169
3603737-2	1987	The activity of acetylcholinesterase in blood cells is shown to be inhibited most of all by thiamine and thiazole.	Thiamine	92-100	acetylcholinesterase	Mus musculus	16-36
3587500-4	1987	Further progression of thiamine deprivation resulted in a generalized reduction in TK activity.	Thiamine	23-31	transketolase	Rattus norvegicus	83-85
3558815-1	1987	We have investigated a thiamine-dependent enzyme, transketolase, in cultured fibroblasts from 41 human subjects, including patients with alcoholism-associated Wernicke-Korsakoff syndrome (n = 3), familial chronic alcoholic males (n = 7), their sons (n = 7), nonalcoholic men (n = 7), their male offspring (n = 7), and three generations of an Amish family (n = 10) without any history of alcoholism.	Thiamine	23-31	transketolase	Homo sapiens	50-63
3558815-3	1987	Our data suggest that an inborn error (i.e., high Km of transketolase for thiamine pyrophosphate) predisposing to thiamine deficiency diseases similar to those reported in Wernicke-Korsakoff syndrome may occur in the general population.	Thiamine	74-82	transketolase	Homo sapiens	56-69
3587500-6	1987	Administration of thiamine to symptomatic thiamine-deprived rats resulted in reversal of neurological symptoms and to normalisation of defective TK activities in less vulnerable structures such as cerebral cortex, striatum and hippocampus; reduction of TK activity, however, persisted in brainstem and cerebellar regions.	Thiamine	18-26	transketolase	Rattus norvegicus	145-147
3587500-6	1987	Administration of thiamine to symptomatic thiamine-deprived rats resulted in reversal of neurological symptoms and to normalisation of defective TK activities in less vulnerable structures such as cerebral cortex, striatum and hippocampus; reduction of TK activity, however, persisted in brainstem and cerebellar regions.	Thiamine	18-26	transketolase	Rattus norvegicus	253-255
3587500-6	1987	Administration of thiamine to symptomatic thiamine-deprived rats resulted in reversal of neurological symptoms and to normalisation of defective TK activities in less vulnerable structures such as cerebral cortex, striatum and hippocampus; reduction of TK activity, however, persisted in brainstem and cerebellar regions.	Thiamine	42-50	transketolase	Rattus norvegicus	145-147
3587500-6	1987	Administration of thiamine to symptomatic thiamine-deprived rats resulted in reversal of neurological symptoms and to normalisation of defective TK activities in less vulnerable structures such as cerebral cortex, striatum and hippocampus; reduction of TK activity, however, persisted in brainstem and cerebellar regions.	Thiamine	42-50	transketolase	Rattus norvegicus	253-255
3587500-9	1987	In contrast to chronic thiamine deprivation, TK activities following pyrithiamine treatment were: equally reduced in magnitude in vulnerable and non-vulnerable brain structures, unchanged following reversal of neurological abnormalities by thiamine administration.	Thiamine	73-81	transketolase	Rattus norvegicus	45-47
3478971-2	1987	Abnormalities in the thiamin-dependent enzyme, transketolase, provide evidence of a high incidence of thiamin deficiency as well as of disturbed thiamin metabolism in chronic alcoholics, which are likely to be caused by reduced vitamin intake as well as impaired absorption.	Thiamine	21-28	transketolase	Homo sapiens	47-60
3478971-2	1987	Abnormalities in the thiamin-dependent enzyme, transketolase, provide evidence of a high incidence of thiamin deficiency as well as of disturbed thiamin metabolism in chronic alcoholics, which are likely to be caused by reduced vitamin intake as well as impaired absorption.	Thiamine	102-109	transketolase	Homo sapiens	47-60
3478971-2	1987	Abnormalities in the thiamin-dependent enzyme, transketolase, provide evidence of a high incidence of thiamin deficiency as well as of disturbed thiamin metabolism in chronic alcoholics, which are likely to be caused by reduced vitamin intake as well as impaired absorption.	Thiamine	102-109	transketolase	Homo sapiens	47-60
3426152-4	1987	Thiamine deficiency also caused a significant decrease in erythrocyte transketolase levels.	Thiamine	0-8	transketolase	Rattus norvegicus	70-83
3426764-5	1987	Since the modified transketolase activation test appears not only to monitor the effectiveness of thiamin therapy but also independently to warn of persisting enzyme abnormalities, it could prove to be of general use in alcohol detoxification units.	Thiamine	98-105	transketolase	Homo sapiens	19-32
3536917-1	1986	We have identified a genetic locus, pho4, in Schizosaccharomyces pombe which encodes a minor expressed cell surface acid phosphatase that is repressed by low concentrations (0.5 microM) of thiamin.	Thiamine	189-196	phosphate-sensing transcription factor PHO4	Saccharomyces cerevisiae S288C	36-40
3536917-6	1986	Thiamin regulation, at least in part, operates by reducing the level of pho4-mRNA.	Thiamine	0-7	phosphate-sensing transcription factor PHO4	Saccharomyces cerevisiae S288C	72-76
3762968-1	1986	We studied a thiamine-dependent enzyme, transketolase, from fibroblasts of a diabetic patient who developed Wernicke"s encephalopathy when treated with tolazamide, in order to delineate if this patient also had transketolase abnormality [high Km for thiamine pyrophosphate (TPP)], as previously reported in postalcoholic Wernicke-Korsakoff syndrome.	Thiamine	13-21	transketolase	Homo sapiens	40-53
3762968-1	1986	We studied a thiamine-dependent enzyme, transketolase, from fibroblasts of a diabetic patient who developed Wernicke"s encephalopathy when treated with tolazamide, in order to delineate if this patient also had transketolase abnormality [high Km for thiamine pyrophosphate (TPP)], as previously reported in postalcoholic Wernicke-Korsakoff syndrome.	Thiamine	13-21	transketolase	Homo sapiens	211-224
24254360-3	1986	Animals fed the thiamine-supplemented diet (50 mg/kg) and Pb showed decreased urinary excretion of delta-ALA and a decreased inhibition of delta-ALAD activity in blood compared to those given Pb with normal thiamine diet.	Thiamine	16-24	aminolevulinate dehydratase	Rattus norvegicus	139-149
3011628-0	1986	Effect of thiamin deficiency on adrenocorticotrophin and vasopressin in the rat hypothalamus.	Thiamine	10-17	arginine vasopressin	Rattus norvegicus	57-68
3765490-0	1986	[Changes in the intracellular glucose-6-phosphate dehydrogenase metabolism in the rat liver during thiamine deficiency].	Thiamine	99-107	glucose-6-phosphate dehydrogenase	Rattus norvegicus	30-63
3765490-2	1986	The alternations, found in the half-life period, in constant rates of synthesis and degradation of the key enzyme of the pentosephosphate pathway, correlated with a decrease of the glucose-6-phosphate dehydrogenase activity in vitamin B1 deficiency.	Thiamine	227-237	glucose-6-phosphate dehydrogenase	Rattus norvegicus	181-214
3523986-5	1986	Insulin and cocarboxylase as well as insulin combined with thiamin and adenine exhibited the best effect on the patterns studied; these drugs normalized the vitamin B1 metabolism and improved the parameters of energy metabolism within 120 min of incubation in erythrocytes isolated from blood of patients with diabetes mellitus.	Thiamine	157-167	insulin	Homo sapiens	0-7
3523986-5	1986	Insulin and cocarboxylase as well as insulin combined with thiamin and adenine exhibited the best effect on the patterns studied; these drugs normalized the vitamin B1 metabolism and improved the parameters of energy metabolism within 120 min of incubation in erythrocytes isolated from blood of patients with diabetes mellitus.	Thiamine	157-167	insulin	Homo sapiens	37-44
3727467-0	1986	[Regulation of glucose-6-phosphate dehydrogenase activity of the rat liver in vitamin B1 deficiency].	Thiamine	78-88	glucose-6-phosphate dehydrogenase	Rattus norvegicus	15-48
4075020-6	1985	Treatment of rabbits for 14 days with the thiamin antagonists pyrithiamine (20 micrograms kg-1) or oxythiamine (0.8 mg kg-1) produced a significant drop in TK activity and increase in the lactate and pyruvate concentrations as well as an increase in TPP effect.	Thiamine	42-49	transketolase	Oryctolagus cuniculus	156-158
3724963-4	1986	Onset of neurological symptoms of thiamine deprivation (ataxia, loss of righting reflex) was accompanied by selective decreases (of the order of 30%) in the activity of alpha-ketoglutarate dehydrogenase (alpha KGDH) in lateral vestibular nucleus and hypothalamus.	Thiamine	34-42	oxoglutarate dehydrogenase	Rattus norvegicus	169-202
3768099-0	1986	The rapid decline in erythrocyte transketolase on cessation of high-dose thiamine administration in Korsakoff patients.	Thiamine	73-81	transketolase	Homo sapiens	33-46
3768099-3	1986	In the first study the changes in the thiamine-dependent enzyme erythrocyte transketolase (TK) which followed the administration of oral thiamine are described.	Thiamine	38-46	transketolase	Homo sapiens	76-89
3768099-3	1986	In the first study the changes in the thiamine-dependent enzyme erythrocyte transketolase (TK) which followed the administration of oral thiamine are described.	Thiamine	38-46	transketolase	Homo sapiens	91-93
3768099-3	1986	In the first study the changes in the thiamine-dependent enzyme erythrocyte transketolase (TK) which followed the administration of oral thiamine are described.	Thiamine	137-145	transketolase	Homo sapiens	76-89
3768099-3	1986	In the first study the changes in the thiamine-dependent enzyme erythrocyte transketolase (TK) which followed the administration of oral thiamine are described.	Thiamine	137-145	transketolase	Homo sapiens	91-93
3022633-0	1986	[Effects of a diet with low fiber and thiamine contents on erythrocyte transketolase activity in goats].	Thiamine	38-46	transketolase	Capra hircus	71-84
3866557-1	1985	An unexpectedly high incidence of biochemical thiamine deficiency (erythrocyte transketolase) was found in groups of mothers and infants, selected for apparent health from a westernized Caucasian community in Australia.	Thiamine	46-54	transketolase	Homo sapiens	79-92
4049549-1	1985	The effect of thiamine treatment on the erythrocyte transketolase activity and the thiamine pyrophosphate effect].	Thiamine	14-22	transketolase	Homo sapiens	52-65
4074790-2	1985	The increase in the intracellular concentrations of isocitrate and alpha-ketoglutarate with a simultaneous decrease of malate in the liver of vitamin-deficient rats points to the inhibition of alpha-ketoglutarate dehydrogenase responsible for the anomalous metabolism under conditions of thiamine deficiency.	Thiamine	288-296	oxoglutarate dehydrogenase	Rattus norvegicus	193-226
6093881-7	1984	A kinetic study of thiamine uptake by rat hepatocytes preloaded with pyrithiamine, a potent inhibitor of thiamine pyrophosphokinase, revealed that the biphasic property of thiamine uptake disappeared and a single carrier system for thiamine with a Kt of 40.5 microM, which was similar to the Kt value of the low affinity process, was retained.	Thiamine	73-81	thiamin pyrophosphokinase 1	Rattus norvegicus	105-131
4063285-1	1985	Thiamin status has been measured using the erythrocyte transketolase (EC 2.2.1.1) assay in twenty-eight normal children and in twenty-five severely-malnourished children throughout the course of recovery.	Thiamine	0-7	transketolase	Homo sapiens	55-68
4052157-6	1985	In the light of these conclusions some recently proposed hypotheses regarding the role of transketolase in the genesis of brain damage in thiamine deficiency are reconsidered and a modified mechanism is proposed consistent with these and other recent findings.	Thiamine	138-146	transketolase	Homo sapiens	90-103
3922165-0	1985	Transketolase activity in the blood of cattle and sheep in relation to thiamine deficiency.	Thiamine	71-79	transketolase	Bos taurus	0-13
6093881-7	1984	A kinetic study of thiamine uptake by rat hepatocytes preloaded with pyrithiamine, a potent inhibitor of thiamine pyrophosphokinase, revealed that the biphasic property of thiamine uptake disappeared and a single carrier system for thiamine with a Kt of 40.5 microM, which was similar to the Kt value of the low affinity process, was retained.	Thiamine	19-27	thiamin pyrophosphokinase 1	Rattus norvegicus	105-131
6093881-7	1984	A kinetic study of thiamine uptake by rat hepatocytes preloaded with pyrithiamine, a potent inhibitor of thiamine pyrophosphokinase, revealed that the biphasic property of thiamine uptake disappeared and a single carrier system for thiamine with a Kt of 40.5 microM, which was similar to the Kt value of the low affinity process, was retained.	Thiamine	73-81	thiamin pyrophosphokinase 1	Rattus norvegicus	105-131
6093881-8	1984	These results strongly suggest that thiamine transport system in rat liver cells is closely connected with thiamine pyrophosphokinase, which accelerates the uptake rat of thiamine by pyrophosphorylation at physiological concentrations of thiamine.	Thiamine	36-44	thiamin pyrophosphokinase 1	Rattus norvegicus	107-133
6465054-6	1984	The activities of brush border sucrase, lactase, maltase, alkaline phosphatase, and leucine aminopeptidase were reduced by 42 to 66% in thiamin deficiency, compared to pair-fed controls.	Thiamine	136-143	lactase	Rattus norvegicus	40-47
6476786-4	1984	The hepatic transketolase activity was highest in rats fed a diet containing 4 mg thiamine/kg diet.	Thiamine	82-90	transketolase	Rattus norvegicus	12-25
6649520-1	1983	In blood of patients with cancer of stomach and mammary gland total thiamin content was measured by means of fluorimetric procedure, thiamindiphosphate (TDP)--by an enzymatic method, activity of transketolase was estimated in presence or in absence of TDP.	Thiamine	68-75	transketolase	Homo sapiens	195-208
6381162-4	1984	Significant decreases, however, were observed in the transketolase activity of pair-fed and thiamine deficient rats.	Thiamine	92-100	transketolase	Rattus norvegicus	53-66
6649520-2	1983	Concentration of total thiamin in blood of healthy persons was 7.65 +/- 0.40 micrograms/100 ml; thiamindiphosphate--5.06 micrograms/100 ml activity of transketolase was 11.59 +/- 0.23 mmol/l.	Thiamine	23-30	transketolase	Homo sapiens	151-164
6298546-5	1983	These results suggest that thiamine deficiency enhances CCl4 damage to membranes of the ER and enhances CCl4 hepatotoxicity.	Thiamine	27-35	C-C motif chemokine ligand 4	Rattus norvegicus	56-60
6191889-7	1983	This heterogeneity might need recognition when thiamin nutritional sufficiency is assessed by the "thiamin diphosphate effect" on erythrocyte transketolase.	Thiamine	47-54	transketolase	Homo sapiens	142-155
6298546-3	1983	CCl4 hepatotoxicity, assessed by serum glutamicpyruvic transaminase (SGPT) activity and histological examination 24 hours after the hepatotoxin, was augmented in the group fed the thiamine deficient diet.	Thiamine	180-188	C-C motif chemokine ligand 4	Rattus norvegicus	0-4
6864328-2	1983	Simultaneously the activities of the thiamin-dependent enzymes (transketolase, pyruvate and oxoglutarate dehydrogenases) were measured as an index of efficiency of fulfilling the coenzyme function of the vitamin under conditions of different thiamin status.	Thiamine	37-44	transketolase	Mus musculus	64-77
6298546-5	1983	These results suggest that thiamine deficiency enhances CCl4 damage to membranes of the ER and enhances CCl4 hepatotoxicity.	Thiamine	27-35	C-C motif chemokine ligand 4	Rattus norvegicus	104-108
6836965-2	1983	As compared with other mice liver subcellular fractions the microsomal fraction proved to be the most sensitive to thiamine deficiency: inhibition of transketolase activity reached 75%.	Thiamine	115-123	transketolase	Mus musculus	150-163
6432511-6	1983	Cytochrome P-450 concentration was higher in the microsomes from thiamin-deficient rats and was induced to a greater degree by phenobarbital than in microsomes from rats fed thiamin-supplemented diets ad libitum.	Thiamine	65-72	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
6432511-6	1983	Cytochrome P-450 concentration was higher in the microsomes from thiamin-deficient rats and was induced to a greater degree by phenobarbital than in microsomes from rats fed thiamin-supplemented diets ad libitum.	Thiamine	174-181	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
6836965-4	1983	As a result of vitamin B1 deprivation of mice with Erlich ascites carcinoma activity of transketolase was decreased by 30% and the TDP-effect increased by 34% in the liver microsomal fraction; in the tumoral cells the enzymatic activity was decreased by 23% and the TDP-effect was increased by 10%.	Thiamine	15-25	transketolase	Mus musculus	88-101
6836965-5	1983	Thiamine-free ration of rats with sarcoma 45, at the initial steps of the tumor growth was responsible for the most distinct decrease in transketolase activity and an increase in the TDP-effect in blood.	Thiamine	0-8	transketolase	Rattus norvegicus	137-150
7097279-4	1982	These data suggest that loss of transketolase activity is likely to be a later consequence of thiamine deficiency in mammalian brain than is decreased activity of pyruvate dehydrogenase complex.	Thiamine	94-102	transketolase	Homo sapiens	32-45
6127634-7	1982	Thiamine deprivation decreased the TK activity by 45% and raised the TPP effect up to 180%.	Thiamine	0-8	transketolase	Mus musculus	35-37
6949752-4	1982	Vitamin B1 deficiency was confirmed by determining erythrocyte transketolase.	Thiamine	0-10	transketolase	Homo sapiens	63-76
7113098-0	1982	[Study of the thiamine supply of healthy school-age children and adolescents by examining transketolase activity and the TDP effect in the blood].	Thiamine	14-22	transketolase	Homo sapiens	90-103
7062238-4	1982	Under urethan anesthesia, thiamine displayed apparent dose-dependent kinetics as measured by the changes in the pharmacokinetic parameters, AUC,Vd(area), t0.5 beta, and total body clearance, ClTB, with dose.	Thiamine	26-34	clathrin, light chain B	Rattus norvegicus	191-195
7129802-2	1982	The mean alpha ETK value indicated inadequate thiamine supply.	Thiamine	46-54	BMX non-receptor tyrosine kinase	Homo sapiens	15-18
6127634-4	1982	The TPKase activity in the liver of mice with EAC decreased by 24% and in thiamine deficiency, by 44%.	Thiamine	74-82	thiamine pyrophosphokinase	Mus musculus	4-10
6127634-8	1982	Thiamine injections restored the TK activity in tumor cells and reduced the TPP effect.	Thiamine	0-8	transketolase	Mus musculus	33-35
6127634-5	1982	The liver PDG, OGDG and TK activities were reduced but slightly in mice with EAC, whereas thiamine deprivation resulted in a decrease of the enzyme activities: PDG by 60%, OGDG by 25% and TK by 45%.	Thiamine	90-98	transketolase	Mus musculus	188-190
7230279-2	1981	Administration of a diet deficient in thiamine resulted in a tendency toward an elevated hepatic and pulmonary microsomal content of cytochrome P-450 and elevated activities of aminopyrine demethylase and aniline hydroxylase compared to those in similar mice fed 5 or 20 mg of thiamine per kilogram of diet.	Thiamine	38-46	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	133-149
7299493-5	1981	Juxtaglomerular granulation in the kidneys indicated that renin secretion was adequate in thiamin-deficient rats.	Thiamine	90-97	renin	Rattus norvegicus	58-63
6121420-2	1981	As compared with controls distinct deficiency of thiamin led a decrease in coenzyme thiamin diphosphate (TPP) down to 15% as well as of transketolase activity (TPP-dependent enzyme) down to 35%, especially during the terminal stage of the avitaminosis; the process was accompanied by cyclic alterations in activity of TPK and TPPase.	Thiamine	49-56	transketolase	Mus musculus	136-149
7198912-4	1981	(1979) 177, 887-894] that the deposition of thiamin-binding protein is coupled to the deposition of riboflavin-binding protein.	Thiamine	44-51	riboflavin binding protein	Gallus gallus	100-126
7296404-10	1981	Sporidesmium sclerotivorum, isolate CS-1, required thiamine for growth and sporulation.	Thiamine	51-59	chorionic somatomammotropin hormone 1	Homo sapiens	36-40
6110711-7	1981	Blood TK was more sensitive to thiamin deprivation than liver TK.	Thiamine	31-38	transketolase	Mus musculus	6-8
7240068-9	1981	The BSC method provides a rapid, accurate, and reproducible method for thiamine assay in different food products, especially for those foods with low thiamine levels.	Thiamine	71-79	solute carrier family 12 member 2	Homo sapiens	4-7
7240068-9	1981	The BSC method provides a rapid, accurate, and reproducible method for thiamine assay in different food products, especially for those foods with low thiamine levels.	Thiamine	150-158	solute carrier family 12 member 2	Homo sapiens	4-7
7236141-3	1981	Erythrocyte transketolase activity decreased in control lambs, and decreased to an even greater extent in thiamin-deficient lambs.	Thiamine	106-113	transketolase	Ovis aries	12-25
7223515-0	1981	Effect of peroral thiamine treatment on thiamine contents and transketolase activity of red blood cells in alcoholic patients.	Thiamine	18-26	transketolase	Homo sapiens	62-75
7223515-1	1981	The thiamine contents, transketolase activity and "thiamine diphosphate effect" (TDP effect) of the transketolase activity were measured in the blood of alcoholic patients during withdrawal, before and after thiamine administration (50 mg) for 10 days.	Thiamine	51-59	transketolase	Homo sapiens	100-113
7223515-7	1981	Thus the TDP effect seems to reflect the relative biochemical deficiency while transketolase activity and thiamine contents seem to be dependent on the amount of apo-enzyme and on the thiamine-binding capacity as well as the degree of thiamine deficiency.	Thiamine	184-192	transketolase	Homo sapiens	79-92
7223515-7	1981	Thus the TDP effect seems to reflect the relative biochemical deficiency while transketolase activity and thiamine contents seem to be dependent on the amount of apo-enzyme and on the thiamine-binding capacity as well as the degree of thiamine deficiency.	Thiamine	184-192	transketolase	Homo sapiens	79-92
6256098-3	1980	The values of the transketolase activity of the two groups were statistically correlated with the levels of the thiamine pyrophosphate effect and the vitamin B1 content of the blood.	Thiamine	150-160	transketolase	Homo sapiens	18-31
7413672-0	1980	Effect of thiamine deficiency on gluconeogenesis and transketolase activity in isolated hepatocytes.	Thiamine	10-18	transketolase	Homo sapiens	53-66
7439259-3	1980	Mean +/- SD, of alpha ETK improved pre-treatment level of 1.174 +/- 0.135 to 1.009 +/- 0.009 after treatment with thiamine.	Thiamine	114-122	EPH receptor A3	Homo sapiens	22-25
489520-1	1979	The thiamine status of 42 physically healthy nonalcoholic psychiatric inpatients was evaluated by measuring transketolase activity in a hemolysate of their red blood cells, before and after addition of thiamine pyrophosphate to the hemolysate.	Thiamine	4-12	transketolase	Homo sapiens	108-121
7218051-0	1980	An evaluation of a modified erythrocyte transketolase assay for assessing thiamine nutritional adequacy.	Thiamine	74-82	transketolase	Homo sapiens	40-53
94830-0	1979	Thiamine intestinal transport and phosphorylation : a study in vitro of potential inhibitors of small intestinal thiamine-pyrophosphokinase using a crude enzymatic preparation.	Thiamine	0-8	thiamin pyrophosphokinase 1	Rattus norvegicus	113-139
94830-3	1979	Eleven thiamine structural analogs and derivatives were assayed for their inhibitory action on the small intestine thiamine-pyrophosphokinase activity.	Thiamine	7-15	thiamin pyrophosphokinase 1	Rattus norvegicus	115-141
7405142-7	1980	The results obtained indicate high transketolase saturation with thiamine diphosphate with low thiamine concentration in blood.	Thiamine	65-73	transketolase	Homo sapiens	35-48
7361704-5	1980	Ten thiamin-depleted subjects were correctly identified by low urinary thiamin excretion, decreasing erythrocyte transketolase activity, and elevation of the thiamin pyrophosphate effect.	Thiamine	4-11	transketolase	Homo sapiens	113-126
7441381-1	1980	A re-investigation of the use of the transketolase-TPP-effect for the assessment of the thiamine status of chronic alcoholics with various degrees of liver cirrhosis was carried out on 36 alcoholics.	Thiamine	88-96	transketolase	Homo sapiens	37-50
7441381-4	1980	This investigation shows that the transketolase-TPP-effect is also present in patients even with severe liver cirrhosis and that a decrease of the TPP-effect can be observed after oral thiamine administration in these subjects.	Thiamine	185-193	transketolase	Homo sapiens	34-47
495541-4	1979	Thiamin requirements were evaluated in terms of erythrocyte transketolase activity and urinary excretion of the vitamin.	Thiamine	0-7	transketolase	Homo sapiens	60-73
495541-7	1979	Urinary excretion of thiamin and erythrocyte transketolase activity appear to be reasonably reliable reflections of thiamin intakes and thiamin nutritional status.	Thiamine	116-123	transketolase	Homo sapiens	45-58
495541-7	1979	Urinary excretion of thiamin and erythrocyte transketolase activity appear to be reasonably reliable reflections of thiamin intakes and thiamin nutritional status.	Thiamine	116-123	transketolase	Homo sapiens	45-58
109083-2	1979	The high specificity of interaction between the thiamin-binding protein and the riboflavin-binding protein of the egg white, with a protein/protein molar ratio of 1.0, led to the development of an alternative procedure that used the riboflavin-binding protein immobilized on CNBr-activated Sepharose as the affinity matrix.	Thiamine	48-55	riboflavin binding protein	Gallus gallus	80-106
483730-6	1979	Thiamine deficiency in the diet is also accompanied by inhibition of the transketolase activity in the gastric mucosa homogenate, which varied from 0.706 +/- 0.032 mcmole (control animals) to 0.344 +/- 0.034 mcmole of sedoheptuloso-7-phsophate/h per 1 mg protein (test animals).	Thiamine	0-8	transketolase	Rattus norvegicus	73-86
454716-0	1979	[Mechanisms of liver transketolase activation in B1-deficient rats after administration of thiamine].	Thiamine	91-99	transketolase	Rattus norvegicus	21-34
454716-3	1979	The data obtained suggest that transketolase activation in the hyaloplasmic fraction of the liver of B1-deficient rats after administration of thiamine in vivo is due to stimulation of the additional synthesis of the enzyme protein rather than to the saturation of the free apoenzyme with newly-formed TDP.	Thiamine	143-151	transketolase	Rattus norvegicus	31-44
515526-2	1979	Thiamine deficiency in these lambs was confirmed by transketolase assay.	Thiamine	0-8	transketolase	Ovis aries	52-65
453718-3	1979	Without thiamine, the transketolase reaction is inhibited.	Thiamine	8-16	transketolase	Homo sapiens	22-35
109083-2	1979	The high specificity of interaction between the thiamin-binding protein and the riboflavin-binding protein of the egg white, with a protein/protein molar ratio of 1.0, led to the development of an alternative procedure that used the riboflavin-binding protein immobilized on CNBr-activated Sepharose as the affinity matrix.	Thiamine	48-55	riboflavin binding protein	Gallus gallus	233-259
542778-0	1979	[Use of the colorimetric micromethod for determination of erythrocyte transketolase activity in the enzyme test for detection of thiamine deficiency].	Thiamine	129-137	transketolase	Homo sapiens	70-83
220801-2	1979	Hydroxythiamin was shown to inhibit specifically the activity of thiamin-dependent enzymes (transketolase and pyruvate dehydrogenase).	Thiamine	7-14	transketolase	Rattus norvegicus	92-105
32828-1	1978	The activity of the red blood cell enzymes transketolase, glutathione reductase, and aspartate transaminase, and their activation by the coenzymes thiamine, riboflavin, and pyridoxine, the pyruvate tolerance test, the leucocyte vitamin C concentration, and the activity in serum of gamma-glutamyl transferase were measured in a series of 35 patients with alcohol-related illness.	Thiamine	147-155	transketolase	Homo sapiens	43-56
32828-1	1978	The activity of the red blood cell enzymes transketolase, glutathione reductase, and aspartate transaminase, and their activation by the coenzymes thiamine, riboflavin, and pyridoxine, the pyruvate tolerance test, the leucocyte vitamin C concentration, and the activity in serum of gamma-glutamyl transferase were measured in a series of 35 patients with alcohol-related illness.	Thiamine	147-155	glutathione-disulfide reductase	Homo sapiens	58-79
32828-2	1978	The incidence of thiamine deficiency was 31% as assessed by the activation of transketolase, and 55% as assessed by the pyruvate tolerance test.	Thiamine	17-25	transketolase	Homo sapiens	78-91
208204-2	1978	A direct dependence is established between the content of thiamine, its coenzyme form, enzyme of thiamine diphosphate synthesis (thiamine pyrophosphokinase) and thiamine diphosphate-containing enzyme (transketolase) in the rat liver in different periods of ontogenesis.	Thiamine	58-66	transketolase	Rattus norvegicus	201-214
32658-4	1978	Reverse correlation between the activity of glucose-6-phosphate dehydrogenase and content of the substrate was observed in heart muscle either after administration of hydroxythiamin or thiamin; the phenomenon suggest that dehydrogenase reactions affect considerably the regulation of glucose-6-phosphate content in the tissue.	Thiamine	174-181	glucose-6-phosphate dehydrogenase	Rattus norvegicus	44-77
153861-0	1978	[Transketolase activity as a parameter for the vitamin B1 provision in some dermatoses (herpes zoster, psoriasis, drug eruptions, excema, and urticaria) (author"s transl)].	Thiamine	47-57	transketolase	Homo sapiens	1-14
149433-4	1978	A seven-fold administration to adrenalectomized animals of nicotinic acid, thiamine or a simple injection of nicotinamide normalize the transketolase activity through raising the TDP level.	Thiamine	75-83	transketolase	Rattus norvegicus	136-149
627916-5	1978	When rats are fed a thiamin deficient diet, the erythrocyte TPP level falls more rapidly than the erythrocyte transketolase activity.	Thiamine	20-27	transketolase	Rattus norvegicus	110-123
97912-3	1978	The degree of thiamine deficiency was measured by the activity coefficient of transketolase in the red blood cells.	Thiamine	14-22	transketolase	Rattus norvegicus	78-91
340187-0	1977	[Transketolase test: a means for the diagnosis of subclinical and clinical thiamine deficiency in cattle].	Thiamine	75-83	transketolase	Bos taurus	1-14
927453-6	1977	The abnormality in transketolase persisted through serial passages in tissue culture in cells grown in medium containing excess thiamine and no ethanol, indicating that the aberrations were genetic rather than dietary.	Thiamine	128-136	transketolase	Homo sapiens	19-32
910736-0	1977	The transketolase assay of thiamine in some diseases.	Thiamine	27-35	transketolase	Homo sapiens	4-17
906271-0	1977	[Effect of thiamine and its derivatives on the activity of cholinesterase of calves" blood].	Thiamine	11-19	butyrylcholinesterase	Bos taurus	59-73
331149-0	1977	Leukocyte transketolase activity: an indicator of thiamin nutriture.	Thiamine	50-57	transketolase	Homo sapiens	10-23
403480-6	1977	Thiamine-deficiency in the experimental animals was confirmed by blood transketolase assays.	Thiamine	0-8	transketolase	Macaca mulatta	71-84
412282-2	1977	The incremental addition of thiamin to the diet depressed mestranol O-demethylation, NADPH cytochrome c reductase, and cytochrome P-450 content in a dose related manner up to 2 microgram thiamin per gram of feed.	Thiamine	28-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	119-135
412282-3	1977	Pair-feeding experiments indicate that thiamin ingestion is responsible for the depression of mestranol O-demethylation and NADPH cytochrome c reductase activity while carbodhydrate ingestion is responsible for the decrease in cytochrome P-450.	Thiamine	39-46	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	227-243
201581-0	1977	Thiamine pyrophosphokinase activity in liver, heart and brain crude extracts of control and thiamine deficient rats.	Thiamine	92-100	thiamin pyrophosphokinase 1	Rattus norvegicus	0-26
23027-6	1977	The stimation of transketolase demonstrates a deficiency in thiamine.	Thiamine	60-68	transketolase	Homo sapiens	17-30
408827-1	1977	Ingestion of high levels of thiamin significantly decreased the activity of cytochrome P-450, NADPH cytochrome c reductase, and the metabolism of aniline and ethylmorphine.	Thiamine	28-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	76-92
591201-1	1977	To clarify the effect of ethanol on thiamine metabolism and activity of transketolase, a thiamine dependent enzyme, in vivo and in vitro experiments were carried out.	Thiamine	36-44	transketolase	Rattus norvegicus	72-85
591201-1	1977	To clarify the effect of ethanol on thiamine metabolism and activity of transketolase, a thiamine dependent enzyme, in vivo and in vitro experiments were carried out.	Thiamine	89-97	transketolase	Rattus norvegicus	72-85
978273-0	1976	Leukocyte transketolase activity as an indicator of thiamin nutriture in rats.	Thiamine	52-59	transketolase	Rattus norvegicus	10-23
978273-1	1976	The purpose of this study was to evaluate the possibility of using leukocyte transketolase activity (TKA) as an index of thiamin status.	Thiamine	121-128	transketolase	Rattus norvegicus	77-90
939994-1	1976	Previous studies have shown that transketolase activity is decreased in the brains of thiamin deficient rats.	Thiamine	86-93	transketolase	Rattus norvegicus	33-46
1004496-2	1976	The effects of thiamine deficiency on thiamine levels, metabolites and thiamine-dependent enzymes on the C-6 glioma and C-1300 neuroblastoma cell lines.	Thiamine	15-23	complement component 6	Mus musculus	105-108
1004496-8	1976	These data indicate that C-6 glioma and C-1300 neuroblastoma cells have the capacity to maintain normal energy metabolites in the presence of large changes in thiamine levels and thiamine dependent enzyme activity.	Thiamine	159-167	complement component 6	Mus musculus	25-28
1004496-8	1976	These data indicate that C-6 glioma and C-1300 neuroblastoma cells have the capacity to maintain normal energy metabolites in the presence of large changes in thiamine levels and thiamine dependent enzyme activity.	Thiamine	179-187	complement component 6	Mus musculus	25-28
939994-2	1976	This study assesses the effect of decreased transketolase levels on the activity of the pentose phosphate cycle in murine thiamin deficient cortex and brainstem.	Thiamine	122-129	transketolase	Mus musculus	44-57
939994-7	1976	In both the brainstem and cortex of thiamin dificient rats, areas in which transketolase activity was decreased up to 65%, the activities of the two regulatory enzymes, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase, were unaltered.	Thiamine	36-43	transketolase	Rattus norvegicus	75-88
1270885-0	1976	Effect of simultaneous thiamin and riboflavin deficiencies on the determination of transketolase and glutathione reductase.	Thiamine	23-30	transketolase	Rattus norvegicus	83-96
185765-3	1976	Thiamin (0.4 g/kg) is shown to cause a decrease in the G-6-Phase activity in the liver of the intact rats and adrenalectomized or hypophysectomized animals.	Thiamine	0-7	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	55-64
185765-4	1976	An assumption is advanced that the found in the experiment a pronounced insulin-like effect of vitamin B with respect to the G-6-Phase activity is connected with an intensified synthesis of the corresponding hormone in the pancreas.	Thiamine	95-104	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	125-134
1270885-0	1976	Effect of simultaneous thiamin and riboflavin deficiencies on the determination of transketolase and glutathione reductase.	Thiamine	23-30	glutathione-disulfide reductase	Rattus norvegicus	101-122
1253408-4	1976	Abnormal transketolase activation correlated well with clinical evidence of vitamin B1 deficiency.	Thiamine	76-86	transketolase	Homo sapiens	9-22
816749-5	1976	The levels of NADPH cytochrome c-reductase, cytochrome b5 and heme were noticeably increased in thiamine deficient animals as compared to normal rats.	Thiamine	96-104	cytochrome b5 type A	Rattus norvegicus	44-57
1210198-0	1975	[Determination of the activity of transketolase in erythrocytes in the study of the vitamin B-1 requirements of the population].	Thiamine	84-95	transketolase	Homo sapiens	34-47
1202712-1	1975	Thiamin - a predecessor of transketolase coenzyme is shown to cause an increase in the intensity of labelled 14C orotic acid incorporation into UDP and UTP of the rat liver though the time of UTP exchange remains unchanged.	Thiamine	0-7	transketolase	Rattus norvegicus	27-40
1262137-4	1976	The thiamine status was measured by determining the thiamine pyrophosphate stimulating effect of transketolase enzyme activity in whole blood.	Thiamine	4-12	transketolase	Homo sapiens	97-110
822434-1	1976	The administration of a diet deficient in thiamin results in elevated hepatic microsomal activity of aniline hydroxylase, ethylmorphone demethylase, NADPH cytochrome c reductase and cytochrome P-450 when compared to similar female rats fed diets supplemented with thiamin.	Thiamine	42-49	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	182-198
822434-3	1976	Binding of aniline to microsomes from rats fed high levels of thiamin is decreased due to a decrease in cytochrome P-450.	Thiamine	62-69	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-120
766392-0	1975	[The transketolase activity in erythrocytes as a criterion for thiamine balance in the body].	Thiamine	63-71	transketolase	Homo sapiens	5-18
766392-1	1975	In deficiency of thiamin the transketolase activity was decreased in patients and in experimental animals.	Thiamine	17-24	transketolase	Homo sapiens	29-42
1210102-3	1975	In dificiency of thiamin, caused by a single administration of hydroxythiamin, content of hexosamines and sialic acids were decreased in liver, pancreas and heart; in blood serum content of ceruloplasmin was decreased but that of glycoproteins was increased.	Thiamine	17-24	ceruloplasmin	Rattus norvegicus	190-203
1112058-0	1975	Transketolase activity of blood hemolysate, a useful index for diagnosing thiamine deficiency.	Thiamine	74-82	transketolase	Homo sapiens	0-13
4371777-0	1974	An examination of the metabolism of thiamin by rat liver alcohol dehydrogenase.	Thiamine	36-43	aldo-keto reductase family 1 member A1	Rattus norvegicus	57-78
4377016-4	1974	Thiamine deficiency caused a significant increase in soluble TTPase activity and a decrease in membrane-associated TTPase activity.	Thiamine	0-8	thiamine triphosphatase	Rattus norvegicus	61-67
4377016-4	1974	Thiamine deficiency caused a significant increase in soluble TTPase activity and a decrease in membrane-associated TTPase activity.	Thiamine	0-8	thiamine triphosphatase	Rattus norvegicus	115-121
1222502-4	1975	The normal values found for transketolase were probably due in most cases to the administration of thiamine before admission.	Thiamine	99-107	transketolase	Homo sapiens	28-41
4838352-0	1974	The thiamine status of patients with cancer as determined by the red cell transketolase activity.	Thiamine	4-12	transketolase	Homo sapiens	74-87
4187476-0	1969	[Biochemical and histochemical studies on the influence of actinomycin C and thiamine on the activity of glycogen phosphorylase (EC 2.4.1.1) and glycogen content of rat liver].	Thiamine	77-85	glycogen phosphorylase L	Rattus norvegicus	105-127
4729804-0	1973	Effects of thiamin antagonists on drug hydroxylation and properties of cytochrome P-450 in the rat.	Thiamine	11-18	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	71-87
5061037-0	1972	Hepatic glutathione reductase and riboflavin concentrations in experimental deficiency of thiamin and riboflavin in rats.	Thiamine	90-97	glutathione-disulfide reductase	Rattus norvegicus	8-29
5053845-0	1972	[Transketolase activity, thiamine excretion and blood thiamine level in man for the evaluation of the vitamin B 1  supply].	Thiamine	102-113	transketolase	Homo sapiens	1-14
5096513-2	1971	The present study describes inhibitory effects of uremic material on nervous tissue transketolase, a thiamine-dependent enzyme of the pentose phosphate pathway which has been reported to have functional importance in the metabolism of myelinated nervous structures.	Thiamine	101-109	transketolase	Homo sapiens	84-97
4343503-0	1972	Thiamine-responsive lactice acidosis in a patient with deficient low-KM pyruvate carboxylase activity in liver.	Thiamine	0-8	pyruvate carboxylase	Homo sapiens	72-92
5305321-0	1969	[On the relationship between thiamine uptake and the content of thiamine, thiamine pyrophosphate and the transketolase activity in rat organs].	Thiamine	29-37	transketolase	Rattus norvegicus	105-118
5397050-0	1969	[Evaluation of the thiamine nutritional state of uremic patients by determination of erythrocyte transketolase activity].	Thiamine	19-27	transketolase	Homo sapiens	97-110
5676522-2	1968	The suggested causal mechanisms of the encephalopathy involve two thiamine-dependent enzymes: (a) impairment of pyruvate decarboxylase activity with decreased cerebral energy (ATP) synthesis, and (b) reduction of transketolase activity with possible impairment of the hexose monophosphate shunt and subsequent decrease in NADPH formation.	Thiamine	66-74	transketolase	Rattus norvegicus	213-226
5469044-2	1970	The influence of glucose and insulin on intestinal resorption of thiamine-S 35].	Thiamine	65-75	insulin	Homo sapiens	29-36
5412651-0	1970	Transketolase activity and urinary excretion of thiamin in the assessment of thiamin-nutrition status of Indians.	Thiamine	77-84	transketolase	Homo sapiens	0-13
5472143-0	1970	Blood transketolase in assessment of thiamine deficiency in alcoholics.	Thiamine	37-45	transketolase	Homo sapiens	6-19
5676522-8	1968	(b) Both cerebral transketolase and pyruvate decarboxylase activities are impaired in low thiamine encephalopathy and the abnormality in the pyruvate decarboxylase is reflected in a rise in brain lactate.	Thiamine	90-98	transketolase	Rattus norvegicus	18-31
5734050-0	1968	[On the incorporation of thiamine (thiazole-2-C14) and 4-methyl-5-(2-chloroethyl)thiazole-2-C14 into the organs of normal and thiamine deficient rats].	Thiamine	25-33	anti-Mullerian hormone receptor type 2	Rattus norvegicus	46-49
5734050-0	1968	[On the incorporation of thiamine (thiazole-2-C14) and 4-methyl-5-(2-chloroethyl)thiazole-2-C14 into the organs of normal and thiamine deficient rats].	Thiamine	126-134	anti-Mullerian hormone receptor type 2	Rattus norvegicus	92-95
5734052-0	1968	[Inactivation of thiamine by substance K and other hemin compounds as well as by different iron salts].	Thiamine	17-25	tachykinin precursor 1	Homo sapiens	29-40
5734053-0	1968	[Studies on the vitamin B1 supply in a city collective by means of the transketolase test].	Thiamine	16-26	transketolase	Homo sapiens	71-84
5408878-0	1969	[Transketolase activity of erythrocytes of chronic alcoholic patients with assumed thiamine deficiency].	Thiamine	83-91	transketolase	Homo sapiens	1-14
14235828-0	1964	THE EFFECTS OF PENICILLIN, DL-PENICILLAMINE, AND D-SORBITOL ON ERYTHROCYTE TRANSKETOLASE ACTIVITY IN THIAMINE-DEFICIENT RATS.	Thiamine	101-109	transketolase	Rattus norvegicus	75-88
14325892-8	1965	A 2% inoculum in a medium composed of commercial defatted soy flakes, phosphate, and thiamine in tap water gave a satisfactory fermentation.	Thiamine	85-93	filamin B	Homo sapiens	97-100
5892294-2	1964	ERG on the experimental acute thiamin deficiency].	Thiamine	30-37	transcriptional regulator ERG	Oryctolagus cuniculus	0-3
5587572-0	1967	The oxidation of C14-pyruvate and of C14-ribose in thiamine deficient intact rats.	Thiamine	51-59	anti-Mullerian hormone receptor type 2	Rattus norvegicus	17-20
5901548-1	1966	Thiamine depletion as measured by erythrocyte transketolase changes.	Thiamine	0-8	transketolase	Homo sapiens	46-59
14341425-0	1965	INHIBITION OF ALCOHOL DEHYDROGENASE BY MODIFIED THIAMINE COMPOUNDS.	Thiamine	48-56	aldo-keto reductase family 1 member A1	Homo sapiens	14-35
14230376-0	1964	TRANSKETOLASE ACTIVITY IN EXPERIMENTAL THIAMINE DEFICIENCY AND HEPATIC NECROSIS.	Thiamine	39-47	transketolase	Homo sapiens	0-13
14251731-0	1964	[ON THE MECHANISM OF INTERACTION OF THIAMINE WITH CYTOCHROME C].	Thiamine	36-44	cytochrome c, somatic	Homo sapiens	50-62
14166932-0	1963	[THE THIAMINE CONTENT MEASURED BY MEANS OF DETERMINATION OF THE TRANSKETOLASE IN ERYTHROCYTES IN BREAST-FED AND ARTIFICIALLY FED CHILDREN].	Thiamine	5-13	transketolase	Homo sapiens	64-77
14022166-0	1963	[Effect of thiamine on the transketolase activity of the pigeon with beriberi].	Thiamine	11-19	transketolase	Homo sapiens	27-40
14106996-4	1963	ADENOSINE DEAMINASE IN THE SPLEEN AND KIDNEYS IN ASCORBIC ACID, BIOTIN AND THIAMINE DEFICIENCIES].	Thiamine	75-83	adenosine deaminase	Homo sapiens	0-19
13873104-0	1962	Erythrocyte transketolase in early thiamine deficiency.	Thiamine	35-43	transketolase	Homo sapiens	12-25
13535877-0	1958	[Mechanism of so-called paradoxical increase of diamine oxidase (histaminase) in the blood following administration of dimedrol and thiamine].	Thiamine	132-140	amine oxidase copper containing 1	Homo sapiens	48-63
13883214-0	1961	[The effect of thiamine on cholinesterase activity and the quantity of acetylcholine in the blood serum in experimental ascariasis].	Thiamine	15-23	butyrylcholinesterase	Homo sapiens	27-41
14482635-0	1962	[Characteristics of the metabolism of thiamine in relation to the transketolase activity of erythrocytes].	Thiamine	38-46	transketolase	Homo sapiens	66-79
13694513-0	1961	[The transketolase activity of the liver of pigeons with vitamin B1 deficiency].	Thiamine	57-67	transketolase	Homo sapiens	5-18
13774618-0	1961	[Thiamine (vitamin B 1) and its effects on the uterine musculature and on the pain during delivery (preliminary report)].	Thiamine	1-9	immunoglobulin kappa variable 7-3 (pseudogene)	Homo sapiens	19-22
13535877-0	1958	[Mechanism of so-called paradoxical increase of diamine oxidase (histaminase) in the blood following administration of dimedrol and thiamine].	Thiamine	132-140	amine oxidase copper containing 1	Homo sapiens	65-76
13381594-0	1956	[Effect of ACTH on the urinary excretion of vitamin B1].	Thiamine	44-54	proopiomelanocortin	Homo sapiens	11-15
13354429-0	1956	The activity in situ of 5"-nucleotidase, phosphomonoesterase and thiamine pyrophosphatase in vitamin B1 deficient brain tissue.	Thiamine	93-103	5'-nucleotidase ecto	Homo sapiens	24-39
13298794-0	1956	[Immunological relations between vitamin B1 and cocarboxylase (pyrophosphate of thiamine)].	Thiamine	80-88	immunoglobulin kappa variable 7-3 (pseudogene)	Homo sapiens	41-61
14361732-0	1955	Effect of riboflavin or thiamin deficiency on the response of liver and kidney adenosinetriphosphatase and D-amino acid oxidase to thyroid and adrenal alterations in rats.	Thiamine	24-31	D-amino-acid oxidase	Rattus norvegicus	107-127
13244665-0	1955	Action of insulin on thiamine phosphorylation in vitro.	Thiamine	21-29	insulin	Homo sapiens	10-17
13404141-0	1956	[Transketolase activity of pigeon liver in vitamin B1 deficiency].	Thiamine	43-53	transketolase	Homo sapiens	1-14
29015621-0	1953	Intestinal Thiamine Synthesis as Influenced by Different Fats.	Thiamine	11-19	chromosome 10 open reading frame 90	Homo sapiens	57-61
13039042-0	1952	[Effect of vitamin B1 on the content of catalase in blood in normal and infected with Staphylococcus aureus rabbits].	Thiamine	11-21	AT695_RS10915	Staphylococcus aureus	40-48
14910767-0	1952	Action of insulin on thiamine phosphorylation.	Thiamine	21-29	insulin	Homo sapiens	10-17
14391377-0	1955	[Action of insulin on the phosphorylation of thiamine in vitro].	Thiamine	45-53	insulin	Homo sapiens	11-18
13242128-0	1955	Studies on cholinesterase; effect of thiamine on the serum cholinesterase activity of human blood.	Thiamine	37-45	butyrylcholinesterase	Homo sapiens	59-73
33571483-1	2021	BACKGROUND AND AIMS: Thiamine-responsive megaloblastic anemia (TRMA), caused by SLC19A2 loss-of-function variants, is characterized by the triad of megaloblastic anemia, progressive sensorineural deafness, and non-type 1 diabetes mellitus.	Thiamine	21-29	solute carrier family 19 member 2	Homo sapiens	80-87
33759569-4	2021	Considerable amount of the microbiota-generated vitamin B1 exists in the form of TPP, and colonocytes can efficiently absorb this TPP via a high-affinity and specific carrier-mediated mechanism that involves the recently cloned colonic TPP transporter (cTPPT; product of SLC44A4 gene).	Thiamine	48-58	solute carrier family 44 member 4	Homo sapiens	271-278
34056411-9	2021	Moreover, the activity of glucose-6-phosphatase and fructose- 1-6-phosphatase (increased in the liver and kidney of diabetic rats) is restored to near-normal levels upon thiamine administration.	Thiamine	170-178	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	26-47
33967805-1	2021	Organic Cation Transporter 1 (OCT1, gene symbol: SLC22A1) is predominately expressed in human liver, localized in the basolateral membrane of hepatocytes and facilitates the uptake of endogenous compounds (e.g. serotonin, acetylcholine, thiamine), and widely prescribed drugs (e.g. metformin, fenoterol, morphine).	Thiamine	237-245	solute carrier family 22 member 1	Homo sapiens	0-28
33967805-1	2021	Organic Cation Transporter 1 (OCT1, gene symbol: SLC22A1) is predominately expressed in human liver, localized in the basolateral membrane of hepatocytes and facilitates the uptake of endogenous compounds (e.g. serotonin, acetylcholine, thiamine), and widely prescribed drugs (e.g. metformin, fenoterol, morphine).	Thiamine	237-245	solute carrier family 22 member 1	Homo sapiens	30-34
33967805-1	2021	Organic Cation Transporter 1 (OCT1, gene symbol: SLC22A1) is predominately expressed in human liver, localized in the basolateral membrane of hepatocytes and facilitates the uptake of endogenous compounds (e.g. serotonin, acetylcholine, thiamine), and widely prescribed drugs (e.g. metformin, fenoterol, morphine).	Thiamine	237-245	solute carrier family 22 member 1	Homo sapiens	49-56
33987140-3	2021	Solute carrier family 35 member F3 (SLC35F3) is a type of transporter uptakes thiamin across the cellular and mitochondrial membrane.	Thiamine	78-85	solute carrier family 35 member F3	Homo sapiens	0-34
33987140-3	2021	Solute carrier family 35 member F3 (SLC35F3) is a type of transporter uptakes thiamin across the cellular and mitochondrial membrane.	Thiamine	78-85	solute carrier family 35 member F3	Homo sapiens	36-43
33867932-8	2021	The biochemical and physiological assessments 8 weeks after SCI reveal that thiamine, but not TEGP, alleviates the SCI-induced perturbations in the rat brain metabolism, accompanied by the decreased expression of (acetyl)p53, increased expression of sirtuin 5 and an 18% improvement in the locomotor recovery.	Thiamine	76-84	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	221-224
33916491-0	2021	Reduced Thiamine Availability and Hyperglycemia Impair Thiamine Transport in Renal Glomerular Cells through Modulation of Thiamine Transporter 2.	Thiamine	8-16	solute carrier family 19 member 3	Homo sapiens	122-144
33916491-1	2021	Thiamine helps transketolase in removing toxic metabolites, counteracting high glucose-induced damage in microvascular cells, and progression of diabetic retinopathy/nephropathy in diabetic animals.	Thiamine	0-8	transketolase	Homo sapiens	15-28
33916491-4	2021	Here, we examined the behavior of thiamine transporter-1 (THTR1), THTR2, and their transcription factor Sp1 in response to high glucose and altered thiamine availability in renal cells involved in diabetic nephropathy.	Thiamine	34-42	solute carrier family 19 member 2	Homo sapiens	58-63
33916491-8	2021	Intracellular thiamine, transketolase activity, and permeability were strongly dependent on thiamine concentrations and, partly, excess glucose.	Thiamine	92-100	transketolase	Homo sapiens	24-37
33868388-3	2021	A major natural thiamine derivative, thiamine diphosphate (ThDP), is a coenzyme of central metabolism, also known to affect transcriptional activity of the master metabolic regulator and genome guardian p53.	Thiamine	16-24	tumor protein p53	Homo sapiens	203-206
33868388-10	2021	Correlation analysis of the p53 expression and enzymatic activities upon variations in cellular thiamine/ThDP levels indicates that p21 knockdown substitutes positive correlation of the p53 expression with the activity of 2-oxoglutarate dehydrogenase complex (OGDHC) for that with the activity of glutamate dehydrogenase (GDH).	Thiamine	96-104	tumor protein p53	Homo sapiens	28-31
33868388-10	2021	Correlation analysis of the p53 expression and enzymatic activities upon variations in cellular thiamine/ThDP levels indicates that p21 knockdown substitutes positive correlation of the p53 expression with the activity of 2-oxoglutarate dehydrogenase complex (OGDHC) for that with the activity of glutamate dehydrogenase (GDH).	Thiamine	96-104	H3 histone pseudogene 16	Homo sapiens	132-135
33868388-10	2021	Correlation analysis of the p53 expression and enzymatic activities upon variations in cellular thiamine/ThDP levels indicates that p21 knockdown substitutes positive correlation of the p53 expression with the activity of 2-oxoglutarate dehydrogenase complex (OGDHC) for that with the activity of glutamate dehydrogenase (GDH).	Thiamine	96-104	tumor protein p53	Homo sapiens	186-189
33868388-10	2021	Correlation analysis of the p53 expression and enzymatic activities upon variations in cellular thiamine/ThDP levels indicates that p21 knockdown substitutes positive correlation of the p53 expression with the activity of 2-oxoglutarate dehydrogenase complex (OGDHC) for that with the activity of glutamate dehydrogenase (GDH).	Thiamine	96-104	glutamate dehydrogenase 1	Homo sapiens	297-320
33868388-10	2021	Correlation analysis of the p53 expression and enzymatic activities upon variations in cellular thiamine/ThDP levels indicates that p21 knockdown substitutes positive correlation of the p53 expression with the activity of 2-oxoglutarate dehydrogenase complex (OGDHC) for that with the activity of glutamate dehydrogenase (GDH).	Thiamine	96-104	glutamate dehydrogenase 1	Homo sapiens	261-264
33231275-0	2021	Thiamine Pyrophosphokinase Deficiency due to Mutations in the TPK1 Gene: A Rare, Treatable Neurodegenerative Disorder.	Thiamine	0-8	thiamin pyrophosphokinase 1	Homo sapiens	62-66
33231275-1	2021	TPK deficiency due to TPK1 mutations is a rare neurodegenerative disorder, also known as thiamine metabolism dysfunction syndrome 5 (OMIM no.	Thiamine	89-97	thiamin pyrophosphokinase 1	Homo sapiens	22-26
33868388-12	2021	Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment.	Thiamine	217-225	tumor protein p53	Homo sapiens	8-11
33868388-12	2021	Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment.	Thiamine	217-225	H3 histone pseudogene 16	Homo sapiens	12-15
33868388-12	2021	Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment.	Thiamine	217-225	glutamic-oxaloacetic transaminase 2	Homo sapiens	103-107
33868388-12	2021	Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment.	Thiamine	217-225	glutamate dehydrogenase 1	Homo sapiens	111-114
33868388-13	2021	Cellular thiamine deficiency may interfere with antiproliferative action of cisplatin due to their common modulation of the p53/p21-dependent metabolic switch between the glutamate oxidation and transamination.	Thiamine	9-17	tumor protein p53	Homo sapiens	124-127
33868388-13	2021	Cellular thiamine deficiency may interfere with antiproliferative action of cisplatin due to their common modulation of the p53/p21-dependent metabolic switch between the glutamate oxidation and transamination.	Thiamine	9-17	H3 histone pseudogene 16	Homo sapiens	128-131
33086386-0	2021	Thiamine Treatment and Favorable Outcome in an Infant with Biallelic TPK1 Variants.	Thiamine	0-8	thiamin pyrophosphokinase 1	Homo sapiens	69-73
33867932-8	2021	The biochemical and physiological assessments 8 weeks after SCI reveal that thiamine, but not TEGP, alleviates the SCI-induced perturbations in the rat brain metabolism, accompanied by the decreased expression of (acetyl)p53, increased expression of sirtuin 5 and an 18% improvement in the locomotor recovery.	Thiamine	76-84	sirtuin 5	Rattus norvegicus	250-259
33166511-12	2021	Thiamine proved its anti-inflammatory property by decreasing the expression of iNOS and interleukin-1(IL-1) and interleukin-6(IL-6).	Thiamine	0-8	interleukin-6	Coturnix japonica	112-125
33749571-4	2022	Dietary thiamine concentrations significantly increased DGC, GRMBW, intestinal activities of amylase, Na+, K+-ATPase, CK, complex I and IV, intestinal microvilli length, number of mitochondrial per field, DeltaPsim, the P-AMPK/T-AMPK ratio, PGC-1beta protein expression as well as the transcriptions of AMPKalpha1, AMPKalpha2, PGC-1beta, Opa-1, ND-1, COX-1 and 2, SGLT-1 and GLUT-2.	Thiamine	8-16	ND1	Megalobrama amblycephala	345-349
33749571-4	2022	Dietary thiamine concentrations significantly increased DGC, GRMBW, intestinal activities of amylase, Na+, K+-ATPase, CK, complex I and IV, intestinal microvilli length, number of mitochondrial per field, DeltaPsim, the P-AMPK/T-AMPK ratio, PGC-1beta protein expression as well as the transcriptions of AMPKalpha1, AMPKalpha2, PGC-1beta, Opa-1, ND-1, COX-1 and 2, SGLT-1 and GLUT-2.	Thiamine	8-16	COX1	Megalobrama amblycephala	351-362
33737877-7	2020	Based on recent publications, we compared the results of the IL-17 response from our clinical and in vitro study to those found in other proinflammatory disease conditions (metabolic conditions, septic shock, viral infections and COVID-19) and effective and safe dose ranges of thiamine.	Thiamine	278-286	interleukin 17A	Mus musculus	61-66
33737877-10	2020	Thiamine-treated DC patients showed significant lowering in IL-17 and increase in the IL-22 levels.	Thiamine	0-8	interleukin 17A	Homo sapiens	60-65
33737877-10	2020	Thiamine-treated DC patients showed significant lowering in IL-17 and increase in the IL-22 levels.	Thiamine	0-8	interleukin 22	Homo sapiens	86-91
33737877-13	2020	Thiamine, a very safe drug even at very high doses, could be repurposed for treating the Th17 mediated IL-17 immune storm, and the subsequent neurological symptoms observed in COVID-19.	Thiamine	0-8	interleukin 17A	Homo sapiens	103-108
32883659-1	2021	OBJECTIVES: Severe pulmonary hypertension (PH) causing right heart failure can occur due to thiamine deficiency in exclusively breastfeeding infants.	Thiamine	92-100	phenylalanine hydroxylase	Homo sapiens	43-45
33649974-0	2021	The Effects of Genetic Mutations and Drugs on the Activity of the Thiamine Transporter, SLC19A2.	Thiamine	66-74	solute carrier family 19 member 2	Homo sapiens	88-95
33649974-1	2021	A rare cause of megaloblastic anemia (MA) is thiamine-responsive megaloblastic anemia (TRMA), a genetic disorder caused by mutations in SLC19A2 (encoding THTR1), a thiamine transporter.	Thiamine	45-53	solute carrier family 19 member 2	Homo sapiens	87-91
33649974-1	2021	A rare cause of megaloblastic anemia (MA) is thiamine-responsive megaloblastic anemia (TRMA), a genetic disorder caused by mutations in SLC19A2 (encoding THTR1), a thiamine transporter.	Thiamine	45-53	solute carrier family 19 member 2	Homo sapiens	136-143
33649974-1	2021	A rare cause of megaloblastic anemia (MA) is thiamine-responsive megaloblastic anemia (TRMA), a genetic disorder caused by mutations in SLC19A2 (encoding THTR1), a thiamine transporter.	Thiamine	45-53	solute carrier family 19 member 2	Homo sapiens	154-159
33649974-1	2021	A rare cause of megaloblastic anemia (MA) is thiamine-responsive megaloblastic anemia (TRMA), a genetic disorder caused by mutations in SLC19A2 (encoding THTR1), a thiamine transporter.	Thiamine	164-172	solute carrier family 19 member 2	Homo sapiens	87-91
33649974-1	2021	A rare cause of megaloblastic anemia (MA) is thiamine-responsive megaloblastic anemia (TRMA), a genetic disorder caused by mutations in SLC19A2 (encoding THTR1), a thiamine transporter.	Thiamine	164-172	solute carrier family 19 member 2	Homo sapiens	136-143
33649974-3	2021	Functional characterization of selected SLC19A2 variants was performed by confocal microscopy and isotopic uptake studies of [3H]-thiamine in HEK293 cells.	Thiamine	130-138	solute carrier family 19 member 2	Homo sapiens	40-47
33649974-6	2021	Ten of 63 drugs inhibited SLC19A2-mediated thiamine transport >= 50% at screening concentrations; however, with the exception of erythromycin, none was predicted to inhibit SLC19A2 at clinically relevant unbound plasma concentrations.	Thiamine	43-51	solute carrier family 19 member 2	Homo sapiens	26-33
33995940-0	2021	Thiamine reduced metabolic syndrome symptoms in rats via down-regulation of hepatic nuclear factor-kbeta and induction activity of glyoxalase-I.	Thiamine	0-8	glyoxalase 1	Rattus norvegicus	131-143
33995940-12	2021	Conclusion: Thiamine decreased body weight and improved metabolism and activity of glyoxalase-I in MS rats with anti-glycation, antioxidant, and anti-inflammatory activities.	Thiamine	12-20	glyoxalase 1	Rattus norvegicus	83-95
33379049-0	2021	Determination of butyrylcholinesterase activity based on thiamine luminescence modulated by MnO2 nanosheets.	Thiamine	57-65	butyrylcholinesterase	Homo sapiens	17-38
33379049-1	2021	In this paper, a novel strategy for biosensing butyrylcholinesterase (BChE) activity is developed based on manganese dioxide (MnO2) nanosheets to modulate the photoluminescence of thiamine (TH).	Thiamine	180-188	butyrylcholinesterase	Homo sapiens	47-68
33379049-1	2021	In this paper, a novel strategy for biosensing butyrylcholinesterase (BChE) activity is developed based on manganese dioxide (MnO2) nanosheets to modulate the photoluminescence of thiamine (TH).	Thiamine	180-188	butyrylcholinesterase	Homo sapiens	70-74
33379049-1	2021	In this paper, a novel strategy for biosensing butyrylcholinesterase (BChE) activity is developed based on manganese dioxide (MnO2) nanosheets to modulate the photoluminescence of thiamine (TH).	Thiamine	190-192	butyrylcholinesterase	Homo sapiens	47-68
33379049-1	2021	In this paper, a novel strategy for biosensing butyrylcholinesterase (BChE) activity is developed based on manganese dioxide (MnO2) nanosheets to modulate the photoluminescence of thiamine (TH).	Thiamine	190-192	butyrylcholinesterase	Homo sapiens	70-74
33498154-0	2021	Sensitive Fluorescence Assay for the Detection of Alkaline Phosphatase Based on a Cu2+-Thiamine System.	Thiamine	87-95	alkaline phosphatase, placental	Homo sapiens	50-70
33498154-1	2021	The authors describe a novel, facile, and sensitive fluorometric strategy based on a Cu2+-thiamine (Cu2+-TH) system for the detection of alkaline phosphatase (ALP) activity and inhibition.	Thiamine	90-98	alkaline phosphatase, placental	Homo sapiens	137-157
33166511-12	2021	Thiamine proved its anti-inflammatory property by decreasing the expression of iNOS and interleukin-1(IL-1) and interleukin-6(IL-6).	Thiamine	0-8	interleukin-6	Coturnix japonica	126-130
33374697-0	2020	A 33-mRNA Classifier Is Able to Produce Inflammopathic, Adaptive, and Coagulopathic Endotypes with Prognostic Significance: The Outcomes of Metabolic Resuscitation Using Ascorbic Acid, Thiamine, and Glucocorticoids in the Early Treatment of Sepsis (ORANGES) Trial.	Thiamine	185-193	glycoprotein A33	Homo sapiens	0-4
33076074-3	2021	Upon the addition of hemin, G-rich segments at the end of H1 and H2 self-assembled into the peroxidase-mimicking hemin/G-quadruplex DNAzymes, which catalyzed the hydrogen peroxide-mediated oxidation of thiamine to achieve fluorescence detection of CEA.	Thiamine	202-210	CEA cell adhesion molecule 3	Homo sapiens	248-251
33076048-0	2021	A thiamine-triggered fluormetric assay for acetylcholinesterase activity and inhibitor screening based on oxidase-like activity of MnO2 nanosheets.	Thiamine	2-10	acetylcholinesterase (Cartwright blood group)	Homo sapiens	43-63
32996449-2	2020	Thiamin status has traditionally been measured through the erythrocyte activation assay (ETKA) or basal transketolase activity (ETK), which indirectly measures thiamin diphosphate (TDP).	Thiamine	0-7	transketolase	Homo sapiens	104-117
33008889-1	2020	SLC19A2 and SLC19A3, also known as thiamine transporters (THTR) 1 and 2, respectively, transport the positively charged thiamine (vitamin B1) into cells to enable its efficient utilization.	Thiamine	35-43	solute carrier family 19 member 2	Homo sapiens	0-7
33008889-1	2020	SLC19A2 and SLC19A3, also known as thiamine transporters (THTR) 1 and 2, respectively, transport the positively charged thiamine (vitamin B1) into cells to enable its efficient utilization.	Thiamine	35-43	solute carrier family 19 member 3	Homo sapiens	12-19
33008889-1	2020	SLC19A2 and SLC19A3, also known as thiamine transporters (THTR) 1 and 2, respectively, transport the positively charged thiamine (vitamin B1) into cells to enable its efficient utilization.	Thiamine	130-140	solute carrier family 19 member 2	Homo sapiens	0-7
33008889-1	2020	SLC19A2 and SLC19A3, also known as thiamine transporters (THTR) 1 and 2, respectively, transport the positively charged thiamine (vitamin B1) into cells to enable its efficient utilization.	Thiamine	130-140	solute carrier family 19 member 3	Homo sapiens	12-19
33008889-1	2020	SLC19A2 and SLC19A3, also known as thiamine transporters (THTR) 1 and 2, respectively, transport the positively charged thiamine (vitamin B1) into cells to enable its efficient utilization.	Thiamine	130-140	solute carrier family 19 member 2	Homo sapiens	35-71
33008889-6	2020	It was saturable as a function of pyridoxine concentration, with an apparent K m of 37.8 and 18.5 muM, for SLC19A2 and SLC19A3, respectively, and inhibited by the pyridoxine analogs pyridoxal and pyridoxamine as well as thiamine.	Thiamine	220-228	solute carrier family 19 member 2	Sus scrofa	107-114
33008889-6	2020	It was saturable as a function of pyridoxine concentration, with an apparent K m of 37.8 and 18.5 muM, for SLC19A2 and SLC19A3, respectively, and inhibited by the pyridoxine analogs pyridoxal and pyridoxamine as well as thiamine.	Thiamine	220-228	solute carrier family 19 member 3	Sus scrofa	119-126
32706593-1	2020	Rationale: In December 2016, a single-center study describing significant improvements in mortality among a small group of patients with severe sepsis and septic shock treated with hydrocortisone, high-dose ascorbic acid, and thiamine (HAT therapy) was published online.Objectives: This study aims to describe the administration of HAT therapy among U.S. adults with septic shock before and after study publication and to compare outcomes between patients who received and did not receive HAT therapy.Methods: We performed a retrospective cohort study of 379 acute care hospitals in the Premier Healthcare Database including patients discharged from October 1, 2015, to September 30, 2018.	Thiamine	226-234	transmembrane serine protease 11D	Homo sapiens	236-239
32706593-1	2020	Rationale: In December 2016, a single-center study describing significant improvements in mortality among a small group of patients with severe sepsis and septic shock treated with hydrocortisone, high-dose ascorbic acid, and thiamine (HAT therapy) was published online.Objectives: This study aims to describe the administration of HAT therapy among U.S. adults with septic shock before and after study publication and to compare outcomes between patients who received and did not receive HAT therapy.Methods: We performed a retrospective cohort study of 379 acute care hospitals in the Premier Healthcare Database including patients discharged from October 1, 2015, to September 30, 2018.	Thiamine	226-234	transmembrane serine protease 11D	Homo sapiens	332-335
32706593-1	2020	Rationale: In December 2016, a single-center study describing significant improvements in mortality among a small group of patients with severe sepsis and septic shock treated with hydrocortisone, high-dose ascorbic acid, and thiamine (HAT therapy) was published online.Objectives: This study aims to describe the administration of HAT therapy among U.S. adults with septic shock before and after study publication and to compare outcomes between patients who received and did not receive HAT therapy.Methods: We performed a retrospective cohort study of 379 acute care hospitals in the Premier Healthcare Database including patients discharged from October 1, 2015, to September 30, 2018.	Thiamine	226-234	transmembrane serine protease 11D	Homo sapiens	332-335
32996449-2	2020	Thiamin status has traditionally been measured through the erythrocyte activation assay (ETKA) or basal transketolase activity (ETK), which indirectly measures thiamin diphosphate (TDP).	Thiamine	0-7	BMX non-receptor tyrosine kinase	Homo sapiens	89-92
33183558-3	2020	Inorganic NO3- tablets consist of NO3- rich beetroot extract, thiamine nitrate, and potassium nitrate in the presence of ascorbic acid, to facilitate NO bioavailability.	Thiamine	62-78	NBL1, DAN family BMP antagonist	Homo sapiens	10-13
33036978-4	2020	SLC19A2 is necessary for optimal growth and ASNase resistance, when standard medium thiamine is lowered ~100-fold to human plasma concentrations.	Thiamine	84-92	solute carrier family 19 member 2	Homo sapiens	0-7
33544541-1	2021	OBJECTIVES: Biallelic mutations in the SLC25A19 gene impair the function of the thiamine mitochondrial carrier, leading to two distinct clinical phenotypes.	Thiamine	80-88	solute carrier family 25 member 19	Homo sapiens	39-47
33544541-10	2021	CONCLUSIONS: Non-Amish SLC25A19 deficiency is an extra-rare cause of Leigh syndrome responsive to thiamine treatment.	Thiamine	98-106	solute carrier family 25 member 19	Homo sapiens	23-31
33037045-0	2020	Differences in metformin and thiamine uptake between human and mouse organic cation transporter OCT1: structural determinants and potential consequences for intrahepatic concentrations.	Thiamine	29-37	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	96-100
33037045-3	2020	Similarly, the effects of OCT1 deficiency on the pharmacokinetics of thiamine were reported to differ between human and mouse.	Thiamine	69-77	solute carrier family 22 member 1	Homo sapiens	26-30
33037045-4	2020	Here, we compared the uptake characteristics of metformin and thiamine between human and mouse OCT1 using stably transfected HEK293 cells.	Thiamine	62-70	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	95-99
33037045-7	2020	Similarly, the affinity for thiamine was 9.5-fold lower in human than in mouse OCT1.	Thiamine	28-36	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	79-83
33037045-10	2020	In conclusion, the contribution of human OCT1 to the cellular uptake of thiamine and especially of metformin may be much lower than that of mouse OCT1.	Thiamine	72-80	solute carrier family 22 member 1	Homo sapiens	41-45
33037045-13	2020	Significance Statement OCT1 is a major hepatic uptake transporter of metformin and thiamine, but we report strong differences in the affinity for both compounds between human and mouse OCT1.	Thiamine	83-91	solute carrier family 22 member 1	Homo sapiens	23-27
33124720-7	2020	We identified eight zwitterions, including ergothioneine, carnitine, carnosine, gabapentin, as well as four cations, including MPP+ , thiamine, and cimetidine, as substrates of SLC22A15.	Thiamine	134-142	solute carrier family 22 member 15	Homo sapiens	177-185
33629063-11	2020	Within the clusters, distinctive basal ganglia MRI patterns were noted in acquired disorders such as cerebral palsy due to hypoxic ischaemic encephalopathy in full-term babies, kernicterus and vigabatrin toxicity and in rare genetic disorders such as 3-methylglutaconic aciduria with deafness, encephalopathy and Leigh-like syndrome, thiamine responsive basal ganglia disease, pantothenate kinase-associated neurodegeneration, TUBB4A and hypermanganesemia.	Thiamine	334-342	tubulin beta 4A class IVa	Homo sapiens	427-433
33036978-5	2020	In addition, humanizing blood thiamine content of mice through diet sensitizes SLC19A2-low leukemia cells to ASNase in vivo.	Thiamine	30-38	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	79-86
32683950-2	2020	Pancreatic acinar cells (PACs) obtain thiamin from their surrounding (circulation) via transport across the plasma membrane, a process that is mediated by THTR-1 and THTR-2.	Thiamine	38-45	solute carrier family 19 member 2	Homo sapiens	155-161
32683950-2	2020	Pancreatic acinar cells (PACs) obtain thiamin from their surrounding (circulation) via transport across the plasma membrane, a process that is mediated by THTR-1 and THTR-2.	Thiamine	38-45	solute carrier family 19 member 3	Homo sapiens	166-172
32683950-4	2020	We addressed this by focusing on the predominant thiamin transporter THTR-1 (encoded by SLC19A2 gene) in PACs.	Thiamine	49-56	solute carrier family 19 member 2	Homo sapiens	69-75
32683950-4	2020	We addressed this by focusing on the predominant thiamin transporter THTR-1 (encoded by SLC19A2 gene) in PACs.	Thiamine	49-56	solute carrier family 19 member 2	Homo sapiens	88-95
32683950-7	2020	Focusing on miR-200a-3p (since it is highly expressed in mouse and human pancreas) we found transfecting PAC 266-6 and human primary PACs (hPACs) with mimic miR-200a-3p lead to a significant inhibition of THTR-1 expression (both protein and mRNA levels) and in thiamin uptake.	Thiamine	261-268	solute carrier family 19 member 2	Homo sapiens	205-211
32869036-9	2020	Based on recent publications, we compared the results of the IL-17 response from our clinical and in vitro study to those found in other proinflammatory disease conditions (metabolic conditions, septic shock, viral infections and COVID-19), including symptoms, and dose ranges of effective and safe administration of thiamine.	Thiamine	317-325	interleukin 17A	Mus musculus	61-66
32869036-12	2020	Three-week of 200 mg daily thiamine treatment significantly lowered the baseline IL-17 levels while increased IL-22 levels (anti-inflammatory response).	Thiamine	27-35	interleukin 17A	Mus musculus	81-86
32869036-12	2020	Three-week of 200 mg daily thiamine treatment significantly lowered the baseline IL-17 levels while increased IL-22 levels (anti-inflammatory response).	Thiamine	27-35	interleukin 22	Homo sapiens	110-115
32869036-13	2020	This was validated by an in vitro macrophage response using a lower thiamine dose equivalent (100 mg), which resulted in attenuation of IL-17 and elevation of IL-22 at the mRNA level compared to the ethanol-only treated group.	Thiamine	68-76	interleukin 17A	Mus musculus	136-141
32869036-13	2020	This was validated by an in vitro macrophage response using a lower thiamine dose equivalent (100 mg), which resulted in attenuation of IL-17 and elevation of IL-22 at the mRNA level compared to the ethanol-only treated group.	Thiamine	68-76	interleukin 22	Homo sapiens	159-164
32869036-16	2020	Discussion The Th17 mediated IL-17 proinflammatory response can potentially be attenuated by thiamine.	Thiamine	93-101	interleukin 17A	Homo sapiens	29-34
32842513-8	2020	Level 1 and 2 evidence supports the use of thiamine, vitamin C, and vitamin D in COVID-like respiratory diseases, ARDS, and sepsis.	Thiamine	43-51	level 1 and 2	None	0-13
33040724-0	2020	Regulation of Thiamine (Vitamin B1)-Dependent Metabolism in Mammals by p53.	Thiamine	14-22	tumor protein p53	Homo sapiens	71-74
32722956-4	2022	RESULTS: Thiamin supplementation significantly decreased serum high-sensitivity C-reactive protein (hs-CRP) (beta - 0.98 mg/L; 95% CI, -1.54, -0.42; p = .001) and plasma malondialdehyde (MDA) levels (beta - 0.86 micromol/L; 95% CI, -1.15, -0.57; p < .001) when compared with the placebo.	Thiamine	9-16	C-reactive protein	Homo sapiens	80-98
32722956-5	2022	In addition, thiamin supplementation downregulated gene expression of tumor necrosis factor-alpha (TNF-alpha) (p = .002) in peripheral blood mononuclear cells of patients with GDM.	Thiamine	13-20	tumor necrosis factor	Homo sapiens	70-97
32722956-5	2022	In addition, thiamin supplementation downregulated gene expression of tumor necrosis factor-alpha (TNF-alpha) (p = .002) in peripheral blood mononuclear cells of patients with GDM.	Thiamine	13-20	tumor necrosis factor	Homo sapiens	99-108
32722956-7	2022	CONCLUSION: Overall, thiamin supplementation for 6 weeks to patients with GDM significantly reduced hs-CRP and MDA levels, and gene expression of TNF-alpha, but did not affect other biomarkers of inflammation and oxidative stress.	Thiamine	21-28	C-reactive protein	Homo sapiens	103-106
32722956-7	2022	CONCLUSION: Overall, thiamin supplementation for 6 weeks to patients with GDM significantly reduced hs-CRP and MDA levels, and gene expression of TNF-alpha, but did not affect other biomarkers of inflammation and oxidative stress.	Thiamine	21-28	tumor necrosis factor	Homo sapiens	146-155
32404369-0	2020	The ThiL enzyme is a valid antibacterial target essential for both thiamine biosynthesis and salvage pathways in Pseudomonas aeruginosa.	Thiamine	67-75	acetyl-CoA acetyltransferase 1	Homo sapiens	4-8
32404369-5	2020	We demonstrate that thiL deletion abolishes not only thiamine biosynthesis but also thiamine salvage capability and results in growth defects of the DeltathiL strain even in the presence of thiamine derivatives, except for TPP.	Thiamine	53-61	acetyl-CoA acetyltransferase 1	Homo sapiens	20-24
32404369-5	2020	We demonstrate that thiL deletion abolishes not only thiamine biosynthesis but also thiamine salvage capability and results in growth defects of the DeltathiL strain even in the presence of thiamine derivatives, except for TPP.	Thiamine	84-92	acetyl-CoA acetyltransferase 1	Homo sapiens	20-24
32404369-5	2020	We demonstrate that thiL deletion abolishes not only thiamine biosynthesis but also thiamine salvage capability and results in growth defects of the DeltathiL strain even in the presence of thiamine derivatives, except for TPP.	Thiamine	84-92	acetyl-CoA acetyltransferase 1	Homo sapiens	20-24
33040724-4	2020	In order to elucidate the mechanism of regulation of thiamine-dependent metabolism by p53, we assessed putative p53-binding sites near transcription starting points in genes coding for transporters and enzymes, whose function is associated with thiamine and/or its derivatives.	Thiamine	53-61	tumor protein p53	Homo sapiens	86-89
33040724-4	2020	In order to elucidate the mechanism of regulation of thiamine-dependent metabolism by p53, we assessed putative p53-binding sites near transcription starting points in genes coding for transporters and enzymes, whose function is associated with thiamine and/or its derivatives.	Thiamine	53-61	tumor protein p53	Homo sapiens	112-115
33193954-1	2020	Thiamine-responsive megaloblastic anaemia (TRMA) is a syndrome associated with megaloblastic anaemia, diabetes mellitus and sensorineural deafness, due to mutations in the SLC19A2gene, which codes for a thiamine carrier protein.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	172-179
33193954-1	2020	Thiamine-responsive megaloblastic anaemia (TRMA) is a syndrome associated with megaloblastic anaemia, diabetes mellitus and sensorineural deafness, due to mutations in the SLC19A2gene, which codes for a thiamine carrier protein.	Thiamine	203-211	solute carrier family 19 member 2	Homo sapiens	172-179
32831862-6	2020	In addition, it is revealed that, after SCI, the highly expressed LncRNA AABR07071383.1 in the post-SCI cis/trans-regulates the expression of mRNA Acpp mRNA that encodes a key enzyme involved in the metabolic process of thiamine in the abirritation of the dorsal root ganglion (DRG), which implies that TCH injection may be more effective when administered with benfotiamine (a common treatment drug).	Thiamine	220-228	acid phosphatase 3	Rattus norvegicus	147-151
32361878-1	2020	TPK deficiency, also known as thiamine metabolism dysfunction syndrome 5, is a rare autosomal recessive disorder of inborn error of metabolism caused by TPK1 gene mutation.	Thiamine	30-38	thiamin pyrophosphokinase 1	Homo sapiens	153-157
32818907-0	2020	Vitamin B1 Supports the Differentiation of T Cells through TGF-beta Superfamily Production in Thymic Stromal Cells.	Thiamine	0-10	transforming growth factor alpha	Homo sapiens	59-67
26425749-9	1993	MANAGEMENT: Treatment of manifestations: Specific treatment is possible for the three nuclear gene-encoded Leigh-like syndromes: biotin-thiamine-responsive basal ganglia disease (BTBGD), biotinidase deficiency, and coenzyme Q10 deficiency caused by mutation of PDSS2.	Thiamine	136-144	decaprenyl diphosphate synthase subunit 2	Homo sapiens	261-266
26425749-11	1993	Prevention of primary manifestations: Prevention of manifestations is possible for biotin-thiamine-responsive basal ganglia disease (BTBGD), biotinidase deficiency, and coenzyme Q10 deficiency caused by mutation of PDSS2.	Thiamine	90-98	decaprenyl diphosphate synthase subunit 2	Homo sapiens	215-220
33040724-0	2020	Regulation of Thiamine (Vitamin B1)-Dependent Metabolism in Mammals by p53.	Thiamine	24-34	tumor protein p53	Homo sapiens	71-74
33040724-3	2020	Thiamine diphosphate (ThDP), which is a major thiamine derivative, affects p53 binding to DNA.	Thiamine	46-54	tumor protein p53	Homo sapiens	75-78
32380162-0	2020	Novel p.P298L SURF1 mutation in thiamine deficient Leigh syndrome patients compromises cytochrome c oxidase activity.	Thiamine	32-40	SURF1 cytochrome c oxidase assembly factor	Homo sapiens	14-19
32100911-0	2020	Non-coenzyme role of vitamin B1 in RANKL-induced osteoclastogenesis and ovariectomy induced osteoporosis.	Thiamine	21-31	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	35-40
32380162-3	2020	We screened all the 9 exons and exon-intron boundaries of SURF1 gene in 165 Indian Leigh syndrome patients who were thiamine responsive too.	Thiamine	116-124	SURF1 cytochrome c oxidase assembly factor	Homo sapiens	58-63
32441748-1	2020	Like fungi and some prokaryotes, plants use a thiazole synthase (THI4) to make the thiazole precursor of thiamin.	Thiamine	105-112	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	65-69
32564742-5	2020	Peptides of two annotated bacterial phosphatases, alkaline phosphatase L from the DING protein family and exopolyphosphatase, were identified in the acidic thiamine eluate.	Thiamine	156-164	ring finger protein 2	Homo sapiens	82-86
32498429-4	2020	In this study, we investigated the genetic association of four single nucleotide polymorphisms (SNPs) within the 3"-untranslated regions of vitamin B-related genes, including TCN2 (encodes transcobalamin II), CD320 (encodes transcobalamin II receptor), SLC19A1 (encodes reduced folate carrier protein 1), and SLC19A2 (encodes thiamine carrier 1), with osteoporosis and osteoporotic vertebral compression fracture (OVCF).	Thiamine	140-149	transcobalamin 2	Homo sapiens	175-179
32498429-4	2020	In this study, we investigated the genetic association of four single nucleotide polymorphisms (SNPs) within the 3"-untranslated regions of vitamin B-related genes, including TCN2 (encodes transcobalamin II), CD320 (encodes transcobalamin II receptor), SLC19A1 (encodes reduced folate carrier protein 1), and SLC19A2 (encodes thiamine carrier 1), with osteoporosis and osteoporotic vertebral compression fracture (OVCF).	Thiamine	140-149	CD320 molecule	Homo sapiens	209-214
32498429-4	2020	In this study, we investigated the genetic association of four single nucleotide polymorphisms (SNPs) within the 3"-untranslated regions of vitamin B-related genes, including TCN2 (encodes transcobalamin II), CD320 (encodes transcobalamin II receptor), SLC19A1 (encodes reduced folate carrier protein 1), and SLC19A2 (encodes thiamine carrier 1), with osteoporosis and osteoporotic vertebral compression fracture (OVCF).	Thiamine	140-149	solute carrier family 19 member 1	Homo sapiens	253-260
32498429-4	2020	In this study, we investigated the genetic association of four single nucleotide polymorphisms (SNPs) within the 3"-untranslated regions of vitamin B-related genes, including TCN2 (encodes transcobalamin II), CD320 (encodes transcobalamin II receptor), SLC19A1 (encodes reduced folate carrier protein 1), and SLC19A2 (encodes thiamine carrier 1), with osteoporosis and osteoporotic vertebral compression fracture (OVCF).	Thiamine	140-149	solute carrier family 19 member 2	Homo sapiens	309-316
31964426-9	2020	In addition, there was a positive correlation between thiamine adequacy and MPO concentration (rho = 0.22, p &lt;0.01) and between calcium adequacy and NEO concentration (rho = 0.23; p &lt; 0.01).	Thiamine	54-62	myeloperoxidase	Homo sapiens	76-79
32142245-2	2020	Vitamin B1, a bifunctional thiazolium N-heterocyclic carbene (NHC) precursor, is the coenzyme for transketolase.	Thiamine	0-10	transketolase	Homo sapiens	98-111
32333971-8	2020	A further four patients were diagnosed with thiamine-responsive megaloblastic anaemia (TRMA), all male, three from the same consanguineous family, and were treated with high-dose thiamine.	Thiamine	44-52	solute carrier family 19 member 2	Homo sapiens	87-91
32317674-4	2020	Four key genes (SNZ2, THI6, THI21 and THI80), participated in the biosynthesis of vitamin B6 and thiamine, were up-regulated significantly in proanthocyanidins treated yeast cells and the gene expression levels were verified by RT-qPCR.	Thiamine	97-105	pyridoxine biosynthesis protein SNZ2	Saccharomyces cerevisiae S288C	16-20
32317674-4	2020	Four key genes (SNZ2, THI6, THI21 and THI80), participated in the biosynthesis of vitamin B6 and thiamine, were up-regulated significantly in proanthocyanidins treated yeast cells and the gene expression levels were verified by RT-qPCR.	Thiamine	97-105	bifunctional hydroxyethylthiazole kinase/thiamine-phosphate diphosphorylase	Saccharomyces cerevisiae S288C	22-26
32317674-4	2020	Four key genes (SNZ2, THI6, THI21 and THI80), participated in the biosynthesis of vitamin B6 and thiamine, were up-regulated significantly in proanthocyanidins treated yeast cells and the gene expression levels were verified by RT-qPCR.	Thiamine	97-105	bifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase	Saccharomyces cerevisiae S288C	28-33
32317674-4	2020	Four key genes (SNZ2, THI6, THI21 and THI80), participated in the biosynthesis of vitamin B6 and thiamine, were up-regulated significantly in proanthocyanidins treated yeast cells and the gene expression levels were verified by RT-qPCR.	Thiamine	97-105	thiamine diphosphokinase	Saccharomyces cerevisiae S288C	38-43
31989470-0	2020	Thiamine Deficiency Modulates p38MAPK and Heme Oxygenase-1 in Mouse Brain: Association with Early Tissue and Behavioral Changes.	Thiamine	0-8	mitogen-activated protein kinase 14	Mus musculus	30-37
31989470-0	2020	Thiamine Deficiency Modulates p38MAPK and Heme Oxygenase-1 in Mouse Brain: Association with Early Tissue and Behavioral Changes.	Thiamine	0-8	heme oxygenase 1	Mus musculus	42-58
32564742-8	2020	The search for mammalian DING phosphatases in the eluates from thiamine-Sepharose revealed X-DING-CD4, mostly eluted by the acidic thiamine solution (pH 5.6).	Thiamine	63-71	ring finger protein 2	Homo sapiens	25-29
32564742-8	2020	The search for mammalian DING phosphatases in the eluates from thiamine-Sepharose revealed X-DING-CD4, mostly eluted by the acidic thiamine solution (pH 5.6).	Thiamine	63-71	ring finger protein 2	Homo sapiens	93-97
32564742-8	2020	The search for mammalian DING phosphatases in the eluates from thiamine-Sepharose revealed X-DING-CD4, mostly eluted by the acidic thiamine solution (pH 5.6).	Thiamine	63-71	CD4 molecule	Homo sapiens	98-101
32564742-8	2020	The search for mammalian DING phosphatases in the eluates from thiamine-Sepharose revealed X-DING-CD4, mostly eluted by the acidic thiamine solution (pH 5.6).	Thiamine	131-139	ring finger protein 2	Homo sapiens	25-29
32564742-8	2020	The search for mammalian DING phosphatases in the eluates from thiamine-Sepharose revealed X-DING-CD4, mostly eluted by the acidic thiamine solution (pH 5.6).	Thiamine	131-139	CD4 molecule	Homo sapiens	98-101
31593619-0	2020	Variability and heritability of thiamine pharmacokinetics with focus on OCT1 effects on membrane transport and pharmacokinetics in humans.	Thiamine	32-40	solute carrier family 22 member 1	Homo sapiens	72-76
31593619-1	2020	Thiamine is substrate of the hepatic uptake transporter OCT1, and pathological lipid metabolism was associated with OCT1-dependent thiamine transport.	Thiamine	0-8	solute carrier family 22 member 1	Homo sapiens	56-60
31593619-6	2020	Further studies in primary human hepatocytes indicated that several cation transporters including OCT1, OCT3, and THTR-2 contribute to hepatic uptake of thiamine.	Thiamine	153-161	solute carrier family 22 member 1	Homo sapiens	98-102
31593619-1	2020	Thiamine is substrate of the hepatic uptake transporter OCT1, and pathological lipid metabolism was associated with OCT1-dependent thiamine transport.	Thiamine	131-139	solute carrier family 22 member 1	Homo sapiens	56-60
31593619-1	2020	Thiamine is substrate of the hepatic uptake transporter OCT1, and pathological lipid metabolism was associated with OCT1-dependent thiamine transport.	Thiamine	131-139	solute carrier family 22 member 1	Homo sapiens	116-120
31593619-4	2020	The variant OCT1*2 had reduced and OCT1*3 to OCT1*6 had deficient thiamine uptake activity.	Thiamine	66-74	solute carrier family 22 member 1	Homo sapiens	12-16
31593619-6	2020	Further studies in primary human hepatocytes indicated that several cation transporters including OCT1, OCT3, and THTR-2 contribute to hepatic uptake of thiamine.	Thiamine	153-161	solute carrier family 22 member 3	Homo sapiens	104-108
31593619-4	2020	The variant OCT1*2 had reduced and OCT1*3 to OCT1*6 had deficient thiamine uptake activity.	Thiamine	66-74	solute carrier family 22 member 1	Homo sapiens	35-39
31593619-6	2020	Further studies in primary human hepatocytes indicated that several cation transporters including OCT1, OCT3, and THTR-2 contribute to hepatic uptake of thiamine.	Thiamine	153-161	solute carrier family 19 member 3	Homo sapiens	114-120
31593619-4	2020	The variant OCT1*2 had reduced and OCT1*3 to OCT1*6 had deficient thiamine uptake activity.	Thiamine	66-74	solute carrier family 22 member 1	Homo sapiens	35-39
32184802-8	2020	From Duroc low feed efficient group, the TPK1 gene was found involved with thiamine metabolism, whereas PARD6G, DLG2, CRB1 were involved with the hippo signaling pathway in high feed efficient group.	Thiamine	75-83	thiamin pyrophosphokinase 1	Sus scrofa	41-45
31657715-10	2020	Descriptive statistics showed that all the patients with decreased thiamine serum levels had either cognitive decline, attention decline, or depression symptoms, and most of them were receiving the 5-fluorouracil anticancer drug and showing decreased serum albumin levels.	Thiamine	67-75	albumin	Homo sapiens	257-264
31726127-2	2020	In order to improve dissolution, bioavailability and sustained release of Thiamine, we prepared Thiamine hydrochloride (TH) and beta-cyclodextrin (beta-CD) host-guest solid inclusion complexes by microwave irradiation and studied the chemical characteristics and drug delivery potential of the complex.	Thiamine	74-82	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	147-154
32034746-0	2020	[Identification of two novel SLC19A3 variants in a Chinese patient with Biotin-thiamine responsive basal ganglia disease].	Thiamine	79-87	solute carrier family 19 member 3	Homo sapiens	29-36
32060165-0	2020	Establishing a case definition of thiamine responsive disorders among infants and young children in Lao PDR: protocol for a prospective cohort study.	Thiamine	34-42	interleukin 4 induced 1	Homo sapiens	100-103
32034746-10	2020	Above finding also enriched the variant spectrum of SLC19A3 gene underlying Biotin-thiamine responsive basal ganglia disease.	Thiamine	83-91	solute carrier family 19 member 3	Homo sapiens	52-59
32027976-12	2020	Finally, we predicted that PI3Kgamma deficiency might affect the synthesis of some antibiotics, bile acid, and thiamine through effects on the microbial community.	Thiamine	111-119	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Mus musculus	27-36
32027976-13	2020	CONCLUSIONS: PI3Kgamma dysfunction led to degeneration of the intestinal microbial community and might alter the synthesis of some antibiotics, bile acids, and thiamine.	Thiamine	160-168	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Mus musculus	13-22
31911438-8	2020	Using bimolecular fluorescence complementation and in vitro Fe-S cluster transfer experiments, we confirmed interactions with two proteins involved in isoprenoid and thiamine biosynthesis, 1-hydroxy-2-methyl-2-(E)-butenyl 4-diphosphate synthase (ISPG) and 4-amino-5-hydroxymethyl-2-methylpyrimidine phosphate synthase (THIC), respectively.	Thiamine	166-174	4-hydroxy-3-methylbut-2-enyl diphosphate synthase	Arabidopsis thaliana	246-250
31911438-8	2020	Using bimolecular fluorescence complementation and in vitro Fe-S cluster transfer experiments, we confirmed interactions with two proteins involved in isoprenoid and thiamine biosynthesis, 1-hydroxy-2-methyl-2-(E)-butenyl 4-diphosphate synthase (ISPG) and 4-amino-5-hydroxymethyl-2-methylpyrimidine phosphate synthase (THIC), respectively.	Thiamine	166-174	thiaminC	Arabidopsis thaliana	319-323
31837780-12	2020	Thiamine supplementation led to lower relative protein expression of IL-1beta, NF-kappaB unit p65, and phosphorylated NF-kappaB unit p65 in ruminal epithelium.	Thiamine	0-8	interleukin-1 beta	Capra hircus	69-77
31726874-0	2020	Thiamine transporter 2 is involved in high glucose-induced damage and altered thiamine availability in cell models of diabetic retinopathy.	Thiamine	78-86	solute carrier family 19 member 3	Homo sapiens	0-22
31388880-0	2020	Thiamine, riboflavin, and nicotinamide inhibit paclitaxel-induced allodynia by reducing TNF-alpha and CXCL-1 in dorsal root ganglia and thalamus and activating ATP-sensitive potassium channels.	Thiamine	0-8	tumor necrosis factor	Homo sapiens	88-97
31388880-0	2020	Thiamine, riboflavin, and nicotinamide inhibit paclitaxel-induced allodynia by reducing TNF-alpha and CXCL-1 in dorsal root ganglia and thalamus and activating ATP-sensitive potassium channels.	Thiamine	0-8	C-X-C motif chemokine ligand 1	Homo sapiens	102-108
31388880-10	2020	Thiamine, riboflavin, and nicotinamide also reduced the concentrations of tumor necrosis factor-alpha (TNF-alpha) and CXCL-1 in dorsal root ganglia (DRG) and thalamus.	Thiamine	0-8	tumor necrosis factor	Homo sapiens	74-101
31388880-10	2020	Thiamine, riboflavin, and nicotinamide also reduced the concentrations of tumor necrosis factor-alpha (TNF-alpha) and CXCL-1 in dorsal root ganglia (DRG) and thalamus.	Thiamine	0-8	tumor necrosis factor	Homo sapiens	103-112
31388880-10	2020	Thiamine, riboflavin, and nicotinamide also reduced the concentrations of tumor necrosis factor-alpha (TNF-alpha) and CXCL-1 in dorsal root ganglia (DRG) and thalamus.	Thiamine	0-8	C-X-C motif chemokine ligand 1	Homo sapiens	118-124
32079515-2	2020	In the step-wise eluates by thiamine (at pH 7.4 or 5.6), NaCl, and urea, the occurrence of glutamate dehydrogenase (GDH) and isoenzymes of malate dehydrogenase (MDH) along with the influence of thiamine and/or ThDP on the enzymatic activities were characterized using mass spectrometry and kinetic experiments.	Thiamine	28-36	malic enzyme 1	Homo sapiens	139-159
32079515-2	2020	In the step-wise eluates by thiamine (at pH 7.4 or 5.6), NaCl, and urea, the occurrence of glutamate dehydrogenase (GDH) and isoenzymes of malate dehydrogenase (MDH) along with the influence of thiamine and/or ThDP on the enzymatic activities were characterized using mass spectrometry and kinetic experiments.	Thiamine	194-202	malic enzyme 1	Homo sapiens	139-159
32079515-3	2020	Maximal activation of the malate dehydrogenase reaction by thiamine is observed after the protein elution with the acidic thiamine solution, which does not elute the MDH1 isoenzyme.	Thiamine	59-67	malic enzyme 1	Homo sapiens	26-46
32079515-3	2020	Maximal activation of the malate dehydrogenase reaction by thiamine is observed after the protein elution with the acidic thiamine solution, which does not elute the MDH1 isoenzyme.	Thiamine	122-130	malic enzyme 1	Homo sapiens	26-46
32079515-8	2020	Simultaneously, the MDH2 content and total GDH activity are higher after the affinity elution at pH 5.6 than at pH 7.4, suggesting the role of the known interaction of GDH with MDH2 in stabilizing the activity of GDH and in the regulation of GDH by thiamine.	Thiamine	249-257	malate dehydrogenase 2	Homo sapiens	20-24
32079515-8	2020	Simultaneously, the MDH2 content and total GDH activity are higher after the affinity elution at pH 5.6 than at pH 7.4, suggesting the role of the known interaction of GDH with MDH2 in stabilizing the activity of GDH and in the regulation of GDH by thiamine.	Thiamine	249-257	malate dehydrogenase 2	Homo sapiens	177-181
31764942-4	2020	OBJECTIVE: In this study, we tested the hypothesis that therapeutic drugs inhibit the intestinal thiamine transporter ThTR-2, which may lead to thiamine deficiency.	Thiamine	97-105	solute carrier family 19 member 3	Homo sapiens	118-124
31764942-9	2020	Complementary analysis using electronic health records suggested that thiamine laboratory values are reduced in individuals receiving prescription drugs found to significantly inhibit ThTR-2, particularly in vulnerable populations (e.g., individuals with alcoholism).	Thiamine	70-78	solute carrier family 19 member 3	Homo sapiens	184-190
31764942-10	2020	CONCLUSIONS: Our comprehensive analysis of prescription drugs suggests that several marketed drugs inhibit ThTR-2, which may contribute to thiamine deficiency, especially in at-risk populations.	Thiamine	139-147	solute carrier family 19 member 3	Homo sapiens	107-113
31726874-10	2020	Thiamine depletion reduced cell viability and proliferation, while thiamine over-supplementation compensated for thiamine transporter 2 reduction by restoring thiamine uptake and transketolase activity.	Thiamine	67-75	solute carrier family 19 member 3	Homo sapiens	113-135
31726874-10	2020	Thiamine depletion reduced cell viability and proliferation, while thiamine over-supplementation compensated for thiamine transporter 2 reduction by restoring thiamine uptake and transketolase activity.	Thiamine	67-75	transketolase	Homo sapiens	179-192
31726874-12	2020	Thiamine transporter 2 modulation in our cell models suggests its major role in thiamine transport in retinal cells and its involvement in high glucose-induced damage and impaired thiamine availability.	Thiamine	80-88	solute carrier family 19 member 3	Homo sapiens	0-22
31726874-12	2020	Thiamine transporter 2 modulation in our cell models suggests its major role in thiamine transport in retinal cells and its involvement in high glucose-induced damage and impaired thiamine availability.	Thiamine	180-188	solute carrier family 19 member 3	Homo sapiens	0-22
31824549-8	2019	The deficiency of thiamine in Gmpgl1 mutant led to reduced activities of the pyruvate dehydrogenase (PDH) and pyruvate decarboxylase (PDC), and decreased contents of six amino acids as compared to that in the wild type plants.	Thiamine	18-26	proline dehydrogenase	Glycine max	77-99
31824549-8	2019	The deficiency of thiamine in Gmpgl1 mutant led to reduced activities of the pyruvate dehydrogenase (PDH) and pyruvate decarboxylase (PDC), and decreased contents of six amino acids as compared to that in the wild type plants.	Thiamine	18-26	proline dehydrogenase	Glycine max	101-104
31338833-5	2019	Five patients with SLC19A2 mutations suffered from thiamine-responsive megaloblastic anaemia and three exhibited the "anaemia, deafness and diabetes" triad.	Thiamine	51-59	solute carrier family 19 member 2	Homo sapiens	19-26
31500509-5	2019	OGD/R treatment repressed the expression of MALAT1 and BDNF and the phosphorylation of PI3K and Akt, and enhanced the miR-1 expression, which were all reversed by vitamin B1 and B12 treatment in N2A neurons.	Thiamine	163-173	brain-derived neurotrophic factor	Rattus norvegicus	55-59
31500509-5	2019	OGD/R treatment repressed the expression of MALAT1 and BDNF and the phosphorylation of PI3K and Akt, and enhanced the miR-1 expression, which were all reversed by vitamin B1 and B12 treatment in N2A neurons.	Thiamine	163-173	AKT serine/threonine kinase 1	Rattus norvegicus	96-99
31500509-5	2019	OGD/R treatment repressed the expression of MALAT1 and BDNF and the phosphorylation of PI3K and Akt, and enhanced the miR-1 expression, which were all reversed by vitamin B1 and B12 treatment in N2A neurons.	Thiamine	163-173	microRNA 1	Rattus norvegicus	118-123
31500509-6	2019	Vitamin B1 and B12 inhibited miR-1 expression through MALAT1, promoted BDNF expression and activated PI3K/Akt signaling through the MALAT1/miR-1 axis.	Thiamine	0-10	microRNA 1	Rattus norvegicus	29-34
31500509-6	2019	Vitamin B1 and B12 inhibited miR-1 expression through MALAT1, promoted BDNF expression and activated PI3K/Akt signaling through the MALAT1/miR-1 axis.	Thiamine	0-10	brain-derived neurotrophic factor	Rattus norvegicus	71-75
31500509-6	2019	Vitamin B1 and B12 inhibited miR-1 expression through MALAT1, promoted BDNF expression and activated PI3K/Akt signaling through the MALAT1/miR-1 axis.	Thiamine	0-10	AKT serine/threonine kinase 1	Rattus norvegicus	106-109
31500509-6	2019	Vitamin B1 and B12 inhibited miR-1 expression through MALAT1, promoted BDNF expression and activated PI3K/Akt signaling through the MALAT1/miR-1 axis.	Thiamine	0-10	microRNA 1	Rattus norvegicus	139-144
31500509-9	2019	Collectively, vitamin B1 and B12 up-regulates BDNF and its downstream PI3K/Akt signaling through MALAT1/miR-1 axis, thus suppressing neuron apoptosis and mitigating nerve injury in cerebral palsy rats.	Thiamine	14-24	brain-derived neurotrophic factor	Rattus norvegicus	46-50
31500509-9	2019	Collectively, vitamin B1 and B12 up-regulates BDNF and its downstream PI3K/Akt signaling through MALAT1/miR-1 axis, thus suppressing neuron apoptosis and mitigating nerve injury in cerebral palsy rats.	Thiamine	14-24	AKT serine/threonine kinase 1	Rattus norvegicus	75-78
31500509-9	2019	Collectively, vitamin B1 and B12 up-regulates BDNF and its downstream PI3K/Akt signaling through MALAT1/miR-1 axis, thus suppressing neuron apoptosis and mitigating nerve injury in cerebral palsy rats.	Thiamine	14-24	microRNA 1	Rattus norvegicus	104-109
31295743-0	2019	Bilateral Striatal Necrosis with Polyneuropathy with a Novel SLC25A19 (Mitochondrial Thiamine Pyrophosphate Carrier OMIMI*606521) Mutation: Treatable Thiamine Metabolic Disorder-A Report of Two Indian Cases.	Thiamine	85-93	solute carrier family 25 member 19	Homo sapiens	61-69
31564168-8	2019	To date, and despite two decades of research into OCT1 functional role, it still remains uncertain what are the define substrates for this uptake transporter, although studies from mice revealed that one of the substrates is vitamin B1.	Thiamine	225-235	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	50-54
31506564-0	2019	Functional analysis of the third identified SLC25A19 mutation causative for the thiamine metabolism dysfunction syndrome 4.	Thiamine	80-88	solute carrier family 25 member 19	Homo sapiens	44-52
31506564-1	2019	Thiamine metabolism dysfunction syndrome-4 (THMD4) includes episodic encephalopathy, often associated with a febrile illness, causing transient neurologic dysfunction and a slowly progressive axonal polyneuropathy.	Thiamine	0-8	solute carrier family 25 member 19	Homo sapiens	44-49
31658248-4	2019	We found that Art2 is the main regulator of substrate- and stress-induced ubiquitylation and endocytosis of the thiamine (vitamin B1) transporters: Thi7, nicotinamide riboside transporter 1 (Nrt1), and Thi72.	Thiamine	112-120	Ecm21p	Saccharomyces cerevisiae S288C	14-18
31658248-4	2019	We found that Art2 is the main regulator of substrate- and stress-induced ubiquitylation and endocytosis of the thiamine (vitamin B1) transporters: Thi7, nicotinamide riboside transporter 1 (Nrt1), and Thi72.	Thiamine	112-120	thiamine transporter THI7	Saccharomyces cerevisiae S288C	148-152
31658248-4	2019	We found that Art2 is the main regulator of substrate- and stress-induced ubiquitylation and endocytosis of the thiamine (vitamin B1) transporters: Thi7, nicotinamide riboside transporter 1 (Nrt1), and Thi72.	Thiamine	112-120	nicotinamide riboside transporter	Saccharomyces cerevisiae S288C	154-189
31658248-4	2019	We found that Art2 is the main regulator of substrate- and stress-induced ubiquitylation and endocytosis of the thiamine (vitamin B1) transporters: Thi7, nicotinamide riboside transporter 1 (Nrt1), and Thi72.	Thiamine	112-120	nicotinamide riboside transporter	Saccharomyces cerevisiae S288C	191-195
31658248-5	2019	Genetic screening allowed for the isolation of transport-defective Thi7 mutants, which impaired thiamine-induced endocytosis.	Thiamine	96-104	thiamine transporter THI7	Saccharomyces cerevisiae S288C	67-71
31295743-10	2019	CONCLUSION: If any child presents with recurrent encephalopathy with flaccid paralysis, dystonia, and neuropathy, a diagnosis of bilateral striatal necrosis with polyneuropathy due to SLC25A19 mutations should be considered and thiamine should be initiated.	Thiamine	228-236	solute carrier family 25 member 19	Homo sapiens	184-192
30817932-6	2019	These ultrasound-induced effects were ameliorated by thiamine and benfotiamine treatment; in particular both antioxidants were able to reverse ultrasound-induced changes in GluA1 and GluA2 subunit expression, and, within the prefrontal cortex, significantly reversed the changes in protein carbonyl and polysialylated form of neural cell adhesion molecule (PSA-NCAM) expression levels.	Thiamine	53-61	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	173-178
31409697-0	2019	Rethinking the PDH Bypass and GABA Shunt as Thiamin-Deficiency Workarounds.	Thiamine	44-51	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	15-18
30817932-6	2019	These ultrasound-induced effects were ameliorated by thiamine and benfotiamine treatment; in particular both antioxidants were able to reverse ultrasound-induced changes in GluA1 and GluA2 subunit expression, and, within the prefrontal cortex, significantly reversed the changes in protein carbonyl and polysialylated form of neural cell adhesion molecule (PSA-NCAM) expression levels.	Thiamine	53-61	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	183-188
31415630-7	2019	As a cofactor for TKT reaction, we evaluated the release of NET formation either in vitamin B1 treatment or in combined use of oxythiamine and vitamin B1, and found that those treatments also exerted a significant suppressive effect on the amount of NET-DNA and ROS production.	Thiamine	84-94	transketolase	Homo sapiens	18-21
31415630-7	2019	As a cofactor for TKT reaction, we evaluated the release of NET formation either in vitamin B1 treatment or in combined use of oxythiamine and vitamin B1, and found that those treatments also exerted a significant suppressive effect on the amount of NET-DNA and ROS production.	Thiamine	143-153	transketolase	Homo sapiens	18-21
31415630-3	2019	Transketolase (TKT) is a thiamine pyrophosphate (vitamin B1)-dependent enzyme that links the pentose phosphate pathway with the glycolytic pathway by feeding excess sugar phosphates into the main carbohydrate metabolic pathways to generate biosynthetic reducing capacity in the form of NADPH as a substrate for ROS generation.	Thiamine	49-59	transketolase	Homo sapiens	0-13
31415630-8	2019	The regulation of TKT by oxythiamine and/or vitamin B1 may therefore be associated with response to the modulation of NET formation by preventing generation of excessive NETs in inflammatory diseases.	Thiamine	44-54	transketolase	Homo sapiens	18-21
31415630-3	2019	Transketolase (TKT) is a thiamine pyrophosphate (vitamin B1)-dependent enzyme that links the pentose phosphate pathway with the glycolytic pathway by feeding excess sugar phosphates into the main carbohydrate metabolic pathways to generate biosynthetic reducing capacity in the form of NADPH as a substrate for ROS generation.	Thiamine	49-59	transketolase	Homo sapiens	15-18
31259722-7	2019	Linearity of the developed method was found in the range 17.5-30 microg mL-1 for thiamine, 35-60 microg mL-1 for pyridoxal phosphate and 87.5-150 microg mL-1 for paracetamol.	Thiamine	81-89	L1 cell adhesion molecule	Mus musculus	72-76
31288420-1	2019	TPK1 mutations are a rare, but potentially treatable, cause of thiamine deficiency.	Thiamine	63-71	thiamin pyrophosphokinase 1	Homo sapiens	0-4
31095747-4	2019	SLC19A3 patients present a profound decrease of free-thiamine in cerebrospinal fluid (CSF) and fibroblasts.	Thiamine	53-61	solute carrier family 19 member 3	Homo sapiens	0-7
31095747-7	2019	In a significant number of patients with SLC19A3, thiamine improves clinical outcome and survival, and prevents further metabolic crisis.	Thiamine	50-58	solute carrier family 19 member 3	Homo sapiens	41-48
31095747-8	2019	In SLC25A19 and TPK1 defects, thiamine has also led to clinical stabilization in single cases.	Thiamine	30-38	solute carrier family 25 member 19	Homo sapiens	3-11
31095747-8	2019	In SLC25A19 and TPK1 defects, thiamine has also led to clinical stabilization in single cases.	Thiamine	30-38	thiamin pyrophosphokinase 1	Homo sapiens	16-20
31095747-9	2019	Moreover, thiamine supplementation leads to normal concentrations of free-thiamine in the CSF of SLC19A3 patients.	Thiamine	10-18	solute carrier family 19 member 3	Homo sapiens	97-104
31095747-9	2019	Moreover, thiamine supplementation leads to normal concentrations of free-thiamine in the CSF of SLC19A3 patients.	Thiamine	74-82	solute carrier family 19 member 3	Homo sapiens	97-104
31390812-7	2019	A linear response was obtained between 0.1 and 20 microg mL-1, which was suitable for the quantification of the vitamin in two commercial products containing vitamin B1.	Thiamine	158-168	L1 cell adhesion molecule	Mus musculus	57-61
31095747-2	2019	Currently, four genetic defects have been described causing impairment of thiamine transport and metabolism: SLC19A2 dysfunction leads to diabetes mellitus, megaloblastic anemia and sensory-neural hearing loss, whereas SLC19A3, SLC25A19, and TPK1-related disorders result in recurrent encephalopathy, basal ganglia necrosis, generalized dystonia, severe disability, and early death.	Thiamine	74-82	solute carrier family 19 member 2	Homo sapiens	109-116
31095747-2	2019	Currently, four genetic defects have been described causing impairment of thiamine transport and metabolism: SLC19A2 dysfunction leads to diabetes mellitus, megaloblastic anemia and sensory-neural hearing loss, whereas SLC19A3, SLC25A19, and TPK1-related disorders result in recurrent encephalopathy, basal ganglia necrosis, generalized dystonia, severe disability, and early death.	Thiamine	74-82	solute carrier family 19 member 3	Homo sapiens	219-226
31095747-2	2019	Currently, four genetic defects have been described causing impairment of thiamine transport and metabolism: SLC19A2 dysfunction leads to diabetes mellitus, megaloblastic anemia and sensory-neural hearing loss, whereas SLC19A3, SLC25A19, and TPK1-related disorders result in recurrent encephalopathy, basal ganglia necrosis, generalized dystonia, severe disability, and early death.	Thiamine	74-82	solute carrier family 25 member 19	Homo sapiens	228-236
31095747-2	2019	Currently, four genetic defects have been described causing impairment of thiamine transport and metabolism: SLC19A2 dysfunction leads to diabetes mellitus, megaloblastic anemia and sensory-neural hearing loss, whereas SLC19A3, SLC25A19, and TPK1-related disorders result in recurrent encephalopathy, basal ganglia necrosis, generalized dystonia, severe disability, and early death.	Thiamine	74-82	thiamin pyrophosphokinase 1	Homo sapiens	242-246
31144472-0	2019	Whole exome sequencing identifies a new mutation in the SLC19A2 gene leading to thiamine-responsive megaloblastic anemia in an Egyptian family.	Thiamine	80-88	solute carrier family 19 member 2	Homo sapiens	56-63
31144472-1	2019	BACKGROUND: The Solute Carrier Family 19 Member 2 (SLC19A2, OMIM *603941) encodes the thiamine transporter 1 (THTR-1) that brings thiamine (Vitamin B1) into cells.	Thiamine	86-94	solute carrier family 19 member 2	Homo sapiens	16-49
31144472-1	2019	BACKGROUND: The Solute Carrier Family 19 Member 2 (SLC19A2, OMIM *603941) encodes the thiamine transporter 1 (THTR-1) that brings thiamine (Vitamin B1) into cells.	Thiamine	86-94	solute carrier family 19 member 2	Homo sapiens	51-58
31144472-1	2019	BACKGROUND: The Solute Carrier Family 19 Member 2 (SLC19A2, OMIM *603941) encodes the thiamine transporter 1 (THTR-1) that brings thiamine (Vitamin B1) into cells.	Thiamine	86-94	solute carrier family 19 member 2	Homo sapiens	110-116
31144472-1	2019	BACKGROUND: The Solute Carrier Family 19 Member 2 (SLC19A2, OMIM *603941) encodes the thiamine transporter 1 (THTR-1) that brings thiamine (Vitamin B1) into cells.	Thiamine	140-150	solute carrier family 19 member 2	Homo sapiens	16-49
31144472-1	2019	BACKGROUND: The Solute Carrier Family 19 Member 2 (SLC19A2, OMIM *603941) encodes the thiamine transporter 1 (THTR-1) that brings thiamine (Vitamin B1) into cells.	Thiamine	140-150	solute carrier family 19 member 2	Homo sapiens	51-58
31144472-1	2019	BACKGROUND: The Solute Carrier Family 19 Member 2 (SLC19A2, OMIM *603941) encodes the thiamine transporter 1 (THTR-1) that brings thiamine (Vitamin B1) into cells.	Thiamine	140-150	solute carrier family 19 member 2	Homo sapiens	86-108
31144472-1	2019	BACKGROUND: The Solute Carrier Family 19 Member 2 (SLC19A2, OMIM *603941) encodes the thiamine transporter 1 (THTR-1) that brings thiamine (Vitamin B1) into cells.	Thiamine	140-150	solute carrier family 19 member 2	Homo sapiens	110-116
31144472-2	2019	THTR-1 is the only thiamine transporter expressed in bone marrow, cochlear, and pancreatic beta cells.	Thiamine	19-27	solute carrier family 19 member 2	Homo sapiens	0-6
31144472-3	2019	THTR-1 loss-of-function leads to the rare recessive genetic disease Thiamine-Responsive Megaloblastic Anemia (TRMA, OMIM #249270).	Thiamine	68-76	solute carrier family 19 member 2	Homo sapiens	0-6
30920302-2	2019	Pancreatic acinar cells (PACs) obtain thiamin from the circulation via a specific carrier-mediated process that involves the plasma membrane thiamin transporters 1 and 2 (THTR-1 and THTR-2; products of SLC19A2 and SLC19A3 genes, respectively).	Thiamine	38-45	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	171-177
30944639-8	2019	Thiamine metabolism (including miR-371a-3p) was the pathway with the highest enrichment of DEMs.	Thiamine	0-8	myosin regulatory light chain interacting protein	Homo sapiens	31-34
30920302-2	2019	Pancreatic acinar cells (PACs) obtain thiamin from the circulation via a specific carrier-mediated process that involves the plasma membrane thiamin transporters 1 and 2 (THTR-1 and THTR-2; products of SLC19A2 and SLC19A3 genes, respectively).	Thiamine	38-45	solute carrier family 19, member 3	Mus musculus	182-188
30920302-2	2019	Pancreatic acinar cells (PACs) obtain thiamin from the circulation via a specific carrier-mediated process that involves the plasma membrane thiamin transporters 1 and 2 (THTR-1 and THTR-2; products of SLC19A2 and SLC19A3 genes, respectively).	Thiamine	38-45	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	202-209
30920302-2	2019	Pancreatic acinar cells (PACs) obtain thiamin from the circulation via a specific carrier-mediated process that involves the plasma membrane thiamin transporters 1 and 2 (THTR-1 and THTR-2; products of SLC19A2 and SLC19A3 genes, respectively).	Thiamine	38-45	solute carrier family 19, member 3	Mus musculus	214-221
30920302-10	2019	These results show, for the first time, that exposure of PACs to flagellin negatively impacts the physiological and molecular parameters of thiamin uptake and that this effect is mediated at the level of transcription of the SLC19A2 and SLC19A3 genes.	Thiamine	140-147	solute carrier family 19, member 3	Mus musculus	237-244
30833467-1	2019	Solute Carrier Family 19 Member 2 (SLC19A2) encodes thiamine transporter 1 (THTR1), which facilitates thiamine transport across the cell membrane.	Thiamine	52-60	solute carrier family 19 member 2	Homo sapiens	0-33
30833467-1	2019	Solute Carrier Family 19 Member 2 (SLC19A2) encodes thiamine transporter 1 (THTR1), which facilitates thiamine transport across the cell membrane.	Thiamine	52-60	solute carrier family 19 member 2	Homo sapiens	35-42
30833467-1	2019	Solute Carrier Family 19 Member 2 (SLC19A2) encodes thiamine transporter 1 (THTR1), which facilitates thiamine transport across the cell membrane.	Thiamine	52-60	solute carrier family 19 member 2	Homo sapiens	76-81
30833467-2	2019	SLC19A2 homozygous mutations have been described as a cause of thiamine-responsive megaloblastic anemia (TRMA), an autosomal recessive syndrome characterized by megaloblastic anemia, diabetes, and sensorineural deafness.	Thiamine	63-71	solute carrier family 19 member 2	Homo sapiens	0-7
30833467-4	2019	We show that SLC19A2-deficient beta-cells are characterized by impaired thiamine uptake, which is not rescued by overexpression of the p.Lys355Gln mutant protein.	Thiamine	72-80	solute carrier family 19 member 2	Homo sapiens	13-20
31142407-5	2019	We present a rare case of an adult patient with TRMA who had been mistakenly diagnosed with myelodysplastic syndrome (MDS), whose anemia was corrected only after thiamine treatment was started.	Thiamine	162-170	solute carrier family 19 member 2	Homo sapiens	48-52
31061755-0	2019	Biotin-Thiamine Responsive Encephalopathy: Report of an Egyptian Family with a Novel SLC19A3 Mutation and Review of the Literature.	Thiamine	7-15	solute carrier family 19 member 3	Homo sapiens	85-92
31061755-1	2019	Biotin-thiamine responsive basal ganglia disease (BTRBGD) is an autosomal recessive neurometabolic disorder with poor genotype-phenotype correlation, caused by mutations in the SLC19A3 gene on chromosome 2q36.6.	Thiamine	7-15	solute carrier family 19 member 3	Homo sapiens	177-184
31138958-6	2019	In the multiple regression analysis adjusted by age, sex, body mass index, and eGFR, whole blood thiamine concentration was a significant negative contributor (standardized coefficient beta = -0.488, p = 0.001) to plasma brain natriuretic peptide.	Thiamine	97-105	epidermal growth factor receptor	Homo sapiens	79-83
30944639-12	2019	miR-371a-3p may be a candidate miRNA for CRT sensitivity in LARC via the thiamine metabolism pathway.	Thiamine	73-81	myosin regulatory light chain interacting protein	Homo sapiens	0-3
30950790-0	2019	A bacterial riboswitch class for the thiamin precursor HMP-PP employs a terminator-embedded aptamer.	Thiamine	37-44	inner membrane mitochondrial protein	Homo sapiens	55-58
30950790-3	2019	In the current report, we describe biochemical and genetic data demonstrating that thiS motif RNAs function as sensors of the thiamin precursor HMP-PP, which is fused with HET-P ultimately to form the final active coenzyme thiamin pyrophosphate (TPP).	Thiamine	126-133	inner membrane mitochondrial protein	Homo sapiens	144-147
30844694-1	2019	Thiamin, riboflavin and pyridoxal phosphate (PLP) concentrations are useful indices for evaluating vitamin B1, B2 and B6 status.	Thiamine	0-7	immunoglobulin kappa variable 5-2	Homo sapiens	99-120
30483896-7	2019	Biochemical characterization of reported TPK1 missense mutations suggested reduced thiamine binding as a new disease mechanism.	Thiamine	83-91	thiamin pyrophosphokinase 1	Homo sapiens	41-45
31951336-0	2019	A novel mutation in the SLC19A2 gene in a Turkish male with thiamine-responsive megaloblastic anemia syndrome.	Thiamine	60-68	solute carrier family 19 member 2	Homo sapiens	24-31
30789823-1	2019	Background The mutations of thiamine pyrophosphokinase-1 (TPK1) gene have been frequently studied in some patients with thiamine metabolism dysfunction syndrome-5 (THMD5), while TPK1 mutations in Chinese patients have been investigated by only homozygous.	Thiamine	28-36	thiamin pyrophosphokinase 1	Homo sapiens	58-62
30789823-1	2019	Background The mutations of thiamine pyrophosphokinase-1 (TPK1) gene have been frequently studied in some patients with thiamine metabolism dysfunction syndrome-5 (THMD5), while TPK1 mutations in Chinese patients have been investigated by only homozygous.	Thiamine	28-36	thiamin pyrophosphokinase 1	Homo sapiens	164-169
30498136-6	2019	Genetic data herein showed that either SNZ2 or SNZ3 are required for efficient thiamine biosynthesis in Saccharomyces cerevisiae Further, SNZ2 or SNZ3 alone could satisfy the cellular requirement for pyridoxal 5"-phosphate (and thiamine), while SNZ1 was sufficient for pyridoxal 5"-phosphate synthesis only if thiamine was provided.	Thiamine	228-236	pyridoxine biosynthesis protein SNZ3	Saccharomyces cerevisiae S288C	146-150
30498136-6	2019	Genetic data herein showed that either SNZ2 or SNZ3 are required for efficient thiamine biosynthesis in Saccharomyces cerevisiae Further, SNZ2 or SNZ3 alone could satisfy the cellular requirement for pyridoxal 5"-phosphate (and thiamine), while SNZ1 was sufficient for pyridoxal 5"-phosphate synthesis only if thiamine was provided.	Thiamine	228-236	pyridoxine biosynthesis protein SNZ2	Saccharomyces cerevisiae S288C	39-43
30498136-6	2019	Genetic data herein showed that either SNZ2 or SNZ3 are required for efficient thiamine biosynthesis in Saccharomyces cerevisiae Further, SNZ2 or SNZ3 alone could satisfy the cellular requirement for pyridoxal 5"-phosphate (and thiamine), while SNZ1 was sufficient for pyridoxal 5"-phosphate synthesis only if thiamine was provided.	Thiamine	228-236	pyridoxine biosynthesis protein SNZ2	Saccharomyces cerevisiae S288C	138-142
30498136-6	2019	Genetic data herein showed that either SNZ2 or SNZ3 are required for efficient thiamine biosynthesis in Saccharomyces cerevisiae Further, SNZ2 or SNZ3 alone could satisfy the cellular requirement for pyridoxal 5"-phosphate (and thiamine), while SNZ1 was sufficient for pyridoxal 5"-phosphate synthesis only if thiamine was provided.	Thiamine	228-236	pyridoxine biosynthesis protein SNZ3	Saccharomyces cerevisiae S288C	146-150
30498136-7	2019	qRT-PCR analysis determined that SNZ2,3 are repressed ten-fold by the presence thiamine.	Thiamine	79-87	pyridoxine biosynthesis protein SNZ2	Saccharomyces cerevisiae S288C	33-39
30498136-8	2019	In total, the data were consistent with a requirement for PLP in thiamine synthesis, perhaps in the Thi5p enzyme, that could only be satisfied by SNZ2 or SNZ3 Additional data showed that Snz3p is a pyridoxal 5"-phosphate synthase in vitro and is sufficient to satisfy the pyridoxal 5"-phosphate requirement in Salmonella enterica when the medium has excess ammonia.	Thiamine	65-73	pyridoxine biosynthesis protein SNZ2	Saccharomyces cerevisiae S288C	146-150
30498136-8	2019	In total, the data were consistent with a requirement for PLP in thiamine synthesis, perhaps in the Thi5p enzyme, that could only be satisfied by SNZ2 or SNZ3 Additional data showed that Snz3p is a pyridoxal 5"-phosphate synthase in vitro and is sufficient to satisfy the pyridoxal 5"-phosphate requirement in Salmonella enterica when the medium has excess ammonia.	Thiamine	65-73	pyridoxine biosynthesis protein SNZ3	Saccharomyces cerevisiae S288C	154-158
30498136-8	2019	In total, the data were consistent with a requirement for PLP in thiamine synthesis, perhaps in the Thi5p enzyme, that could only be satisfied by SNZ2 or SNZ3 Additional data showed that Snz3p is a pyridoxal 5"-phosphate synthase in vitro and is sufficient to satisfy the pyridoxal 5"-phosphate requirement in Salmonella enterica when the medium has excess ammonia.	Thiamine	65-73	pyridoxine biosynthesis protein SNZ3	Saccharomyces cerevisiae S288C	187-192
30472222-3	2019	The second procedure focused on the preparation and characterization of a new polymeric conjugate between the poly(anhydride) backbone and thiamine prior the nanoparticle formation (T-NPB).	Thiamine	139-147	neuropeptide B	Homo sapiens	184-187
30498136-0	2019	SNZ3 Encodes a PLP Synthase Involved in Thiamine Synthesis in Saccharomyces cerevisiae.	Thiamine	40-48	pyridoxine biosynthesis protein SNZ3	Saccharomyces cerevisiae S288C	0-4
30498136-6	2019	Genetic data herein showed that either SNZ2 or SNZ3 are required for efficient thiamine biosynthesis in Saccharomyces cerevisiae Further, SNZ2 or SNZ3 alone could satisfy the cellular requirement for pyridoxal 5"-phosphate (and thiamine), while SNZ1 was sufficient for pyridoxal 5"-phosphate synthesis only if thiamine was provided.	Thiamine	79-87	pyridoxine biosynthesis protein SNZ2	Saccharomyces cerevisiae S288C	39-43
30498136-6	2019	Genetic data herein showed that either SNZ2 or SNZ3 are required for efficient thiamine biosynthesis in Saccharomyces cerevisiae Further, SNZ2 or SNZ3 alone could satisfy the cellular requirement for pyridoxal 5"-phosphate (and thiamine), while SNZ1 was sufficient for pyridoxal 5"-phosphate synthesis only if thiamine was provided.	Thiamine	79-87	pyridoxine biosynthesis protein SNZ3	Saccharomyces cerevisiae S288C	47-51
30498136-6	2019	Genetic data herein showed that either SNZ2 or SNZ3 are required for efficient thiamine biosynthesis in Saccharomyces cerevisiae Further, SNZ2 or SNZ3 alone could satisfy the cellular requirement for pyridoxal 5"-phosphate (and thiamine), while SNZ1 was sufficient for pyridoxal 5"-phosphate synthesis only if thiamine was provided.	Thiamine	79-87	pyridoxine biosynthesis protein SNZ2	Saccharomyces cerevisiae S288C	138-142
30498136-6	2019	Genetic data herein showed that either SNZ2 or SNZ3 are required for efficient thiamine biosynthesis in Saccharomyces cerevisiae Further, SNZ2 or SNZ3 alone could satisfy the cellular requirement for pyridoxal 5"-phosphate (and thiamine), while SNZ1 was sufficient for pyridoxal 5"-phosphate synthesis only if thiamine was provided.	Thiamine	79-87	pyridoxine biosynthesis protein SNZ3	Saccharomyces cerevisiae S288C	146-150
30498136-6	2019	Genetic data herein showed that either SNZ2 or SNZ3 are required for efficient thiamine biosynthesis in Saccharomyces cerevisiae Further, SNZ2 or SNZ3 alone could satisfy the cellular requirement for pyridoxal 5"-phosphate (and thiamine), while SNZ1 was sufficient for pyridoxal 5"-phosphate synthesis only if thiamine was provided.	Thiamine	79-87	pyridoxine biosynthesis protein SNZ1	Saccharomyces cerevisiae S288C	245-249
30498136-6	2019	Genetic data herein showed that either SNZ2 or SNZ3 are required for efficient thiamine biosynthesis in Saccharomyces cerevisiae Further, SNZ2 or SNZ3 alone could satisfy the cellular requirement for pyridoxal 5"-phosphate (and thiamine), while SNZ1 was sufficient for pyridoxal 5"-phosphate synthesis only if thiamine was provided.	Thiamine	228-236	pyridoxine biosynthesis protein SNZ2	Saccharomyces cerevisiae S288C	39-43
30498136-6	2019	Genetic data herein showed that either SNZ2 or SNZ3 are required for efficient thiamine biosynthesis in Saccharomyces cerevisiae Further, SNZ2 or SNZ3 alone could satisfy the cellular requirement for pyridoxal 5"-phosphate (and thiamine), while SNZ1 was sufficient for pyridoxal 5"-phosphate synthesis only if thiamine was provided.	Thiamine	228-236	pyridoxine biosynthesis protein SNZ2	Saccharomyces cerevisiae S288C	138-142
31951336-2	2019	A novel mutation in the SLC19A2 gene in a Turkish male with thiamine-responsive megaloblastic anemia syndrome.	Thiamine	60-68	solute carrier family 19 member 2	Homo sapiens	24-31
31951337-0	2019	A novel mutation in the SLC19A2 gene in a Turkish male with thiamine-responsive megaloblastic anemia syndrome.	Thiamine	60-68	solute carrier family 19 member 2	Homo sapiens	24-31
31951337-2	2019	A novel mutation in the SLC19A2 gene in a Turkish male with thiamine-responsive megaloblastic anemia syndrome.	Thiamine	60-68	solute carrier family 19 member 2	Homo sapiens	24-31
31951337-4	2019	Thiamine-responsive megaloblastic anemia (TRMA) is a very rare syndrome characterized by the triad of early onset megaloblastic anemia, sensorineural deafness and diabetes mellitus.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	42-46
30544975-1	2018	The organic cation transporter 1 (OCT1, SLC22A1) is strongly expressed in the human liver and facilitates the hepatic uptake of drugs such as morphine, metformin, tropisetron, sumatriptan and fenoterol and of endogenous substances such as thiamine.	Thiamine	239-247	solute carrier family 22 member 1	Homo sapiens	4-32
30544975-1	2018	The organic cation transporter 1 (OCT1, SLC22A1) is strongly expressed in the human liver and facilitates the hepatic uptake of drugs such as morphine, metformin, tropisetron, sumatriptan and fenoterol and of endogenous substances such as thiamine.	Thiamine	239-247	solute carrier family 22 member 1	Homo sapiens	34-38
30544975-1	2018	The organic cation transporter 1 (OCT1, SLC22A1) is strongly expressed in the human liver and facilitates the hepatic uptake of drugs such as morphine, metformin, tropisetron, sumatriptan and fenoterol and of endogenous substances such as thiamine.	Thiamine	239-247	solute carrier family 22 member 1	Homo sapiens	40-47
30464635-6	2018	In a subgroup analysis based on vitamin B subclass, B1, B3, B6, and B9 vitamins were associated with decreased EC risk (vitamin B1: OR=0.68, 95% CI: 0.56-0.82; vitamin B3: OR=0.70, 95% CI: 0.53-0.94; vitamin B6: OR=0.64, 95% CI: 0.49-0.83; and vitamin B9: OR=0.69, 95% CI: 0.55-0.86).	Thiamine	120-130	immunoglobulin kappa variable 7-3 (pseudogene)	Homo sapiens	52-70
31762684-10	2018	Enhancement in mass cell volume (MCV) level and decline in mean corpuscular hemoglobin (MCH) levels were observed in both thiamine deficient groups with respect to control.	Thiamine	122-130	modifier of chinchilla	Mus musculus	88-91
30311825-10	2018	Daily supplementation with an individualized ALA, carnosine, and thiamine supplement effectively reduced glucose concentration in type 2 diabetic patients, probably by increasing insulin production from the pancreas.	Thiamine	65-73	insulin	Homo sapiens	179-186
30008376-0	2018	Stabilization of the hypoxia-inducible transcription Factor-1 alpha (HIF-1alpha) in thiamine deficiency is mediated by pyruvate accumulation.	Thiamine	84-92	hypoxia inducible factor 1, alpha subunit	Mus musculus	69-79
30054086-1	2018	BACKGROUND: Biotin-thiamine responsive basal ganglia disease (BTBGD) is an autosomal recessive disorder caused by mutations in the SLC19A3 gene and characterized by recurrent sub-acute episodes of encephalopathy that typically starts in early childhood.	Thiamine	19-27	solute carrier family 19 member 3	Homo sapiens	131-138
30459934-3	2018	Upon uptake, thiamine pyrophosphokinase-1 (TPK1) facilitates the rapid phosphorylation of thiamine into thiamine pyrophosphate (TPP).	Thiamine	13-21	thiamin pyrophosphokinase 1	Homo sapiens	43-47
30459934-11	2018	These findings suggest that the adaptive regulation of TPK1 may be an essential component in the cellular response to oxidative stress, and that during supplemental thiamine conditions its expression may be exploited by tumor cells for a redox advantage contributing to tumor progression.	Thiamine	165-173	thiamin pyrophosphokinase 1	Homo sapiens	55-59
30138624-2	2018	The substrates and inhibitors of hOCT1 are structurally and physiochemically diverse and include some widely prescribed drugs (metformin and imatinib), vitamins (thiamine), and neurotransmitters (serotonin).	Thiamine	162-170	solute carrier family 22 member 1	Homo sapiens	33-38
29777685-9	2018	By the third day after TBI, thiamine treatment also decreased expression of TNF-R1.	Thiamine	28-36	TNF receptor superfamily member 1A	Rattus norvegicus	76-82
29966293-1	2018	Thiamine, named as vitamin B1, is an important cofactor for the critical enzymes regarding to glucose metabolism, like transketolase, pyruvate dehydrogenase, and alpha-ketoglutarate dehydrogenase.	Thiamine	0-8	oxoglutarate (alpha-ketoglutarate) dehydrogenase (lipoamide)	Mus musculus	162-195
29860433-1	2018	Impaired glucose metabolism, decreased levels of thiamine and its phosphate esters, and reduced activity of thiamine-dependent enzymes, such as pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and transketolase occur in Alzheimer"s disease (AD).	Thiamine	108-116	oxoglutarate (alpha-ketoglutarate) dehydrogenase (lipoamide)	Mus musculus	168-201
29860433-1	2018	Impaired glucose metabolism, decreased levels of thiamine and its phosphate esters, and reduced activity of thiamine-dependent enzymes, such as pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and transketolase occur in Alzheimer"s disease (AD).	Thiamine	108-116	transketolase	Mus musculus	206-219
30022846-6	2018	RFS is characterized by severe electrolyte shifts (mainly hypophosphatemia, hypomagnesemia and hypokalemia), vitamin deficiency (mainly thiamine), fluid overload and salt retention leading to organ dysfunction and cardiac arrhythmias.	Thiamine	136-144	FRTS1	Homo sapiens	0-3
29986774-1	2018	As the co-enzyme of pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, thiamine plays a critical role in carbohydrate metabolism in dairy cows.	Thiamine	82-90	oxoglutarate dehydrogenase	Bos taurus	47-80
29966293-1	2018	Thiamine, named as vitamin B1, is an important cofactor for the critical enzymes regarding to glucose metabolism, like transketolase, pyruvate dehydrogenase, and alpha-ketoglutarate dehydrogenase.	Thiamine	19-29	oxoglutarate (alpha-ketoglutarate) dehydrogenase (lipoamide)	Mus musculus	162-195
29997610-8	2018	HAP4 globally regulated thiamine synthesis, biomass synthesis, respiration, and osmotolerance of cells, which conferred the recombinant strain hap4-OE with faster glucose metabolism and enhanced stress resistance.	Thiamine	24-32	transcription factor HAP4	Saccharomyces cerevisiae S288C	0-4
29997610-8	2018	HAP4 globally regulated thiamine synthesis, biomass synthesis, respiration, and osmotolerance of cells, which conferred the recombinant strain hap4-OE with faster glucose metabolism and enhanced stress resistance.	Thiamine	24-32	transcription factor HAP4	Saccharomyces cerevisiae S288C	143-147
29450569-3	2018	We investigated the genotype, phenotype and response to thiamine (vitamin B1) in a cohort of individuals with TRMA-related diabetes.	Thiamine	56-64	solute carrier family 19 member 2	Homo sapiens	110-114
29903777-1	2018	Thiamine-responsive megaloblastic anaemia (TRMA) is a syndrome associated with megaloblastic anaemia, diabetes mellitus and sensorineural deafness, due to mutations in the SLC19A2 gene, which codes for a thiamine carrier protein.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	43-47
29903777-1	2018	Thiamine-responsive megaloblastic anaemia (TRMA) is a syndrome associated with megaloblastic anaemia, diabetes mellitus and sensorineural deafness, due to mutations in the SLC19A2 gene, which codes for a thiamine carrier protein.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	172-179
29903777-1	2018	Thiamine-responsive megaloblastic anaemia (TRMA) is a syndrome associated with megaloblastic anaemia, diabetes mellitus and sensorineural deafness, due to mutations in the SLC19A2 gene, which codes for a thiamine carrier protein.	Thiamine	204-212	solute carrier family 19 member 2	Homo sapiens	43-47
29903777-1	2018	Thiamine-responsive megaloblastic anaemia (TRMA) is a syndrome associated with megaloblastic anaemia, diabetes mellitus and sensorineural deafness, due to mutations in the SLC19A2 gene, which codes for a thiamine carrier protein.	Thiamine	204-212	solute carrier family 19 member 2	Homo sapiens	172-179
29914147-7	2018	Thiamine had a number of effects in MCF7; it (1) reduced extracellular lactate levels in growth media, (2) increased cellular pyruvate dehydrogenase (PDH) activities and the baseline and maximum cellular oxygen consumption rates, and (3) decreased non-glycolytic acidification, glycolysis, and glycolytic capacity.	Thiamine	0-8	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	126-148
29914147-7	2018	Thiamine had a number of effects in MCF7; it (1) reduced extracellular lactate levels in growth media, (2) increased cellular pyruvate dehydrogenase (PDH) activities and the baseline and maximum cellular oxygen consumption rates, and (3) decreased non-glycolytic acidification, glycolysis, and glycolytic capacity.	Thiamine	0-8	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	150-153
30090160-0	2018	Thiamin-Responsive PDH Deficiency due to a PDHA1 Variant.	Thiamine	0-7	pyruvate dehydrogenase E1 subunit alpha 1	Homo sapiens	43-48
29659562-0	2018	Organic cation transporter 1 (OCT1) modulates multiple cardiometabolic traits through effects on hepatic thiamine content.	Thiamine	105-113	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	0-28
29659562-0	2018	Organic cation transporter 1 (OCT1) modulates multiple cardiometabolic traits through effects on hepatic thiamine content.	Thiamine	105-113	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	30-34
29659562-3	2018	Here, we show that OCT1, widely characterized as a drug transporter, plays a key role in modulating hepatic glucose and lipid metabolism, potentially by mediating thiamine (vitamin B1) uptake and hence its levels in the liver.	Thiamine	163-171	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	19-23
29659562-3	2018	Here, we show that OCT1, widely characterized as a drug transporter, plays a key role in modulating hepatic glucose and lipid metabolism, potentially by mediating thiamine (vitamin B1) uptake and hence its levels in the liver.	Thiamine	173-183	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	19-23
29659562-4	2018	Deletion of Oct1 in mice resulted in reduced activity of thiamine-dependent enzymes, including pyruvate dehydrogenase (PDH), which disrupted the hepatic glucose-fatty acid cycle and shifted the source of energy production from glucose to fatty acids, leading to a reduction in glucose utilization, increased gluconeogenesis, and altered lipid metabolism.	Thiamine	57-65	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	12-16
28942193-8	2018	THD also demonstrated a potential of interrupting Nrf2-Keap1 protein-protein interaction (PPI).	Thiamine	0-3	NFE2 like bZIP transcription factor 2	Homo sapiens	50-54
29469010-5	2018	RESULTS: Thiamine deficiency was detected in 61 patients within the first 10 d of ICU stay, 57 cases being diagnosed on admission and 4 new cases on the 5th d. C-reactive protein concentration during ICU stay was independently associated with decreased blood thiamine concentrations (P = 0.003).	Thiamine	9-17	C-reactive protein	Homo sapiens	160-178
29469010-5	2018	RESULTS: Thiamine deficiency was detected in 61 patients within the first 10 d of ICU stay, 57 cases being diagnosed on admission and 4 new cases on the 5th d. C-reactive protein concentration during ICU stay was independently associated with decreased blood thiamine concentrations (P = 0.003).	Thiamine	259-267	C-reactive protein	Homo sapiens	160-178
28942193-8	2018	THD also demonstrated a potential of interrupting Nrf2-Keap1 protein-protein interaction (PPI).	Thiamine	0-3	kelch like ECH associated protein 1	Homo sapiens	55-60
28942193-10	2018	Taken together, we conclude that NLD and THD are two novel Nrf2 activators with potential application of preventing acute and chronic oxidative insults in human lung tissue.	Thiamine	41-44	NFE2 like bZIP transcription factor 2	Homo sapiens	59-63
29101630-1	2018	Biotin Thiamine responsive Basal Ganglia Disease (BTBGD) is a rare treatable autosomal recessive metabolic disorder caused by mutations in SLC19A3 gene.	Thiamine	7-15	solute carrier family 19 member 3	Homo sapiens	139-146
29969779-0	2018	A Novel Mutation of SLC19A2 in a Chinese Zhuang Ethnic Family with Thiamine-Responsive Megaloblastic Anemia.	Thiamine	67-75	solute carrier family 19 member 2	Homo sapiens	20-27
29208764-3	2018	Pyruvate dehydrogenase and 2-oxoglutarate dehydrogenase complexes as well as transketolase are the examples of thiamine-dependent enzymes present in eukaryotes, including human.	Thiamine	111-119	transketolase	Homo sapiens	77-90
29969779-1	2018	BACKGROUND/AIMS: Thiamine-responsive megaloblastic anemia syndrome is a rare autosomal recessive disorder resulting from mutations in SLC19A2, and is mainly characterized by megaloblastic anemia, diabetes, and progressive sensorineural hearing loss.	Thiamine	17-25	solute carrier family 19 member 2	Homo sapiens	134-141
29123435-3	2017	We report a case of early infantile Leigh-like SLC19A3 gene defects of patients who died at 4 months of age with no response to a high dose of biotin and thiamine.	Thiamine	154-162	solute carrier family 19 member 3	Homo sapiens	47-54
28371426-0	2018	Recovered insulin production after thiamine administration in permanent neonatal diabetes mellitus with a novel solute carrier family 19 member 2 (SLC19A2) mutation.	Thiamine	35-43	insulin	Homo sapiens	10-17
28371426-0	2018	Recovered insulin production after thiamine administration in permanent neonatal diabetes mellitus with a novel solute carrier family 19 member 2 (SLC19A2) mutation.	Thiamine	35-43	solute carrier family 19 member 2	Homo sapiens	112-145
28371426-0	2018	Recovered insulin production after thiamine administration in permanent neonatal diabetes mellitus with a novel solute carrier family 19 member 2 (SLC19A2) mutation.	Thiamine	35-43	solute carrier family 19 member 2	Homo sapiens	147-154
28371426-1	2018	BACKGROUND: Solute carrier family 19 member 2 (SLC19A2) gene deficiency is one of the causes of permanent neonatal diabetes mellitus (PNDM) and can be effectively managed by thiamine supplementation.	Thiamine	174-182	solute carrier family 19 member 2	Homo sapiens	12-45
28371426-1	2018	BACKGROUND: Solute carrier family 19 member 2 (SLC19A2) gene deficiency is one of the causes of permanent neonatal diabetes mellitus (PNDM) and can be effectively managed by thiamine supplementation.	Thiamine	174-182	solute carrier family 19 member 2	Homo sapiens	47-54
28371426-8	2018	After oral thiamine administration, the patient"s fasting C-peptide levels increased gradually, and there was a marked decrease in insulin requirements.	Thiamine	11-19	insulin	Homo sapiens	131-138
29379566-5	2018	After treatment of thiamine, diabetes was controlled and insulin was discontinued.	Thiamine	19-27	insulin	Homo sapiens	57-64
28004468-0	2017	First 2 cases with thiamine-responsive megaloblastic anemia in the Czech Republic, a rare form of monogenic diabetes mellitus: a novel mutation in the thiamine transporter SLC19A2 gene-intron 1 mutation c.204+2T&gt;G. Thiamine-responsive megaloblastic anemia (TRMA) is a rare autosomal recessive disorder caused by mutations in the SLC19A2 gene.	Thiamine	19-27	solute carrier family 19 member 2	Homo sapiens	172-179
28004468-0	2017	First 2 cases with thiamine-responsive megaloblastic anemia in the Czech Republic, a rare form of monogenic diabetes mellitus: a novel mutation in the thiamine transporter SLC19A2 gene-intron 1 mutation c.204+2T&gt;G. Thiamine-responsive megaloblastic anemia (TRMA) is a rare autosomal recessive disorder caused by mutations in the SLC19A2 gene.	Thiamine	19-27	solute carrier family 19 member 2	Homo sapiens	332-339
28004468-0	2017	First 2 cases with thiamine-responsive megaloblastic anemia in the Czech Republic, a rare form of monogenic diabetes mellitus: a novel mutation in the thiamine transporter SLC19A2 gene-intron 1 mutation c.204+2T&gt;G. Thiamine-responsive megaloblastic anemia (TRMA) is a rare autosomal recessive disorder caused by mutations in the SLC19A2 gene.	Thiamine	218-226	solute carrier family 19 member 2	Homo sapiens	172-179
28696212-0	2017	Compound heterozygous SLC19A3 mutations further refine the critical promoter region for biotin-thiamine-responsive basal ganglia disease.	Thiamine	95-103	solute carrier family 19 member 3	Homo sapiens	22-29
28696212-1	2017	Mutations in the gene SLC19A3 result in thiamine metabolism dysfunction syndrome 2, also known as biotin-thiamine-responsive basal ganglia disease (BTBGD).	Thiamine	40-48	solute carrier family 19 member 3	Homo sapiens	22-29
28696212-1	2017	Mutations in the gene SLC19A3 result in thiamine metabolism dysfunction syndrome 2, also known as biotin-thiamine-responsive basal ganglia disease (BTBGD).	Thiamine	105-113	solute carrier family 19 member 3	Homo sapiens	22-29
29045486-0	2017	Thiamine deficiency activates hypoxia inducible factor-1alpha to facilitate pro-apoptotic responses in mouse primary astrocytes.	Thiamine	0-8	hypoxia inducible factor 1, alpha subunit	Mus musculus	30-61
29089959-7	2017	Quantitative real-time PCR was performed to measure transcript abundances of four key thiamine biosynthesis genes (THI4, THIC, TH1, and TPK) on days 1, 7, 15, and 30 in response to H. toruloidea colonization.	Thiamine	86-94	negative elongation factor complex member C/D	Homo sapiens	127-130
29045486-10	2017	Pharmacological inhibition of HIF-1alpha activity using YC1 and thiamine repletion both reduced expression of pro-apoptotic HIF-1alpha target genes and apoptotic cell death in TD.	Thiamine	64-72	hypoxia inducible factor 1, alpha subunit	Mus musculus	30-40
29045486-10	2017	Pharmacological inhibition of HIF-1alpha activity using YC1 and thiamine repletion both reduced expression of pro-apoptotic HIF-1alpha target genes and apoptotic cell death in TD.	Thiamine	64-72	hypoxia inducible factor 1, alpha subunit	Mus musculus	124-134
29045486-11	2017	These results demonstrate that induction of HIF-1alpha mediated transcriptional up-regulation of pro-apoptotic/inflammatory signaling contributes to astrocyte cell death during thiamine deficiency.	Thiamine	177-185	hypoxia inducible factor 1, alpha subunit	Mus musculus	44-54
28958614-13	2017	Riboflavin, thiamine and dexamethasone reduced TNF-alpha and IL-6 production.	Thiamine	12-20	tumor necrosis factor	Rattus norvegicus	47-56
27440134-0	2017	Thiamine Levels During Intensive Insulin Therapy in Critically Ill Patients.	Thiamine	0-8	insulin	Homo sapiens	33-40
27440134-3	2017	In this study, we investigated the prevalence of thiamine deficiency at admission to the intensive care unit (ICU) and hypothesized that intensive insulin therapy, aimed at regulating glucose levels, increases thiamine utilization and therefore might cause or worsen deficiency in patients with limited thiamine stores.	Thiamine	49-57	insulin	Homo sapiens	147-154
27440134-3	2017	In this study, we investigated the prevalence of thiamine deficiency at admission to the intensive care unit (ICU) and hypothesized that intensive insulin therapy, aimed at regulating glucose levels, increases thiamine utilization and therefore might cause or worsen deficiency in patients with limited thiamine stores.	Thiamine	210-218	insulin	Homo sapiens	147-154
27440134-3	2017	In this study, we investigated the prevalence of thiamine deficiency at admission to the intensive care unit (ICU) and hypothesized that intensive insulin therapy, aimed at regulating glucose levels, increases thiamine utilization and therefore might cause or worsen deficiency in patients with limited thiamine stores.	Thiamine	210-218	insulin	Homo sapiens	147-154
28958614-13	2017	Riboflavin, thiamine and dexamethasone reduced TNF-alpha and IL-6 production.	Thiamine	12-20	interleukin 6	Rattus norvegicus	61-65
28958614-14	2017	The association of dexamethasone with thiamine induced greater inhibition of IL-6 production when compared with that induced by dexamethasone.	Thiamine	38-46	interleukin 6	Rattus norvegicus	77-81
28958614-15	2017	CONCLUSIONS: Riboflavin and thiamine exacerbate the anti-inflammatory activity of dexamethasone and reduce production of TNF-alpha and IL-6.	Thiamine	28-36	tumor necrosis factor	Rattus norvegicus	121-130
28958614-15	2017	CONCLUSIONS: Riboflavin and thiamine exacerbate the anti-inflammatory activity of dexamethasone and reduce production of TNF-alpha and IL-6.	Thiamine	28-36	interleukin 6	Rattus norvegicus	135-139
28878400-0	2017	Thiamine antagonists trigger p53-dependent apoptosis in differentiated SH-SY5Y cells.	Thiamine	0-8	tumor protein p53	Homo sapiens	29-32
28803855-4	2017	A two-week-long pretreatment regime with imipramine (7.5mg/kg/day) or thiamine (200mg/kg/day), which is known to have antidepressant properties, reduced the GSK3beta over-expression and decreased floating behaviour on Day 5.	Thiamine	70-78	glycogen synthase kinase 3 beta	Mus musculus	157-165
28803855-7	2017	In this model, GSK3alpha mRNA changes were prevented by imipramine or thiamine treatment.	Thiamine	70-78	glycogen synthase kinase 3 alpha	Mus musculus	15-24
28856750-3	2017	Herein, we describe the clinical and genetic characterization of 79 patients with inherited thiamine defects causing encephalopathy in childhood, identifying outcome predictors in patients with pathogenic SLC19A3 variants, the most common genetic etiology.	Thiamine	92-100	solute carrier family 19 member 3	Homo sapiens	205-212
28878400-1	2017	Accumulating evidences suggest that p53 is a key coordinator of cellular events triggered by oxidative stress often associated with the impairment in thiamine metabolism and its functions.	Thiamine	150-158	tumor protein p53	Homo sapiens	36-39
28501402-12	2017	Thiamine supplementation decreased ruminal LPS (49,361 vs. 134,380 endotoxin units/mL) and attenuated the HG-induced inflammation response as indicated by a reduction in plasma IL6, and decreasing gene and protein expression of pro-inflammatory cytokines in rumen epithelium.	Thiamine	0-8	interferon beta-2	Bos taurus	177-180
28747443-0	2017	Thiamine-responsive disease due to mutation of tpk1: Importance of avoiding misdiagnosis.	Thiamine	0-8	thiamin pyrophosphokinase 1	Homo sapiens	47-51
29068569-8	2017	CONCLUSIONS: The above results and reported changes in expression of GAPDH, IDH1 and SLC19A3 genes observed upon thiamine deficit conditions suggest that intracellular thiamine status and energy metabolism can have a role in HD pathogenesis.	Thiamine	113-121	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	69-74
29068569-8	2017	CONCLUSIONS: The above results and reported changes in expression of GAPDH, IDH1 and SLC19A3 genes observed upon thiamine deficit conditions suggest that intracellular thiamine status and energy metabolism can have a role in HD pathogenesis.	Thiamine	113-121	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	76-80
29068569-8	2017	CONCLUSIONS: The above results and reported changes in expression of GAPDH, IDH1 and SLC19A3 genes observed upon thiamine deficit conditions suggest that intracellular thiamine status and energy metabolism can have a role in HD pathogenesis.	Thiamine	113-121	solute carrier family 19 member 3	Homo sapiens	85-92
29068569-8	2017	CONCLUSIONS: The above results and reported changes in expression of GAPDH, IDH1 and SLC19A3 genes observed upon thiamine deficit conditions suggest that intracellular thiamine status and energy metabolism can have a role in HD pathogenesis.	Thiamine	168-176	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	69-74
29068569-8	2017	CONCLUSIONS: The above results and reported changes in expression of GAPDH, IDH1 and SLC19A3 genes observed upon thiamine deficit conditions suggest that intracellular thiamine status and energy metabolism can have a role in HD pathogenesis.	Thiamine	168-176	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	76-80
29068569-8	2017	CONCLUSIONS: The above results and reported changes in expression of GAPDH, IDH1 and SLC19A3 genes observed upon thiamine deficit conditions suggest that intracellular thiamine status and energy metabolism can have a role in HD pathogenesis.	Thiamine	168-176	solute carrier family 19 member 3	Homo sapiens	85-92
27550086-0	2017	Multi-spectroscopic and voltammetric evidences for binding, conformational changes of bovine serum albumin with thiamine.	Thiamine	112-120	albumin	Homo sapiens	93-106
28501402-13	2017	Western bottling analysis showed that thiamine suppressed the protein expression of TLR4 and the phosphorylation of nuclear factor kappa B (NFkappaB) unit p65.	Thiamine	38-46	toll like receptor 4	Bos taurus	84-88
28506637-5	2017	This reduction was prevented when the mice were treated (200mg/kg/day in drinking water for 20days) with thiamine or benfotiamine, that were recently found to prevent stress-induced behavioral changes and glycogen synthase kinase-3beta (GSK-3beta) upregulation in the CNS.	Thiamine	105-113	glycogen synthase kinase 3 beta	Mus musculus	205-235
28506637-5	2017	This reduction was prevented when the mice were treated (200mg/kg/day in drinking water for 20days) with thiamine or benfotiamine, that were recently found to prevent stress-induced behavioral changes and glycogen synthase kinase-3beta (GSK-3beta) upregulation in the CNS.	Thiamine	105-113	glycogen synthase kinase 3 beta	Mus musculus	237-246
28501402-13	2017	Western bottling analysis showed that thiamine suppressed the protein expression of TLR4 and the phosphorylation of nuclear factor kappa B (NFkappaB) unit p65.	Thiamine	38-46	synaptotagmin 1	Bos taurus	155-158
28501402-15	2017	Thiamine could attenuate the epithelial inflammation during high-grain feeding, and the protective effects may be due to its ability to suppress TLR4-mediated NFkappaB signaling pathways.	Thiamine	0-8	toll like receptor 4	Bos taurus	145-149
28402605-0	2017	Biotin-thiamine responsive basal ganglia disease: Identification of a pyruvate peak on brain spectroscopy, novel mutation in SLC19A3, and calculation of prevalence based on allele frequencies from aggregated next-generation sequencing data.	Thiamine	7-15	solute carrier family 19 member 3	Homo sapiens	125-132
28665968-0	2017	High-dose thiamine prevents brain lesions and prolongs survival of Slc19a3-deficient mice.	Thiamine	10-18	solute carrier family 19, member 3	Mus musculus	67-74
28665968-1	2017	SLC19A3 deficiency, also called thiamine metabolism dysfunction syndrome-2 (THMD2; OMIM 607483), is an autosomal recessive neurodegenerative disorder caused by mutations in SLC19A3, the gene encoding thiamine transporter 2.	Thiamine	32-40	solute carrier family 19 member 3	Homo sapiens	76-81
28665968-1	2017	SLC19A3 deficiency, also called thiamine metabolism dysfunction syndrome-2 (THMD2; OMIM 607483), is an autosomal recessive neurodegenerative disorder caused by mutations in SLC19A3, the gene encoding thiamine transporter 2.	Thiamine	32-40	solute carrier family 19, member 3	Mus musculus	0-7
28665968-1	2017	SLC19A3 deficiency, also called thiamine metabolism dysfunction syndrome-2 (THMD2; OMIM 607483), is an autosomal recessive neurodegenerative disorder caused by mutations in SLC19A3, the gene encoding thiamine transporter 2.	Thiamine	32-40	solute carrier family 19, member 3	Mus musculus	200-222
28665968-4	2017	These findings may bear some features of thiamine-deficient mice generated by pyrithiamine injection and a thiamine-deficient diet, suggesting that the primary cause of THMD2 could be thiamine pyrophosphate (TPP) deficiency.	Thiamine	41-49	solute carrier family 19 member 3	Homo sapiens	169-174
28665968-9	2017	These results showed that acute neurodegeneration caused by thiamine deficiency is preventable in most parts, and prompt high-dose thiamine administration is critical for the treatment of THMD2.	Thiamine	131-139	solute carrier family 19 member 3	Homo sapiens	188-193
28402605-1	2017	Biotin-thiamine responsive basal ganglia disease is an inborn error of metabolism caused by mutations in SLC19A3, encoding a transporter of thiamine across the plasma membrane.	Thiamine	7-15	solute carrier family 19 member 3	Homo sapiens	105-112
28402605-1	2017	Biotin-thiamine responsive basal ganglia disease is an inborn error of metabolism caused by mutations in SLC19A3, encoding a transporter of thiamine across the plasma membrane.	Thiamine	140-148	solute carrier family 19 member 3	Homo sapiens	105-112
28032668-8	2017	The link found between TKT genetic variability and nerve function measures is considered here in the context of DPN genetic studies and of experimental and clinical findings regarding thiamine and benfotiamine.	Thiamine	184-192	transketolase	Homo sapiens	23-26
28504500-0	2017	Infantile-onset thiamine responsive megaloblastic anemia syndrome with SLC19A2 mutation: a case report.	Thiamine	16-24	solute carrier family 19 member 2	Homo sapiens	71-78
28504500-1	2017	BACKGROUND: Thiamine-responsive megaloblastic anemia syndrome (TRMA), also known as Rogers syndrome, is characterized by megaloblastic anemia, sensorineural hearing loss, and diabetes mellitus.	Thiamine	12-20	solute carrier family 19 member 2	Homo sapiens	63-67
28504500-2	2017	Disturbances of the thiamine transport into the cells results from homozygous or compound heterozygous mutations in the SLC19A2 gene.	Thiamine	20-28	solute carrier family 19 member 2	Homo sapiens	120-127
27140189-0	2017	Thiamine Deficiency Increases Ca2+ Current and CaV1.2 L-type Ca2+ Channel Levels in Cerebellum Granular Neurons.	Thiamine	0-8	carbonic anhydrase 2	Homo sapiens	30-33
27825907-10	2017	Our data indicate that thiamine and benfotiamine have antidepressant/anti-stress effects in naive animals that are associated with reduced GSK-3beta expression and conditioning of adverse memories.	Thiamine	23-31	glycogen synthase kinase 3 beta	Mus musculus	139-148
27825907-11	2017	Thus thiamine and benfotiamine may modulate GSK-3beta functions in a manner that is dependent on whether the contextual conditioning is adaptive or maladaptive.	Thiamine	5-13	glycogen synthase kinase 3 beta	Mus musculus	44-53
27825907-0	2017	Thiamine and benfotiamine improve cognition and ameliorate GSK-3beta-associated stress-induced behaviours in mice.	Thiamine	0-8	glycogen synthase kinase 3 beta	Mus musculus	59-68
27825907-2	2017	Indirect evidence suggests that thiamine may contribute to these pathologies by controlling the activities of glycogen synthase kinase (GSK)-3beta.	Thiamine	32-40	glycogen synthase kinase 3 beta	Mus musculus	110-146
27825907-4	2017	However, hitherto direct evidence for the effects of thiamine on GSK-3beta function has not been reported.	Thiamine	53-61	glycogen synthase kinase 3 beta	Mus musculus	65-74
27140189-0	2017	Thiamine Deficiency Increases Ca2+ Current and CaV1.2 L-type Ca2+ Channel Levels in Cerebellum Granular Neurons.	Thiamine	0-8	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	47-53
27140189-0	2017	Thiamine Deficiency Increases Ca2+ Current and CaV1.2 L-type Ca2+ Channel Levels in Cerebellum Granular Neurons.	Thiamine	0-8	carbonic anhydrase 2	Homo sapiens	61-64
27140189-1	2017	Thiamine (vitamin B1) is co-factor for three pivotal enzymes for glycolytic metabolism: pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase.	Thiamine	0-8	transketolase	Homo sapiens	151-164
27140189-1	2017	Thiamine (vitamin B1) is co-factor for three pivotal enzymes for glycolytic metabolism: pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase.	Thiamine	10-20	transketolase	Homo sapiens	151-164
27140189-5	2017	Here, using an in vitro model to study the effects of thiamine deficiency on cerebellum granule neurons, we show an increase in Ca2+ current density and CaV1.2 expression.	Thiamine	54-62	carbonic anhydrase 2	Homo sapiens	128-131
27140189-5	2017	Here, using an in vitro model to study the effects of thiamine deficiency on cerebellum granule neurons, we show an increase in Ca2+ current density and CaV1.2 expression.	Thiamine	54-62	calcium voltage-gated channel subunit alpha1 C	Homo sapiens	153-159
28182200-0	2017	Chronic Ethanol Consumption and Thiamine Deficiency Modulate beta-Amyloid Peptide Level and Oxidative Stress in the Brain.	Thiamine	32-40	amyloid beta precursor protein	Homo sapiens	61-81
28352471-11	2017	The closest candidate gene is TPK1, a thiamine-dependent enzyme and part of the PKA complex.	Thiamine	38-46	thiamin pyrophosphokinase 1	Canis lupus familiaris	30-34
28076318-0	2017	Beta cell function and clinical course in three siblings with thiamine-responsive megaloblastic anemia (TRMA) treated with thiamine supplementation.	Thiamine	62-70	solute carrier family 19 member 2	Homo sapiens	104-108
28076318-1	2017	Three siblings with thiamine-responsive megaloblastic anemia (TRMA) with a homozygous c.454delGGCATinsAT mutation in SLC19A2 are described.	Thiamine	20-28	solute carrier family 19 member 2	Homo sapiens	117-124
28076318-0	2017	Beta cell function and clinical course in three siblings with thiamine-responsive megaloblastic anemia (TRMA) treated with thiamine supplementation.	Thiamine	123-131	solute carrier family 19 member 2	Homo sapiens	104-108
28076318-7	2017	The clinical course in this family suggests that there is an effect of thiamine on pancreatic beta cell function in patients with TRMA given the resolution of impaired fasting glucose with increasing thiamine dose in one sibling and the lack of diabetes to date in the siblings that were treated early with thiamine.	Thiamine	71-79	solute carrier family 19 member 2	Homo sapiens	130-134
28076318-1	2017	Three siblings with thiamine-responsive megaloblastic anemia (TRMA) with a homozygous c.454delGGCATinsAT mutation in SLC19A2 are described.	Thiamine	20-28	solute carrier family 19 member 2	Homo sapiens	62-66
28076318-7	2017	The clinical course in this family suggests that there is an effect of thiamine on pancreatic beta cell function in patients with TRMA given the resolution of impaired fasting glucose with increasing thiamine dose in one sibling and the lack of diabetes to date in the siblings that were treated early with thiamine.	Thiamine	200-208	solute carrier family 19 member 2	Homo sapiens	130-134
28076318-7	2017	The clinical course in this family suggests that there is an effect of thiamine on pancreatic beta cell function in patients with TRMA given the resolution of impaired fasting glucose with increasing thiamine dose in one sibling and the lack of diabetes to date in the siblings that were treated early with thiamine.	Thiamine	200-208	solute carrier family 19 member 2	Homo sapiens	130-134
28677371-0	2017	Neuropathological characteristics of the brain in two patients with SLC19A3 mutations related to the biotin-thiamine-responsive basal ganglia disease.	Thiamine	108-116	solute carrier family 19 member 3	Homo sapiens	68-75
27905264-1	2017	BACKGROUND: Biotin-thiamine-responsive basal ganglia disease (BTBGD) is an autosomal recessive neurometabolic disorder caused by mutations in the SLC19A3 gene.	Thiamine	19-27	solute carrier family 19 member 3	Homo sapiens	146-153
27803021-8	2017	Further studies with drugs containing a 2,4-diaminopyrimidine resulted in the discovery that the antibiotic trimethoprim also potently inhibits thiamine uptake mediated by THTR-1 (IC50 = 6.84 microM) and THTR-2 (IC50 = 5.56 microM).	Thiamine	144-152	solute carrier family 19 member 2	Homo sapiens	172-178
27803021-8	2017	Further studies with drugs containing a 2,4-diaminopyrimidine resulted in the discovery that the antibiotic trimethoprim also potently inhibits thiamine uptake mediated by THTR-1 (IC50 = 6.84 microM) and THTR-2 (IC50 = 5.56 microM).	Thiamine	144-152	solute carrier family 19 member 3	Homo sapiens	204-210
27983623-7	2016	In particular, these structural differences may affect the well-known regulation of GDH by nucleotides which is related to recent identification of thiamine derivatives as novel GDH modulators.	Thiamine	148-156	glutamate dehydrogenase 1	Homo sapiens	84-87
27743994-11	2016	This work demonstrates the direct binding and activation of SLC19A3 expression by HIF-1alpha during hypoxic stress, suggesting an important adaptive regulatory role for HIF-1alpha in maintaining thiamine homeostasis.	Thiamine	195-203	solute carrier family 19 member 3	Homo sapiens	60-67
27743994-11	2016	This work demonstrates the direct binding and activation of SLC19A3 expression by HIF-1alpha during hypoxic stress, suggesting an important adaptive regulatory role for HIF-1alpha in maintaining thiamine homeostasis.	Thiamine	195-203	hypoxia inducible factor 1 subunit alpha	Homo sapiens	82-92
27743994-11	2016	This work demonstrates the direct binding and activation of SLC19A3 expression by HIF-1alpha during hypoxic stress, suggesting an important adaptive regulatory role for HIF-1alpha in maintaining thiamine homeostasis.	Thiamine	195-203	hypoxia inducible factor 1 subunit alpha	Homo sapiens	169-179
27983623-7	2016	In particular, these structural differences may affect the well-known regulation of GDH by nucleotides which is related to recent identification of thiamine derivatives as novel GDH modulators.	Thiamine	148-156	glutamate dehydrogenase 1	Homo sapiens	178-181
27983623-8	2016	The thiamine-dependent regulation of GDH is in good agreement with the fact that the non-coenzyme forms of thiamine, i.e., thiamine triphosphate and its adenylated form are generated in response to amino acid and carbon starvation.	Thiamine	4-12	glutamate dehydrogenase 1	Homo sapiens	37-40
27983623-8	2016	The thiamine-dependent regulation of GDH is in good agreement with the fact that the non-coenzyme forms of thiamine, i.e., thiamine triphosphate and its adenylated form are generated in response to amino acid and carbon starvation.	Thiamine	107-115	glutamate dehydrogenase 1	Homo sapiens	37-40
27984051-8	2016	Likewise, glucose transporter-1 (Glut-1), which is mostly expressed in endothelial cells, was also severely decreased in this pyrithiamine induced thiamine deficient rat model.	Thiamine	130-138	solute carrier family 2 member 1	Rattus norvegicus	10-31
27773789-1	2016	Decreased thiamine and reduced activity of thiamine diphosphate (ThDP)-dependent 2-oxoglutarate dehydrogenase (OGDH) cause neurodegeneration.	Thiamine	10-18	oxoglutarate dehydrogenase	Rattus norvegicus	111-115
27773789-5	2016	Indeed, in rat astrocytes and brain cortex, OGDH inhibition by succinyl phosphonate (SP) enlarged the pool of thiamine compounds.	Thiamine	110-118	oxoglutarate dehydrogenase	Rattus norvegicus	44-48
27773789-8	2016	The presented data indicate that functional interplay between OGDH, other proteins of the tricarbocylic acid cycle and proteins of thiamine metabolism is an important determinant of physiology-specific networks and their homeostatic mechanisms.	Thiamine	131-139	oxoglutarate dehydrogenase	Rattus norvegicus	62-66
27984051-8	2016	Likewise, glucose transporter-1 (Glut-1), which is mostly expressed in endothelial cells, was also severely decreased in this pyrithiamine induced thiamine deficient rat model.	Thiamine	130-138	solute carrier family 2 member 1	Rattus norvegicus	33-39
26372107-6	2016	In this study, the binding of thiamine hydrochloride (vitamin B1) to bovine serum albumin (BSA) was evaluated using a new proposed vitamin B1 (thiamine)-selective membrane electrode under various experimental conditions, such as pH, ionic strength, and protein concentration; in addition molecular modeling was applied as well.	Thiamine	54-64	albumin	Homo sapiens	76-95
27904781-4	2016	Transketolase (TKT), a thiamine-dependent enzyme that plays a role in the channeling of excess glucose phosphates to glycolysis in the pentose phosphate pathway, was identified as a direct target of miR-497.	Thiamine	23-31	transketolase	Homo sapiens	0-13
27904781-4	2016	Transketolase (TKT), a thiamine-dependent enzyme that plays a role in the channeling of excess glucose phosphates to glycolysis in the pentose phosphate pathway, was identified as a direct target of miR-497.	Thiamine	23-31	transketolase	Homo sapiens	15-18
27904781-4	2016	Transketolase (TKT), a thiamine-dependent enzyme that plays a role in the channeling of excess glucose phosphates to glycolysis in the pentose phosphate pathway, was identified as a direct target of miR-497.	Thiamine	23-31	microRNA 497	Homo sapiens	199-206
27488863-0	2016	Long-term treatment with thiamine as possible medical therapy for Friedreich ataxia.	Thiamine	25-33	frataxin	Homo sapiens	66-83
27488863-2	2016	Previous studies reported low thiamine levels in cerebrospinal fluid and pyruvate dehydrogenase dysfunction in Friedreich ataxia (FRDA).	Thiamine	30-38	frataxin	Homo sapiens	111-128
27488863-11	2016	Further studies are mandatory to evaluate thiamine role on FXN regulation, to exclude placebo effect, to verify our clinical results, and to confirm restorative and neuroprotective action of thiamine in FRDA.	Thiamine	42-50	frataxin	Homo sapiens	59-62
28284395-4	2016	SLC19A1 transports folate and SLC19A2 and SLC19A3 transport thiamine.	Thiamine	60-68	solute carrier family 19 member 1	Homo sapiens	0-7
28284395-4	2016	SLC19A1 transports folate and SLC19A2 and SLC19A3 transport thiamine.	Thiamine	60-68	solute carrier family 19 member 3	Homo sapiens	42-49
27872694-8	2016	RESULTS: The results indicated that vitamin B1(150 and 200 mg/kg) attenuated the paw edema, thermal hyperalgesia, and serum levels of TNF-alpha and IL-1beta during both phases of CFA-induced inflammation in a dose-dependent manner.	Thiamine	36-46	tumor necrosis factor	Rattus norvegicus	134-143
27872694-8	2016	RESULTS: The results indicated that vitamin B1(150 and 200 mg/kg) attenuated the paw edema, thermal hyperalgesia, and serum levels of TNF-alpha and IL-1beta during both phases of CFA-induced inflammation in a dose-dependent manner.	Thiamine	36-46	interleukin 1 beta	Rattus norvegicus	148-156
27872694-9	2016	Effective dose of vitamin B1(150 mg/kg) reduced inflammatory symptoms and serum levels of TNF-alpha and IL-1beta compare to indomethacin during the chronic phase of inflammation.	Thiamine	18-28	tumor necrosis factor	Rattus norvegicus	90-99
27872694-9	2016	Effective dose of vitamin B1(150 mg/kg) reduced inflammatory symptoms and serum levels of TNF-alpha and IL-1beta compare to indomethacin during the chronic phase of inflammation.	Thiamine	18-28	interleukin 1 beta	Rattus norvegicus	104-112
26372107-6	2016	In this study, the binding of thiamine hydrochloride (vitamin B1) to bovine serum albumin (BSA) was evaluated using a new proposed vitamin B1 (thiamine)-selective membrane electrode under various experimental conditions, such as pH, ionic strength, and protein concentration; in addition molecular modeling was applied as well.	Thiamine	131-141	albumin	Homo sapiens	76-95
26372107-6	2016	In this study, the binding of thiamine hydrochloride (vitamin B1) to bovine serum albumin (BSA) was evaluated using a new proposed vitamin B1 (thiamine)-selective membrane electrode under various experimental conditions, such as pH, ionic strength, and protein concentration; in addition molecular modeling was applied as well.	Thiamine	30-38	albumin	Homo sapiens	76-95
26372107-9	2016	According to the electrochemical and molecular docking results, it can be concluded that the hydrophobic interactions and hydrogen binding are major interactions between BSA and vitamin B1.	Thiamine	178-188	albumin	Homo sapiens	170-173
27185216-2	2016	Thiamine is an essential co-factor of PDH.	Thiamine	0-8	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	38-41
27198804-0	2016	The uremic toxin oxythiamine causes functional thiamine deficiency in end-stage renal disease by inhibiting transketolase activity.	Thiamine	20-28	transketolase	Homo sapiens	108-121
27460839-0	2016	High-Throughput Detection of Thiamine Using Periplasmic Binding Protein-Based Biorecognition.	Thiamine	29-37	phosphatidylethanolamine binding protein 1	Homo sapiens	44-71
27460839-2	2016	As an alternative, we demonstrate use of a periplasmic binding protein (PBP) to provide high affinity recognition for thiamine (vitamin B1), an analyte of great importance to human and environmental health for which, like so many other small molecules, no suitable biorecognition element is available.	Thiamine	118-126	phosphatidylethanolamine binding protein 1	Homo sapiens	43-70
27460839-2	2016	As an alternative, we demonstrate use of a periplasmic binding protein (PBP) to provide high affinity recognition for thiamine (vitamin B1), an analyte of great importance to human and environmental health for which, like so many other small molecules, no suitable biorecognition element is available.	Thiamine	118-126	phosphatidylethanolamine binding protein 1	Homo sapiens	72-75
27460839-2	2016	As an alternative, we demonstrate use of a periplasmic binding protein (PBP) to provide high affinity recognition for thiamine (vitamin B1), an analyte of great importance to human and environmental health for which, like so many other small molecules, no suitable biorecognition element is available.	Thiamine	128-138	phosphatidylethanolamine binding protein 1	Homo sapiens	43-70
27460839-2	2016	As an alternative, we demonstrate use of a periplasmic binding protein (PBP) to provide high affinity recognition for thiamine (vitamin B1), an analyte of great importance to human and environmental health for which, like so many other small molecules, no suitable biorecognition element is available.	Thiamine	128-138	phosphatidylethanolamine binding protein 1	Homo sapiens	72-75
27460839-4	2016	The high-throughput method relies upon the thiamine periplasmic binding protein (TBP) from Escherichia coli for thiamine biorecognition and dye-encapsulating liposomes for signal-enhancement.	Thiamine	43-51	phosphatidylethanolamine binding protein 1	Homo sapiens	52-79
27460839-4	2016	The high-throughput method relies upon the thiamine periplasmic binding protein (TBP) from Escherichia coli for thiamine biorecognition and dye-encapsulating liposomes for signal-enhancement.	Thiamine	112-120	phosphatidylethanolamine binding protein 1	Homo sapiens	52-79
27185216-11	2016	The beneficial effects of thiamine were accompanied by improved oxygen consumption in mitochondria, restored thiamine pyrophosphate levels, and increased PDH activity in the brain at 10 days.	Thiamine	26-34	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	154-157
27191787-2	2016	There are four major genetic defects (SLC19A2, SLC19A3, SLC25A19 and TPK1) involved in the metabolism and transport of thiamine through cellular and mitochondrial membranes.	Thiamine	119-127	solute carrier family 19 member 3	Homo sapiens	47-54
27329029-9	2016	Among children with diabetes diagnosed between 6 and 12months, 1 patient had an INS mutation and one patient was homozygous for an SLC19A2 mutation which confirmed a diagnosis of thiamine-responsive megaloblastic anaemia syndrome.	Thiamine	179-187	solute carrier family 19 member 2	Homo sapiens	131-138
27191787-2	2016	There are four major genetic defects (SLC19A2, SLC19A3, SLC25A19 and TPK1) involved in the metabolism and transport of thiamine through cellular and mitochondrial membranes.	Thiamine	119-127	solute carrier family 19 member 2	Homo sapiens	38-45
27191787-2	2016	There are four major genetic defects (SLC19A2, SLC19A3, SLC25A19 and TPK1) involved in the metabolism and transport of thiamine through cellular and mitochondrial membranes.	Thiamine	119-127	solute carrier family 25 member 19	Homo sapiens	56-64
27191787-2	2016	There are four major genetic defects (SLC19A2, SLC19A3, SLC25A19 and TPK1) involved in the metabolism and transport of thiamine through cellular and mitochondrial membranes.	Thiamine	119-127	thiamin pyrophosphokinase 1	Homo sapiens	69-73
27191787-6	2016	Expert commentary: Doses of thiamine vary according to the genetic defect: for SLC19A2, the usual dose is 25-200 mg/day (1-4 mg/kg per day), for SLC19A3, 10-40 mg/kg per day, and for TPK1, 30 mg/kg per day.	Thiamine	28-36	solute carrier family 19 member 2	Homo sapiens	79-86
27191787-6	2016	Expert commentary: Doses of thiamine vary according to the genetic defect: for SLC19A2, the usual dose is 25-200 mg/day (1-4 mg/kg per day), for SLC19A3, 10-40 mg/kg per day, and for TPK1, 30 mg/kg per day.	Thiamine	28-36	solute carrier family 19 member 3	Homo sapiens	145-152
27191787-6	2016	Expert commentary: Doses of thiamine vary according to the genetic defect: for SLC19A2, the usual dose is 25-200 mg/day (1-4 mg/kg per day), for SLC19A3, 10-40 mg/kg per day, and for TPK1, 30 mg/kg per day.	Thiamine	28-36	thiamin pyrophosphokinase 1	Homo sapiens	183-187
27191787-7	2016	Thiamine supplementation in SLC19A3-mutated patients restores CSF and intracellular thiamine levels, resulting in successful clinical benefits.	Thiamine	0-8	solute carrier family 19 member 3	Homo sapiens	28-35
27191787-7	2016	Thiamine supplementation in SLC19A3-mutated patients restores CSF and intracellular thiamine levels, resulting in successful clinical benefits.	Thiamine	84-92	solute carrier family 19 member 3	Homo sapiens	28-35
27191787-8	2016	In conclusion, evidence collected so far suggests that the administration of thiamine improves outcome in SLC19A-2, SLC19A3- and TPK1-mutated patients, so most efforts should be aimed at early diagnosis of these disorders.	Thiamine	77-85	solute carrier family 19 member 2	Homo sapiens	106-114
27191787-8	2016	In conclusion, evidence collected so far suggests that the administration of thiamine improves outcome in SLC19A-2, SLC19A3- and TPK1-mutated patients, so most efforts should be aimed at early diagnosis of these disorders.	Thiamine	77-85	solute carrier family 19 member 3	Homo sapiens	116-123
27191787-8	2016	In conclusion, evidence collected so far suggests that the administration of thiamine improves outcome in SLC19A-2, SLC19A3- and TPK1-mutated patients, so most efforts should be aimed at early diagnosis of these disorders.	Thiamine	77-85	thiamin pyrophosphokinase 1	Homo sapiens	129-133
26999808-1	2016	Thiamin is essential for normal metabolism in pancreatic acinar cells (PAC) and is obtained from their microenvironment through specific plasma-membrane transporters, converted to thiamin pyrophosphate (TPP) in the cytoplasm, followed by uptake of TPP by mitochondria through the mitochondrial TPP (MTPP) transporter (MTPPT; product of SLC25A19 gene).	Thiamine	0-7	solute carrier family 25 (mitochondrial thiamine pyrophosphate carrier), member 19	Mus musculus	336-344
27006489-6	2016	A combination of biochemical, physiological, and genetic approaches permitted us to show that PUT3 mediates phloem transport of both thiamine and polyamines.	Thiamine	133-141	Amino acid permease family protein	Arabidopsis thaliana	94-98
26745793-6	2016	The fluorescence emission intensity enhancement of Cu(2+) ion modified C-dots in the presence of thiamine exhibits a linear relationship within the thiamine concentration range of 10-50 muM.	Thiamine	97-105	latexin	Homo sapiens	186-189
26745793-6	2016	The fluorescence emission intensity enhancement of Cu(2+) ion modified C-dots in the presence of thiamine exhibits a linear relationship within the thiamine concentration range of 10-50 muM.	Thiamine	148-156	latexin	Homo sapiens	186-189
27006489-8	2016	The pivotal role of PUT3 mediated thiamine and polyamine homeostasis in plants, and its importance for plant fitness is revealed through these findings.	Thiamine	34-42	Amino acid permease family protein	Arabidopsis thaliana	20-24
26744303-7	2016	Moreover, it was found that vitamin D3 combined with vitamin B1 or vitamin B2 exhibited significant synergistic effects on inhibition of alpha-glucosidase.	Thiamine	53-63	sucrase-isomaltase	Homo sapiens	137-154
26971083-5	2016	In preclinical models, reduced thiamine can drive AD-like abnormalities, including memory deficits, neuritic plaques, and hyperphosphorylation of tau.	Thiamine	31-39	microtubule associated protein tau	Homo sapiens	146-149
26863430-0	2016	Novel SLC19A3 Promoter Deletion and Allelic Silencing in Biotin-Thiamine-Responsive Basal Ganglia Encephalopathy.	Thiamine	64-72	solute carrier family 19 member 3	Homo sapiens	6-13
26863430-1	2016	BACKGROUND: Biotin-thiamine responsive basal ganglia disease is a severe, but potentially treatable disorder caused by mutations in the SLC19A3 gene.	Thiamine	19-27	solute carrier family 19 member 3	Homo sapiens	136-143
26657515-4	2016	Thiamine derivatives were analysed by high performance liquid chromatography in 106 whole blood and 38 cerebrospinal fluid samples from paediatric controls, 16 cerebrospinal fluid samples from patients with Leigh syndrome, six of whom harboured mutations in the SLC19A3 gene, and 49 patients with other neurological disorders.	Thiamine	0-8	solute carrier family 19 member 3	Homo sapiens	262-269
26549656-0	2016	Novel nonsense mutation (p.Ile411Metfs*12) in the SLC19A2 gene causing Thiamine Responsive Megaloblastic Anemia in an Indian patient.	Thiamine	71-79	solute carrier family 19 member 2	Homo sapiens	50-57
26549656-1	2016	Thiamine-responsive megaloblastic anemia (TRMA), an autosomal recessive disorder, is caused by mutations in SLC19A2 gene encodes a high affinity thiamine transporter (THTR-1).	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	42-46
26549656-1	2016	Thiamine-responsive megaloblastic anemia (TRMA), an autosomal recessive disorder, is caused by mutations in SLC19A2 gene encodes a high affinity thiamine transporter (THTR-1).	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	108-115
26549656-1	2016	Thiamine-responsive megaloblastic anemia (TRMA), an autosomal recessive disorder, is caused by mutations in SLC19A2 gene encodes a high affinity thiamine transporter (THTR-1).	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	167-173
26549656-5	2016	Thiamine transport activity by the clinical variant was severely inhibited than wild-type THTR-1.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	90-96
26657515-5	2016	Free-thiamine was remarkably reduced in the cerebrospinal fluid of five SLC19A3 patients before treatment.	Thiamine	5-13	solute carrier family 19 member 3	Homo sapiens	72-79
26657515-6	2016	In contrast, free-thiamine was slightly decreased in 15.2% of patients with other neurological conditions, and above the reference range in one SLC19A3 patient on thiamine supplementation.	Thiamine	18-26	solute carrier family 19 member 3	Homo sapiens	144-151
26657515-6	2016	In contrast, free-thiamine was slightly decreased in 15.2% of patients with other neurological conditions, and above the reference range in one SLC19A3 patient on thiamine supplementation.	Thiamine	163-171	solute carrier family 19 member 3	Homo sapiens	144-151
26657515-10	2016	In conclusion, we found a profound deficiency of free-thiamine in the CSF and fibroblasts of patients with thiamine transporter-2 deficiency.	Thiamine	54-62	solute carrier family 19 member 3	Homo sapiens	107-129
26528626-3	2015	Recently, our laboratory demonstrated that organic cation transporter 1, OCT1, the major hepatic uptake transporter for metformin, was also the primary hepatic uptake transporter for thiamine, vitamin B1.	Thiamine	183-191	solute carrier family 22 member 1	Homo sapiens	43-71
28214879-11	2016	Glucose tolerance was initially increased, suggesting augmented insulin sensitivity, as we had found in biotin deficiency; however, in the case of thiamine, it was diminished from the 3rd week on, when the deficient animals became undernourished, and paralleled the changes in AKT and mTOR, 2 main proteins in the insulin signaling pathway.	Thiamine	147-155	thymoma viral proto-oncogene 1	Mus musculus	277-280
28214879-11	2016	Glucose tolerance was initially increased, suggesting augmented insulin sensitivity, as we had found in biotin deficiency; however, in the case of thiamine, it was diminished from the 3rd week on, when the deficient animals became undernourished, and paralleled the changes in AKT and mTOR, 2 main proteins in the insulin signaling pathway.	Thiamine	147-155	mechanistic target of rapamycin kinase	Mus musculus	285-289
26955771-6	2016	We found that seven of them could bind to the protein NFkappaB (catechin, leucoanthocyanidin, niacin, phenylethylamine, theobromine, theophylline, and thiamin).	Thiamine	151-158	nuclear factor kappa B subunit 1	Homo sapiens	54-62
26528626-3	2015	Recently, our laboratory demonstrated that organic cation transporter 1, OCT1, the major hepatic uptake transporter for metformin, was also the primary hepatic uptake transporter for thiamine, vitamin B1.	Thiamine	193-203	solute carrier family 22 member 1	Homo sapiens	43-71
26528626-3	2015	Recently, our laboratory demonstrated that organic cation transporter 1, OCT1, the major hepatic uptake transporter for metformin, was also the primary hepatic uptake transporter for thiamine, vitamin B1.	Thiamine	193-203	solute carrier family 22 member 1	Homo sapiens	73-77
26528626-3	2015	Recently, our laboratory demonstrated that organic cation transporter 1, OCT1, the major hepatic uptake transporter for metformin, was also the primary hepatic uptake transporter for thiamine, vitamin B1.	Thiamine	183-191	solute carrier family 22 member 1	Homo sapiens	73-77
26633299-2	2015	Pancreatic acinar cells (PAC) obtain thiamin from the circulation using a specific carrier-mediated process mediated by both thiamin transporters -1 and -2 (THTR-1 and THTR-2; encoded by the SLC19A2 and SLC19A3 genes, respectively).	Thiamine	37-44	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	157-163
26528626-7	2015	Furthermore, metformin as well as other drugs including phenformin, chloroquine, verapamil, famotidine, and amprolium inhibited hTHTR-2 mediated uptake of both thiamine and metformin.	Thiamine	160-168	solute carrier family 19 member 3	Homo sapiens	128-135
26633299-2	2015	Pancreatic acinar cells (PAC) obtain thiamin from the circulation using a specific carrier-mediated process mediated by both thiamin transporters -1 and -2 (THTR-1 and THTR-2; encoded by the SLC19A2 and SLC19A3 genes, respectively).	Thiamine	37-44	solute carrier family 19, member 3	Mus musculus	168-174
26633299-2	2015	Pancreatic acinar cells (PAC) obtain thiamin from the circulation using a specific carrier-mediated process mediated by both thiamin transporters -1 and -2 (THTR-1 and THTR-2; encoded by the SLC19A2 and SLC19A3 genes, respectively).	Thiamine	37-44	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	191-198
26633299-2	2015	Pancreatic acinar cells (PAC) obtain thiamin from the circulation using a specific carrier-mediated process mediated by both thiamin transporters -1 and -2 (THTR-1 and THTR-2; encoded by the SLC19A2 and SLC19A3 genes, respectively).	Thiamine	37-44	solute carrier family 19, member 3	Mus musculus	203-210
26212886-4	2015	Malate dehydrogenase, glutamate dehydrogenase and pyridoxal kinase were identified as abundant proteins binding to thiamin- or thiazolium-modified sorbents.	Thiamine	115-122	malic enzyme 1	Homo sapiens	0-20
27164172-9	2015	The low-thiamine value group (&lt; 35.4 ng/ml; 26.8 +- 5.3 ng/ml) exhibited lower levels of serum aspartate aminotransferase and alanine aminotransferase than the high-thiamine value group (&gt;= 35.4 ng/ml; 73.5 +- 102.5 ng/ml) although there was no significance in nutritional marker, Alb, geriatric nutritional risk index , protein catabolic rate and creatinine generation rate.	Thiamine	8-16	glutamic--pyruvic transaminase	Homo sapiens	129-153
27164172-9	2015	The low-thiamine value group (&lt; 35.4 ng/ml; 26.8 +- 5.3 ng/ml) exhibited lower levels of serum aspartate aminotransferase and alanine aminotransferase than the high-thiamine value group (&gt;= 35.4 ng/ml; 73.5 +- 102.5 ng/ml) although there was no significance in nutritional marker, Alb, geriatric nutritional risk index , protein catabolic rate and creatinine generation rate.	Thiamine	8-16	albumin	Homo sapiens	287-290
26316591-2	2015	Cells obtain thiamin from their surroundings and enzymatically convert it into thiamin pyrophosphate (TPP) in the cytoplasm; TPP is then taken up by mitochondria via a specific carrier the mitochondrial TPP transporter (MTPPT; product of the SLC25A19 gene).	Thiamine	13-20	solute carrier family 25 (mitochondrial thiamine pyrophosphate carrier), member 19	Mus musculus	242-250
26324451-10	2015	IMPORTANCE: This work describes a metabolic link between the sugar-phosphate stress response and the yeast thiamine biosynthetic enzyme Thi5p when heterologously expressed in Salmonella enterica during growth on minimal glucose medium.	Thiamine	107-115	4-amino-5-hydroxymethyl-2-methylpyrimidine phosphate synthase	Saccharomyces cerevisiae S288C	136-141
25982678-0	2015	The impact of thiamine supplementation on blood pressure, serum lipids and C-reactive protein in individuals with hyperglycemia: a randomised, double-blind cross-over trial.	Thiamine	14-22	C-reactive protein	Homo sapiens	75-93
25982678-5	2015	RESULTS: DBP was significantly decreased in participants consuming thiamine supplements for six weeks (67.9 +- 5.8 mm Hg) relative to baseline (71.4 +- 7.4 mm Hg, p=0.005) and week 3 (70.9.	Thiamine	67-75	D-box binding PAR bZIP transcription factor	Homo sapiens	9-12
26722561-0	2015	Biochemical changes correlated with blood thiamine and its phosphate esters levels in patients with diabetes type 1 (DMT1).	Thiamine	42-50	doublesex and mab-3 related transcription factor 1	Homo sapiens	117-121
26722561-2	2015	However, little is known on the positive effects of thiamine in diabetic type 1 (DMT1) patients.	Thiamine	52-60	doublesex and mab-3 related transcription factor 1	Homo sapiens	81-85
26722561-3	2015	The objectives of this study were to evaluate the biochemical changes related to thiamine deficiency in patients with DMT1 outcomes among Saudi adults.	Thiamine	81-89	doublesex and mab-3 related transcription factor 1	Homo sapiens	118-122
26722561-4	2015	We hypothesized that blood thiamine deficiency in patients with DMT1 manifestations might lead to an increase in metabolic syndrome.	Thiamine	27-35	doublesex and mab-3 related transcription factor 1	Homo sapiens	64-68
26722561-12	2015	The results support a pivotal role of blood thiamine and its phosphate esters in preventing the biochemical changes and complications in patients with DMT1.	Thiamine	44-52	doublesex and mab-3 related transcription factor 1	Homo sapiens	151-155
26376452-10	2015	CONCLUSIONS: These findings support protective effects of thiamine and one-carbon metabolism vitamins (folate, riboflavin, and vitamin B6) against BC in general; while folate may also protect against ER+PR+ and HER2- disease; and thiamine against ER-PR-, and HER2+ disease.	Thiamine	58-66	erb-b2 receptor tyrosine kinase 2	Homo sapiens	211-215
26454882-9	2015	Total thiamin leaf content in THI1 plants was up approximately 2-fold compared with the wild type.	Thiamine	6-13	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	30-34
26454882-11	2015	Resulting THI1 x THIC plants accumulated up to 3.4- and 2.6-fold more total thiamin than wild-type plants in leaf and seeds, respectively.	Thiamine	76-83	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	10-14
26454882-11	2015	Resulting THI1 x THIC plants accumulated up to 3.4- and 2.6-fold more total thiamin than wild-type plants in leaf and seeds, respectively.	Thiamine	76-83	thiaminC	Arabidopsis thaliana	17-21
26212886-7	2015	Thiamin and ThDP regulate malate dehydrogenase isoforms and pyridoxal kinase.	Thiamine	0-7	malic enzyme 1	Homo sapiens	26-46
26157489-1	2015	BACKGROUND: The organic cation transporter OCT1 (SLC22A1) mediates the uptake of vitamin B1, cationic drugs, and xenobiotics into hepatocytes.	Thiamine	81-91	solute carrier family 22 member 1	Homo sapiens	43-47
25707023-0	2015	Thiamine responsive megaloblastic anemia syndrome: a novel homozygous SLC19A2 gene mutation identified.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	70-77
25707023-3	2015	TRMAS is a Mendelian disorder; a gene SLC19A2 coding high affinity thiamine transporter mediating vitamin B1 uptake through cell membrane has been identified.	Thiamine	67-75	solute carrier family 19 member 2	Homo sapiens	38-45
25707023-3	2015	TRMAS is a Mendelian disorder; a gene SLC19A2 coding high affinity thiamine transporter mediating vitamin B1 uptake through cell membrane has been identified.	Thiamine	98-108	solute carrier family 19 member 2	Homo sapiens	38-45
25117056-0	2015	Thiamine Deficiency-Mediated Brain Mitochondrial Pathology in Alaskan Huskies with Mutation in SLC19A3.1.	Thiamine	0-8	thiamine transporter 2	Canis lupus familiaris	95-102
25701312-1	2015	PURPOSE: To investigate the role of organic cation transporters (Octs) and multidrug and toxin extrusion protein 1 (Mate1) in the disposition of thiamine.	Thiamine	145-153	solute carrier family 47, member 1	Mus musculus	75-114
25701312-1	2015	PURPOSE: To investigate the role of organic cation transporters (Octs) and multidrug and toxin extrusion protein 1 (Mate1) in the disposition of thiamine.	Thiamine	145-153	solute carrier family 47, member 1	Mus musculus	116-121
25701312-6	2015	RESULTS: Thiamine is a substrate of Oct1 and Oct2, but not Oct3.	Thiamine	9-17	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	36-40
25701312-6	2015	RESULTS: Thiamine is a substrate of Oct1 and Oct2, but not Oct3.	Thiamine	9-17	POU domain, class 2, transcription factor 2	Mus musculus	45-49
25701312-7	2015	Oct1/2 defect caused a significant reduction in the uptake of [(3)H]thiamine by hepatocytes in vitro, and elevated the plasma thiamine concentration by 5.8-fold in vivo.	Thiamine	68-76	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	0-6
25701312-10	2015	The total thiamine and thiamine-d3 concentrations were moderately reduced in the intestine of Oct1/2(-/-) mice but were unchanged in the kidney, liver, or brain.	Thiamine	10-18	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	94-100
25701312-11	2015	The milk-to-plasma concentration ratio of thiamine was decreased by 28-fold in the Oct1/2(-/-) mice.	Thiamine	42-50	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	83-89
25701312-12	2015	CONCLUSIONS: Oct1 is possibly responsible for the plasma clearance of thiamine via tissue uptake and for milk secretion.	Thiamine	70-78	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	13-17
25701312-13	2015	Oct1/2 and Mate1 are involved in the renal tubular secretion of thiamine.	Thiamine	64-72	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	0-6
25701312-13	2015	Oct1/2 and Mate1 are involved in the renal tubular secretion of thiamine.	Thiamine	64-72	solute carrier family 47, member 1	Mus musculus	11-16
26157489-1	2015	BACKGROUND: The organic cation transporter OCT1 (SLC22A1) mediates the uptake of vitamin B1, cationic drugs, and xenobiotics into hepatocytes.	Thiamine	81-91	solute carrier family 22 member 1	Homo sapiens	49-56
25816395-3	2015	Thiamine administration was also reported to prevent deterioration in fasting glucose and insulin levels, and to improve glucose tolerance in hyperglycemic patients.	Thiamine	0-8	insulin	Homo sapiens	90-97
25849583-1	2015	Benfotiamine is a synthetic thiamine analogue that stimulates transketolase, a cellular enzyme essential for glucose metabolism.	Thiamine	28-36	transketolase	Homo sapiens	62-75
25645231-1	2015	A novel method was developed for spectral resolution and further determination of five-component mixture including Vitamin B complex (B1, B6, B12 and Benfotiamine) along with the commonly co-formulated Diclofenac.	Thiamine	115-124	immunoglobulin kappa variable 7-3 (pseudogene)	Homo sapiens	134-140
25788274-3	2015	Thiamine pyrophosphokinase-1 (TPK1), a key component of Vitamin B1/thiamine metabolism, was identified as a target for radiosensitization.	Thiamine	56-66	thiamin pyrophosphokinase 1	Homo sapiens	0-28
26122215-3	2015	Vitamin B1 influences pro-apoptotic proteins, mitochondrial membrane potential, cytochrome C release, protein kinases, p38-MAPK, suppresses oxidative stress-induced NF-kappaB and has anti-inflammatory properties.	Thiamine	0-10	mitogen-activated protein kinase 14	Homo sapiens	119-122
26122215-4	2015	Deficiency of vitamin B1 may cause beriberi, dysfunction of the nervous system, neuroinflammation, T cell infiltration, chemokine CCL2 activation, over expression of proinflammatory cytokines, such as IL-1, TNF, IL-6, and arachidonic acid products, and induces expression of CD40 by the microglia and CD40L by astrocytes which provoke the death of neurons.	Thiamine	14-24	C-C motif chemokine ligand 2	Homo sapiens	130-134
26122215-4	2015	Deficiency of vitamin B1 may cause beriberi, dysfunction of the nervous system, neuroinflammation, T cell infiltration, chemokine CCL2 activation, over expression of proinflammatory cytokines, such as IL-1, TNF, IL-6, and arachidonic acid products, and induces expression of CD40 by the microglia and CD40L by astrocytes which provoke the death of neurons.	Thiamine	14-24	interleukin 1 beta	Homo sapiens	201-205
26122215-4	2015	Deficiency of vitamin B1 may cause beriberi, dysfunction of the nervous system, neuroinflammation, T cell infiltration, chemokine CCL2 activation, over expression of proinflammatory cytokines, such as IL-1, TNF, IL-6, and arachidonic acid products, and induces expression of CD40 by the microglia and CD40L by astrocytes which provoke the death of neurons.	Thiamine	14-24	tumor necrosis factor	Homo sapiens	207-210
26122215-4	2015	Deficiency of vitamin B1 may cause beriberi, dysfunction of the nervous system, neuroinflammation, T cell infiltration, chemokine CCL2 activation, over expression of proinflammatory cytokines, such as IL-1, TNF, IL-6, and arachidonic acid products, and induces expression of CD40 by the microglia and CD40L by astrocytes which provoke the death of neurons.	Thiamine	14-24	interleukin 6	Homo sapiens	212-216
26122215-4	2015	Deficiency of vitamin B1 may cause beriberi, dysfunction of the nervous system, neuroinflammation, T cell infiltration, chemokine CCL2 activation, over expression of proinflammatory cytokines, such as IL-1, TNF, IL-6, and arachidonic acid products, and induces expression of CD40 by the microglia and CD40L by astrocytes which provoke the death of neurons.	Thiamine	14-24	CD40 molecule	Homo sapiens	275-279
26122215-4	2015	Deficiency of vitamin B1 may cause beriberi, dysfunction of the nervous system, neuroinflammation, T cell infiltration, chemokine CCL2 activation, over expression of proinflammatory cytokines, such as IL-1, TNF, IL-6, and arachidonic acid products, and induces expression of CD40 by the microglia and CD40L by astrocytes which provoke the death of neurons.	Thiamine	14-24	CD40 ligand	Homo sapiens	301-306
25383846-1	2015	BACKGROUND: To report ophthalmologic fundus autofluorescence and spectral domain optical coherence tomography findings in a patient with thiamine responsive megaloblastic anemia (TRMA).	Thiamine	137-145	solute carrier family 19 member 2	Homo sapiens	179-183
25788274-3	2015	Thiamine pyrophosphokinase-1 (TPK1), a key component of Vitamin B1/thiamine metabolism, was identified as a target for radiosensitization.	Thiamine	56-66	thiamin pyrophosphokinase 1	Homo sapiens	30-34
25788274-3	2015	Thiamine pyrophosphokinase-1 (TPK1), a key component of Vitamin B1/thiamine metabolism, was identified as a target for radiosensitization.	Thiamine	67-75	thiamin pyrophosphokinase 1	Homo sapiens	0-28
25788274-3	2015	Thiamine pyrophosphokinase-1 (TPK1), a key component of Vitamin B1/thiamine metabolism, was identified as a target for radiosensitization.	Thiamine	67-75	thiamin pyrophosphokinase 1	Homo sapiens	30-34
25788274-5	2015	Other means of blocking this pathway, knockdown of thiamine transporter-1 (THTR1) or treatment with the thiamine analogue pyrithiamine hydrobromide (PyrH) caused significant tumor specific radiosensitization.	Thiamine	51-59	solute carrier family 19 member 2	Homo sapiens	75-80
25670766-0	2015	Overexpression of plastid transketolase in tobacco results in a thiamine auxotrophic phenotype.	Thiamine	64-72	Transketolase	Arabidopsis thaliana	26-39
25526377-9	2015	Thiamine level was significantly associated with PDH quantity at all time points (P = 0.01).	Thiamine	0-8	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	49-52
25484137-0	2015	Bioinformatic and metabolomic analysis reveals miR-155 regulates thiamine level in breast cancer.	Thiamine	65-73	microRNA 155	Homo sapiens	47-54
25484137-2	2015	Thiamine, commonly known as vitamin B1, is one of critical cofactors for energy metabolic enzymes including pyruvate dehydrogenase, alpha ketoglutarate dehydrogenase, and transketolase.	Thiamine	0-8	transketolase	Homo sapiens	171-184
25484137-2	2015	Thiamine, commonly known as vitamin B1, is one of critical cofactors for energy metabolic enzymes including pyruvate dehydrogenase, alpha ketoglutarate dehydrogenase, and transketolase.	Thiamine	28-38	transketolase	Homo sapiens	171-184
25484137-3	2015	Here we report a novel role of miR-155 in cancer metabolism through the up-regulation of thiamine in breast cancer cells.	Thiamine	89-97	microRNA 155	Homo sapiens	31-38
25484137-4	2015	A bioinformatic analysis of miRNA array and metabolite-profiling data from NCI-60 cancer cell panel revealed thiamine as a metabolite positively correlated with the miR-155 expression level.	Thiamine	109-117	microRNA 155	Homo sapiens	165-172
25484137-5	2015	We confirmed it in MCF7, MDA-MB-436 and two human primary breast cancer cells by showing reduced thiamine levels upon a knock-down of miR-155.	Thiamine	97-105	microRNA 155	Homo sapiens	134-141
25484137-6	2015	To understand how the miR-155 controls thiamine level, a set of key molecules for thiamine homeostasis were further analyzed after the knockdown of miR-155.	Thiamine	39-47	microRNA 155	Homo sapiens	22-29
25484137-6	2015	To understand how the miR-155 controls thiamine level, a set of key molecules for thiamine homeostasis were further analyzed after the knockdown of miR-155.	Thiamine	82-90	microRNA 155	Homo sapiens	22-29
25484137-8	2015	Finally, we confirm the finding by showing a positive correlation between miR-155 and thiamine level in 71 triple negative breast tumors.	Thiamine	86-94	microRNA 155	Homo sapiens	74-81
25484137-9	2015	Taken altogether, our study demonstrates a role of miR-155 in thiamine homeostasis and suggests a function of this oncogenic miRNA on breast cancer metabolism.	Thiamine	62-70	microRNA 155	Homo sapiens	51-58
25670766-4	2015	These phenotypes were complemented by germinating the seeds of transketolase-overexpressing lines in media containing either thiamine pyrophosphate or thiamine.	Thiamine	125-133	Transketolase	Arabidopsis thaliana	63-76
25670766-5	2015	Thiamine levels in the seeds and cotyledons were lower in transketolase-overexpressing lines than in wild-type plants.	Thiamine	0-8	Transketolase	Arabidopsis thaliana	58-71
25670766-6	2015	When transketolase-overexpressing plants were supplemented with thiamine or thiamine pyrophosphate throughout the life cycle, they grew normally and the seed produced from these plants generated plants that did not have a growth or chlorotic phenotype.	Thiamine	64-72	Transketolase	Arabidopsis thaliana	5-18
25670766-8	2015	The mechanism determining transketolase protein levels remains to be elucidated, but the data presented provide evidence that this may contribute to the complex regulatory mechanisms maintaining thiamine homeostasis in plants.	Thiamine	195-203	Transketolase	Arabidopsis thaliana	26-39
25063874-0	2014	Thiamine deficiency promotes T cell infiltration in experimental autoimmune encephalomyelitis: the involvement of CCL2.	Thiamine	0-8	chemokine (C-C motif) ligand 2	Mus musculus	114-118
25590804-0	2015	PKR downregulation prevents neurodegeneration and beta-amyloid production in a thiamine-deficient model.	Thiamine	79-87	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	0-3
25878670-0	2015	A novel homozygous SLC19A2 mutation in a Portuguese patient with diabetes mellitus and thiamine-responsive megaloblastic anaemia.	Thiamine	87-95	solute carrier family 19 member 2	Homo sapiens	19-26
25878670-1	2015	Thiamine-responsive megaloblastic anaemia (TRMA) is a rare syndrome where patients present with early onset diabetes mellitus, megaloblastic anaemia and sensorineural deafness.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	43-47
24770900-0	2015	Mild thiamine deficiency and chronic ethanol consumption modulate acetylcholinesterase activity change and spatial memory performance in a water maze task.	Thiamine	5-13	acetylcholinesterase (Cartwright blood group)	Homo sapiens	66-86
24770900-2	2015	In the present work, the chronic effects of ethanol and its association to a mild thiamine deficiency episode (subclinical model) on neocortical and hippocampal acetylcholinesterase activity were assessed along with their possible association to spatial cognitive dysfunction.	Thiamine	82-90	acetylcholinesterase (Cartwright blood group)	Homo sapiens	161-181
24770900-3	2015	The results indicate that in the beginning of the neurodegenerative process, before the appearance of brain lesions, chronic ethanol consumption reverses the effects of mild thiamine deficiency on both spatial cognitive performance and acetylcholinesterase activity without having significant effects on any morphometric parameter.	Thiamine	174-182	acetylcholinesterase (Cartwright blood group)	Homo sapiens	236-256
26875494-1	2015	Glycine oxidase, encoded by the thiO gene, participates in the biosynthesis of thiamin by providing glyoxyl imine to form the thiazole moiety of thiamin.	Thiamine	79-86	glycine oxidase ThiO	Pseudomonas putida KT2440	32-36
26875494-1	2015	Glycine oxidase, encoded by the thiO gene, participates in the biosynthesis of thiamin by providing glyoxyl imine to form the thiazole moiety of thiamin.	Thiamine	145-152	glycine oxidase ThiO	Pseudomonas putida KT2440	32-36
25267444-8	2014	The observation of covalent enzymatic intermediates in hyperreactive conformations such as Schiff-bases with twisted double-bond linkages in transaldolase and physically distorted substrate-thiamin conjugates with elongated substrate bonds to be cleaved in transketolase, which probably epitomize a canonical feature of enzyme catalysis, will be also highlighted.	Thiamine	190-197	transketolase	Homo sapiens	257-270
25381355-0	2014	Response to Comment on "Thiamine deficiency promotes T cell infiltration in experimental autoimmune encephalomyelitis: the involvement of CCL2".	Thiamine	24-32	C-C motif chemokine ligand 2	Homo sapiens	138-142
25348237-0	2014	Conserved active site cysteine residue of archaeal THI4 homolog is essential for thiamine biosynthesis in Haloferax volcanii.	Thiamine	81-89	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	51-55
25348237-6	2014	Usage of the eukaryotic THI4-type sulfur relay was initially considered less likely for thiamine biosynthesis in archaea, since the active-site cysteine residue of yeast THI4p that donates the sulfur to the thiazole ring by a suicide mechanism is replaced by a histidine residue in many archaeal THI4 homologs and these are described as D-ribose-1,5-bisphosphate isomerases.	Thiamine	88-96	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	24-28
25348237-6	2014	Usage of the eukaryotic THI4-type sulfur relay was initially considered less likely for thiamine biosynthesis in archaea, since the active-site cysteine residue of yeast THI4p that donates the sulfur to the thiazole ring by a suicide mechanism is replaced by a histidine residue in many archaeal THI4 homologs and these are described as D-ribose-1,5-bisphosphate isomerases.	Thiamine	88-96	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	170-175
25348237-6	2014	Usage of the eukaryotic THI4-type sulfur relay was initially considered less likely for thiamine biosynthesis in archaea, since the active-site cysteine residue of yeast THI4p that donates the sulfur to the thiazole ring by a suicide mechanism is replaced by a histidine residue in many archaeal THI4 homologs and these are described as D-ribose-1,5-bisphosphate isomerases.	Thiamine	88-96	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	170-174
25348237-11	2014	volcanii uses a yeast THI4-type mechanism for sulfur relay to form the thiazole ring of thiamine.	Thiamine	88-96	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	22-26
25348237-12	2014	We extend this finding to a relatively large group of archaea, including haloarchaea, ammonium oxidizing archaea, and some methanogen and Pyrococcus species, by observing that these organisms code for THI4 homologs that have a conserved active site cysteine residue which is likely used in thiamine biosynthesis.	Thiamine	290-298	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	201-205
25348237-13	2014	Thus, archaeal members of IPR002922 THI4 family that have a conserved cysteine active site should be reexamined for a function in thiamine biosynthesis.	Thiamine	130-138	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	36-40
25063672-0	2014	The Janus kinase 2 inhibitor fedratinib inhibits thiamine uptake: a putative mechanism for the onset of Wernicke"s encephalopathy.	Thiamine	49-57	Janus kinase 2	Homo sapiens	4-18
25560422-12	2015	After 8 hours of insulin therapy, seven of 20 patients (35%) had thiamine deficiency, and four of these seven patients also had thiamine deficiency at presentation.	Thiamine	65-73	insulin	Homo sapiens	17-24
25560422-12	2015	After 8 hours of insulin therapy, seven of 20 patients (35%) had thiamine deficiency, and four of these seven patients also had thiamine deficiency at presentation.	Thiamine	128-136	insulin	Homo sapiens	17-24
25560422-13	2015	Sixty-eight percent of patients had a decrease in thiamine levels after 8 hours of insulin therapy, with a mean fall of 20 +- 31.4 nmol/L.	Thiamine	50-58	insulin	Homo sapiens	83-90
25994133-0	2015	Impact of exercise and vitamin B1 intake on hippocampal brain-derived neurotrophic factor and spatial memory performance in a rat model of stress.	Thiamine	23-33	brain-derived neurotrophic factor	Rattus norvegicus	56-89
25994133-7	2015	However, either swimming training or thiamine intake for 30 d was proved to induce a significant increase both in BDNF and Ach in conjunction with improved performance in the T maze, marked anxiolytic effect and enhanced ambulation in the open field test, as compared to the stress group.	Thiamine	37-45	brain-derived neurotrophic factor	Rattus norvegicus	114-118
25994133-9	2015	It was concluded that decreased BDNF and Ach after stress exposure could be a mechanism for the deleterious actions of stress on memory function; swimming exercise or vitamin B1 supplementation for 30 d was a protective tool to improve coping with chronic stress by modulating BDNF and Ach content along with enhancement of memory functions and motor activities.	Thiamine	167-177	brain-derived neurotrophic factor	Rattus norvegicus	277-281
25494835-4	2014	Thiamine biosynthesis is regulated in response to thiamine availability and is coordinated by the thiamine sensor Thi3p, which activates Pdc2p and Thi2p.	Thiamine	0-8	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	114-119
25494835-4	2014	Thiamine biosynthesis is regulated in response to thiamine availability and is coordinated by the thiamine sensor Thi3p, which activates Pdc2p and Thi2p.	Thiamine	0-8	Pdc2p	Saccharomyces cerevisiae S288C	137-142
25494835-4	2014	Thiamine biosynthesis is regulated in response to thiamine availability and is coordinated by the thiamine sensor Thi3p, which activates Pdc2p and Thi2p.	Thiamine	0-8	Thi2p	Saccharomyces cerevisiae S288C	147-152
25494835-4	2014	Thiamine biosynthesis is regulated in response to thiamine availability and is coordinated by the thiamine sensor Thi3p, which activates Pdc2p and Thi2p.	Thiamine	50-58	Pdc2p	Saccharomyces cerevisiae S288C	137-142
25494835-4	2014	Thiamine biosynthesis is regulated in response to thiamine availability and is coordinated by the thiamine sensor Thi3p, which activates Pdc2p and Thi2p.	Thiamine	98-106	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	114-119
25494835-4	2014	Thiamine biosynthesis is regulated in response to thiamine availability and is coordinated by the thiamine sensor Thi3p, which activates Pdc2p and Thi2p.	Thiamine	98-106	Pdc2p	Saccharomyces cerevisiae S288C	137-142
25494835-4	2014	Thiamine biosynthesis is regulated in response to thiamine availability and is coordinated by the thiamine sensor Thi3p, which activates Pdc2p and Thi2p.	Thiamine	98-106	Thi2p	Saccharomyces cerevisiae S288C	147-152
25494835-5	2014	We used a genetic approach to identify quantitative trait loci (QTLs) in wine yeast and we discovered that a set of thiamine genes displayed expression-QTL on a common locus, which contains the thiamine regulator THI3.	Thiamine	116-124	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	213-217
25494835-5	2014	We used a genetic approach to identify quantitative trait loci (QTLs) in wine yeast and we discovered that a set of thiamine genes displayed expression-QTL on a common locus, which contains the thiamine regulator THI3.	Thiamine	194-202	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	213-217
25494835-7	2014	We showed that alteration of THI3 results in reduced expression of the genes involved in thiamine biosynthesis (THI11/12/13 and THI74) and increased expression of the pyruvate decarboxylase gene PDC1.	Thiamine	89-97	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	29-33
25494835-7	2014	We showed that alteration of THI3 results in reduced expression of the genes involved in thiamine biosynthesis (THI11/12/13 and THI74) and increased expression of the pyruvate decarboxylase gene PDC1.	Thiamine	89-97	4-amino-5-hydroxymethyl-2-methylpyrimidine phosphate synthase	Saccharomyces cerevisiae S288C	112-117
25494835-12	2014	CONCLUSIONS: This highlights a switch from PDC1 to PDC5 gene expression during thiamine deficiency, which may improve the thiamine affinity or conservation during the enzymatic reaction.	Thiamine	79-87	indolepyruvate decarboxylase 1	Saccharomyces cerevisiae S288C	43-47
25494835-12	2014	CONCLUSIONS: This highlights a switch from PDC1 to PDC5 gene expression during thiamine deficiency, which may improve the thiamine affinity or conservation during the enzymatic reaction.	Thiamine	79-87	indolepyruvate decarboxylase 5	Saccharomyces cerevisiae S288C	51-55
25494835-12	2014	CONCLUSIONS: This highlights a switch from PDC1 to PDC5 gene expression during thiamine deficiency, which may improve the thiamine affinity or conservation during the enzymatic reaction.	Thiamine	122-130	indolepyruvate decarboxylase 1	Saccharomyces cerevisiae S288C	43-47
25494835-12	2014	CONCLUSIONS: This highlights a switch from PDC1 to PDC5 gene expression during thiamine deficiency, which may improve the thiamine affinity or conservation during the enzymatic reaction.	Thiamine	122-130	indolepyruvate decarboxylase 5	Saccharomyces cerevisiae S288C	51-55
25494835-13	2014	In addition, we observed that the lab allele of THI3 and of the thiamin transporter THI7 have diverged from the original alleles, consistent with an adaptation of lab strains to rich media containing an excess of thiamine.	Thiamine	213-221	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	48-52
25494835-13	2014	In addition, we observed that the lab allele of THI3 and of the thiamin transporter THI7 have diverged from the original alleles, consistent with an adaptation of lab strains to rich media containing an excess of thiamine.	Thiamine	213-221	thiamine transporter THI7	Saccharomyces cerevisiae S288C	84-88
25063874-4	2014	We have previously shown that thiamine deficiency (TD) induced CCL2 in neurons.	Thiamine	30-38	chemokine (C-C motif) ligand 2	Mus musculus	63-67
25027701-1	2014	BACKGROUND: In a recent study one third of Lao patients presenting with uncomplicated Plasmodium falciparum malaria had biochemical evidence of thiamin deficiency, which was associated with a higher incidence of adverse events.	Thiamine	144-151	interleukin 4 induced 1	Homo sapiens	43-46
27896110-0	2014	Whole exome sequencing reveals compound heterozygous mutations in SLC19A3 causing biotin-thiamine responsive basal ganglia disease.	Thiamine	89-97	solute carrier family 19 member 3	Homo sapiens	66-73
27896110-1	2014	Biotin-thiamine responsive basal ganglia disease (BTBGD) is a rare metabolic condition caused by mutations in the SLC19A3 gene.	Thiamine	7-15	solute carrier family 19 member 3	Homo sapiens	114-121
24452856-6	2014	Furthermore, gene expression under the control of the eno or gpd promoter was not repressed by the components of YES medium while nmt1 promoter was inhibited by thiamine in yeast extract.	Thiamine	161-169	glycylpeptide N-tetradecanoyltransferase NMT1	Saccharomyces cerevisiae S288C	130-134
24961373-5	2014	Metabolomic and isotopic uptake methods identified thiamine as a principal endogenous substrate of OCT1.	Thiamine	51-59	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	99-103
24737227-4	2014	The increase in modified Y2O3:Eu NPs fluorescence signal as a function of thiamine concentration was found to be linear in the concentration range of 0-44 muM.	Thiamine	74-82	latexin	Homo sapiens	155-158
24737227-5	2014	The limit of detection (LOD) of thiamine by this method was 0.144 muM.	Thiamine	32-40	latexin	Homo sapiens	66-69
24957181-2	2014	METHODS: We report the clinical follow-up after thiamine and biotin supplementation in four children with ThTR2 deficiency presenting with Leigh and biotin-thiamine-responsive basal ganglia disease phenotypes.	Thiamine	48-56	solute carrier family 19 member 3	Homo sapiens	106-111
24957181-2	2014	METHODS: We report the clinical follow-up after thiamine and biotin supplementation in four children with ThTR2 deficiency presenting with Leigh and biotin-thiamine-responsive basal ganglia disease phenotypes.	Thiamine	156-164	solute carrier family 19 member 3	Homo sapiens	106-111
24637331-0	2014	THI1, a protein involved in the biosynthesis of thiamin in Arabidopsis thaliana: structural analysis of THI1(A140V) mutant.	Thiamine	48-55	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	0-4
24637331-0	2014	THI1, a protein involved in the biosynthesis of thiamin in Arabidopsis thaliana: structural analysis of THI1(A140V) mutant.	Thiamine	48-55	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	104-108
24637331-3	2014	Here, we investigated THI1 and its mutant THI1(A140V), responsible for the thiamin auxotrophy in a A. thaliana mutant line, aiming to clarify the impact of this mutation in the stability and activity of THI1.	Thiamine	75-82	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	22-26
24637331-3	2014	Here, we investigated THI1 and its mutant THI1(A140V), responsible for the thiamin auxotrophy in a A. thaliana mutant line, aiming to clarify the impact of this mutation in the stability and activity of THI1.	Thiamine	75-82	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	42-46
24637331-3	2014	Here, we investigated THI1 and its mutant THI1(A140V), responsible for the thiamin auxotrophy in a A. thaliana mutant line, aiming to clarify the impact of this mutation in the stability and activity of THI1.	Thiamine	75-82	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	42-46
24637331-4	2014	Recently, the THI1 orthologue (THI4) was revealed to be responsible for the donation of the sulfur atom from a cysteine residue to the thiazole ring in the thiamine intermediate.	Thiamine	156-164	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	14-18
24637331-4	2014	Recently, the THI1 orthologue (THI4) was revealed to be responsible for the donation of the sulfur atom from a cysteine residue to the thiazole ring in the thiamine intermediate.	Thiamine	156-164	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	31-35
24637331-9	2014	Hence, despite keeping its function in the early steps during the synthesis of TPP precursor, our studies have shown a decrease in the THI1(A140V) stability, which might be slowing down the biological activity of the mutant, and thus contributing to thiamin auxotrophy.	Thiamine	250-257	thiazole biosynthetic enzyme, chloroplast (ARA6) (THI1) (THI4)	Arabidopsis thaliana	135-139
24961373-7	2014	Metformin and the biguanide analog, phenformin, competitively inhibited OCT1-mediated thiamine uptake.	Thiamine	86-94	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	72-76
24961373-10	2014	The studies implicate OCT1 as well as metformin in thiamine disposition, suggesting an intriguing and parallel mechanism for metformin and its major hepatic transporter in metabolic function.	Thiamine	51-59	solute carrier family 22 (organic cation transporter), member 1	Mus musculus	22-26
24789339-3	2014	Thiamine is transported into cells by two carriers, THTR1 and THTR2, and deficiency of these results in thiamine-responsive megaloblastic anaemia and biotin-responsive basal ganglia disease respectively.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	52-57
24789339-3	2014	Thiamine is transported into cells by two carriers, THTR1 and THTR2, and deficiency of these results in thiamine-responsive megaloblastic anaemia and biotin-responsive basal ganglia disease respectively.	Thiamine	0-8	solute carrier family 19 member 3	Homo sapiens	62-67
24789339-3	2014	Thiamine is transported into cells by two carriers, THTR1 and THTR2, and deficiency of these results in thiamine-responsive megaloblastic anaemia and biotin-responsive basal ganglia disease respectively.	Thiamine	104-112	solute carrier family 19 member 3	Homo sapiens	62-67
23638917-1	2014	BACKGROUND: Thiamine responsive megaloblastic anemia syndrome (TRMA), an autosomal recessive disorder is caused by mutations in the SLC19A2 gene which encodes for thiamine transporter 1 (THTR1) protein.	Thiamine	12-20	solute carrier family 19 member 2	Homo sapiens	63-67
23638917-1	2014	BACKGROUND: Thiamine responsive megaloblastic anemia syndrome (TRMA), an autosomal recessive disorder is caused by mutations in the SLC19A2 gene which encodes for thiamine transporter 1 (THTR1) protein.	Thiamine	12-20	solute carrier family 19 member 2	Homo sapiens	132-139
23638917-1	2014	BACKGROUND: Thiamine responsive megaloblastic anemia syndrome (TRMA), an autosomal recessive disorder is caused by mutations in the SLC19A2 gene which encodes for thiamine transporter 1 (THTR1) protein.	Thiamine	12-20	solute carrier family 19 member 2	Homo sapiens	163-185
23638917-1	2014	BACKGROUND: Thiamine responsive megaloblastic anemia syndrome (TRMA), an autosomal recessive disorder is caused by mutations in the SLC19A2 gene which encodes for thiamine transporter 1 (THTR1) protein.	Thiamine	12-20	solute carrier family 19 member 2	Homo sapiens	187-192
24760553-7	2014	The approach used to analyze genetic association with the SAM/SAH metabolites is called middle-out: SNPs in 275 genes involved in the one-carbon pathway (folate, pyridoxal/pyridoxine, thiamin) or were correlated with SAM/SAH (vitamin A, E, Hcy) were analyzed instead of the entire 1M SNP data set.	Thiamine	184-191	acyl-CoA synthetase medium chain family member 3	Homo sapiens	58-65
24525018-1	2014	Pancreatic acinar cells (PAC) obtain thiamin from the circulation via a carrier-mediated process that involves thiamin transporters 1 and 2 (THTR-1 and THTR-2; products of SLC19A2 and SLC19A3, respectively).	Thiamine	37-44	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	141-147
24509276-8	2014	Sequence homology to a putative yeast thiamine (vitamin B1) transporter prompted us to express human SLC35F3 in Escherichia coli, which catalyzed [(3)H]-thiamine uptake.	Thiamine	38-46	solute carrier family 35 member F3	Homo sapiens	101-108
24509276-8	2014	Sequence homology to a putative yeast thiamine (vitamin B1) transporter prompted us to express human SLC35F3 in Escherichia coli, which catalyzed [(3)H]-thiamine uptake.	Thiamine	153-161	solute carrier family 35 member F3	Homo sapiens	101-108
24509276-9	2014	SLC35F3 risk-allele homozygotes (T/T) displayed decreased erythrocyte thiamine content on microbiological assay.	Thiamine	70-78	solute carrier family 35 member F3	Homo sapiens	0-7
24509276-10	2014	In twin pairs, the SLC35F3 risk allele predicted heritable cardiovascular traits previously associated with thiamine deficiency, including elevated cardiac stroke volume with decreased vascular resistance, and elevated pressor responses to environmental (cold) stress.	Thiamine	108-116	solute carrier family 35 member F3	Homo sapiens	19-26
24525018-1	2014	Pancreatic acinar cells (PAC) obtain thiamin from the circulation via a carrier-mediated process that involves thiamin transporters 1 and 2 (THTR-1 and THTR-2; products of SLC19A2 and SLC19A3, respectively).	Thiamine	37-44	solute carrier family 19, member 3	Mus musculus	152-158
24525018-1	2014	Pancreatic acinar cells (PAC) obtain thiamin from the circulation via a carrier-mediated process that involves thiamin transporters 1 and 2 (THTR-1 and THTR-2; products of SLC19A2 and SLC19A3, respectively).	Thiamine	37-44	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	172-179
24355766-0	2014	Identification of four SLC19A2 mutations in four Chinese thiamine responsive megaloblastic anemia patients without diabetes.	Thiamine	57-65	solute carrier family 19 member 2	Homo sapiens	23-30
24525018-1	2014	Pancreatic acinar cells (PAC) obtain thiamin from the circulation via a carrier-mediated process that involves thiamin transporters 1 and 2 (THTR-1 and THTR-2; products of SLC19A2 and SLC19A3, respectively).	Thiamine	37-44	solute carrier family 19, member 3	Mus musculus	184-191
24525018-7	2014	Chronic alcohol exposure of PAC also led to a significant reduction in the expression of the SP1 transcription factor, which upon correction (via expression) led to the prevention of alcohol inhibitory effects on not only the activity of SLC19A2 and SLC19A3 promoters but also on the expression of THTR-1 and -2 mRNA and thiamin uptake.	Thiamine	321-328	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	238-245
24525018-8	2014	These results demonstrate that the inhibitory effect of chronic alcohol exposure on physiological/molecular parameters of thiamin uptake by PAC is mediated via specific cis-regulatory elements in SLC19A2 and SLC19A3 minimal promoters.	Thiamine	122-129	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	196-203
24525018-8	2014	These results demonstrate that the inhibitory effect of chronic alcohol exposure on physiological/molecular parameters of thiamin uptake by PAC is mediated via specific cis-regulatory elements in SLC19A2 and SLC19A3 minimal promoters.	Thiamine	122-129	solute carrier family 19, member 3	Mus musculus	208-215
24372704-0	2014	Stress-induced upregulation of SLC19A3 is impaired in biotin-thiamine-responsive basal ganglia disease.	Thiamine	61-69	solute carrier family 19 member 3	Homo sapiens	31-38
24372704-1	2014	Biotin-thiamine-responsive basal ganglia disease (BTBGD) is a potentially treatable disorder caused by mutations in the SLC19A3 gene, encoding the human thiamine transporter 2.	Thiamine	7-15	solute carrier family 19 member 3	Homo sapiens	120-127
24372704-1	2014	Biotin-thiamine-responsive basal ganglia disease (BTBGD) is a potentially treatable disorder caused by mutations in the SLC19A3 gene, encoding the human thiamine transporter 2.	Thiamine	7-15	solute carrier family 19 member 3	Homo sapiens	153-175
24607307-2	2014	We analyzed for the first time, the role of all known mutations within three specific thiamine carrier genes, SLC19 A2, SLC19 A3, and SLC25 A19, in a patient with atrophic beriberi, a multiorgan nutritional disease caused by thiamine deficiency.	Thiamine	86-94	solute carrier family 19 member 2	Homo sapiens	110-118
24607307-2	2014	We analyzed for the first time, the role of all known mutations within three specific thiamine carrier genes, SLC19 A2, SLC19 A3, and SLC25 A19, in a patient with atrophic beriberi, a multiorgan nutritional disease caused by thiamine deficiency.	Thiamine	86-94	solute carrier family 19 member 3	Homo sapiens	120-128
24607307-2	2014	We analyzed for the first time, the role of all known mutations within three specific thiamine carrier genes, SLC19 A2, SLC19 A3, and SLC25 A19, in a patient with atrophic beriberi, a multiorgan nutritional disease caused by thiamine deficiency.	Thiamine	86-94	solute carrier family 25 member 19	Homo sapiens	134-143
24607307-2	2014	We analyzed for the first time, the role of all known mutations within three specific thiamine carrier genes, SLC19 A2, SLC19 A3, and SLC25 A19, in a patient with atrophic beriberi, a multiorgan nutritional disease caused by thiamine deficiency.	Thiamine	225-233	solute carrier family 19 member 2	Homo sapiens	110-118
24607307-2	2014	We analyzed for the first time, the role of all known mutations within three specific thiamine carrier genes, SLC19 A2, SLC19 A3, and SLC25 A19, in a patient with atrophic beriberi, a multiorgan nutritional disease caused by thiamine deficiency.	Thiamine	225-233	solute carrier family 25 member 19	Homo sapiens	134-143
24452394-3	2014	Recent focuses on metabolic targets for cancer therapy have exploited the altered regulation of the thiamine-dependent enzyme pyruvate dehydrogenase (PDH).	Thiamine	100-108	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	126-148
24282057-1	2014	BACKGROUND: The human thiamine transporter-2 (hTHTR-2) is involved in the intestinal absorption of thiamine.	Thiamine	22-30	solute carrier family 19 member 3	Homo sapiens	46-53
24282057-10	2014	Co-expression of hTHTR-2 with TM4SF4 in HuTu-80 cells led to a significant induction in thiamine uptake.	Thiamine	88-96	solute carrier family 19 member 3	Homo sapiens	17-24
24282057-10	2014	Co-expression of hTHTR-2 with TM4SF4 in HuTu-80 cells led to a significant induction in thiamine uptake.	Thiamine	88-96	transmembrane 4 superfamily member 4	Mus musculus	30-36
24282057-11	2014	In contrast, silencing TM4SF4 with gene-specific siRNA led to a significant decrease in thiamine uptake.	Thiamine	88-96	transmembrane 4 L six family member 4	Homo sapiens	23-29
24452394-3	2014	Recent focuses on metabolic targets for cancer therapy have exploited the altered regulation of the thiamine-dependent enzyme pyruvate dehydrogenase (PDH).	Thiamine	100-108	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	150-153
24452394-6	2014	Recently, it has been shown that the thiamine coenzyme, thiamine pyrophosphate reduces PDK-mediated phosphorylation of PDH.	Thiamine	37-45	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	119-122
24452394-9	2014	Comparative effects of high-dose thiamine and DCA on PDH phosphorylation were measured by Western blot.	Thiamine	33-41	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	53-56
24452394-13	2014	Both thiamine and DCA reduced the extent of PDH phosphorylation, reduced glucose consumption, lactate production, and mitochondrial membrane potential.	Thiamine	5-13	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	44-47
24452394-14	2014	High-dose thiamine and DCA did not increase ROS, but increased caspase-3 activity.	Thiamine	10-18	caspase 3	Homo sapiens	63-72
24133060-6	2013	The inhibition in thiamin uptake by ETEC was associated with a significant reduction in expression of human thiamin transporter-1 and -2 (hTHTR1 and hTHTR2) at the protein and mRNA levels as well as in the activity of the SLC19A2 and SLC19A3 promoters.	Thiamine	18-25	solute carrier family 19 member 2	Homo sapiens	138-144
24096332-3	2014	Using a thiamine-repressible promoter (pthiA), we showed that genetic repression of Hsp90 significantly reduced virulence in a murine model of invasive aspergillosis.	Thiamine	8-16	heat shock protein, 3	Mus musculus	84-89
24454921-11	2014	Thus, these studies demonstrate that acute intracellular thiamine depletion by recombinant thiaminase results in metabolic changes in thiamine-dependent metabolism, and demonstrate a previously unrecognized role of mTOR signaling in the regulation of thiamine-dependent metabolism.	Thiamine	57-65	mechanistic target of rapamycin kinase	Homo sapiens	215-219
24454921-11	2014	Thus, these studies demonstrate that acute intracellular thiamine depletion by recombinant thiaminase results in metabolic changes in thiamine-dependent metabolism, and demonstrate a previously unrecognized role of mTOR signaling in the regulation of thiamine-dependent metabolism.	Thiamine	134-142	mechanistic target of rapamycin kinase	Homo sapiens	215-219
24454921-11	2014	Thus, these studies demonstrate that acute intracellular thiamine depletion by recombinant thiaminase results in metabolic changes in thiamine-dependent metabolism, and demonstrate a previously unrecognized role of mTOR signaling in the regulation of thiamine-dependent metabolism.	Thiamine	134-142	mechanistic target of rapamycin kinase	Homo sapiens	215-219
25028661-0	2014	Downregulation of transketolase activity is related to inhibition of hippocampal progenitor cell proliferation induced by thiamine deficiency.	Thiamine	122-130	transketolase	Homo sapiens	18-31
25028661-1	2014	In animal experiments, hippocampal neurogenesis and the activity of thiamine-dependent transketolase decrease markedly under conditions of thiamine deficiency.	Thiamine	68-76	transketolase	Homo sapiens	87-100
25028661-5	2014	Taken together, our results suggest that modulation of transketolase activity might be one of the mechanisms by which thiamine regulates the proliferation of hippocampal progenitor cells.	Thiamine	118-126	transketolase	Homo sapiens	55-68
24597996-4	2014	A two-sample t test estimated the association between frusemide use and thiamin concentration and regression between thiamin concentration and EGFR.	Thiamine	117-124	epidermal growth factor receptor	Homo sapiens	143-147
24597996-6	2014	There was a weak linear relationship between thiamin concentration and EGFR, with thiamin concentration being 17.0 nmol/L lower per 30 ml/min greater EGFR, P=0.076.	Thiamine	82-89	epidermal growth factor receptor	Homo sapiens	150-154
23907530-9	2014	The specific uptake of thiamine was observed in MATE1-, MATE2-K- or OCT2-expressing HEK293 cells with Km of 3.5 +- 1.0, 3.9 +- 0.8 and 59.9 +- 6.7 muM, respectively.	Thiamine	23-31	solute carrier family 47 member 1	Homo sapiens	48-53
23907530-9	2014	The specific uptake of thiamine was observed in MATE1-, MATE2-K- or OCT2-expressing HEK293 cells with Km of 3.5 +- 1.0, 3.9 +- 0.8 and 59.9 +- 6.7 muM, respectively.	Thiamine	23-31	solute carrier family 47 member 2	Homo sapiens	56-63
23907530-9	2014	The specific uptake of thiamine was observed in MATE1-, MATE2-K- or OCT2-expressing HEK293 cells with Km of 3.5 +- 1.0, 3.9 +- 0.8 and 59.9 +- 6.7 muM, respectively.	Thiamine	23-31	POU class 2 homeobox 2	Homo sapiens	68-72
23907530-9	2014	The specific uptake of thiamine was observed in MATE1-, MATE2-K- or OCT2-expressing HEK293 cells with Km of 3.5 +- 1.0, 3.9 +- 0.8 and 59.9 +- 6.7 muM, respectively.	Thiamine	23-31	latexin	Homo sapiens	147-150
24376884-10	2013	For CHO cells stably expressing wild-type alphaIIbbeta3 that is an inactive form, overexpression of a talin head domain (THD) induced alphaIIbbeta3 activation and the THD-induced alphaIIbbeta3 activation was impaired by ILK siRNA through a significant reduction in the expression of the IPP complex.	Thiamine	121-124	integrin-linked protein kinase	Cricetulus griseus	220-223
24133060-6	2013	The inhibition in thiamin uptake by ETEC was associated with a significant reduction in expression of human thiamin transporter-1 and -2 (hTHTR1 and hTHTR2) at the protein and mRNA levels as well as in the activity of the SLC19A2 and SLC19A3 promoters.	Thiamine	18-25	solute carrier family 19 member 3	Homo sapiens	149-155
24133060-6	2013	The inhibition in thiamin uptake by ETEC was associated with a significant reduction in expression of human thiamin transporter-1 and -2 (hTHTR1 and hTHTR2) at the protein and mRNA levels as well as in the activity of the SLC19A2 and SLC19A3 promoters.	Thiamine	18-25	solute carrier family 19 member 2	Homo sapiens	222-229
24133060-6	2013	The inhibition in thiamin uptake by ETEC was associated with a significant reduction in expression of human thiamin transporter-1 and -2 (hTHTR1 and hTHTR2) at the protein and mRNA levels as well as in the activity of the SLC19A2 and SLC19A3 promoters.	Thiamine	18-25	solute carrier family 19 member 3	Homo sapiens	234-241
24244374-2	2013	These cells take up thiamin via specific carrier-mediated process that involves thiamin transporter-1 and -2 (THTR-1 and THTR-2; products of SLC19A2 and SLC19A3 genes, respectively).	Thiamine	20-27	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	110-116
24244374-2	2013	These cells take up thiamin via specific carrier-mediated process that involves thiamin transporter-1 and -2 (THTR-1 and THTR-2; products of SLC19A2 and SLC19A3 genes, respectively).	Thiamine	20-27	solute carrier family 19, member 3	Mus musculus	121-127
24244374-2	2013	These cells take up thiamin via specific carrier-mediated process that involves thiamin transporter-1 and -2 (THTR-1 and THTR-2; products of SLC19A2 and SLC19A3 genes, respectively).	Thiamine	20-27	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	141-148
24244374-2	2013	These cells take up thiamin via specific carrier-mediated process that involves thiamin transporter-1 and -2 (THTR-1 and THTR-2; products of SLC19A2 and SLC19A3 genes, respectively).	Thiamine	20-27	solute carrier family 19, member 3	Mus musculus	153-160
24244374-6	2013	Similarly chronic exposure of mice to NNK (IP 10 mg/100 g body weight, three times/week for 2 weeks) leads to a significant inhibition in thiamin uptake by freshly isolated pancreatic acinar cells, as well as in the level of expression of THTR-1 and -2 protein and mRNA.	Thiamine	138-145	chemokine (C-X-C motif) ligand 10	Mus musculus	43-48
24968580-7	2013	The activities of AST, ALT, GGT, scavenging enzymes as well as markers of inflammation and fibrosis in serum, liver and brain were reversed to a certain extent by thiamine.	Thiamine	163-171	gamma-glutamyltransferase 1	Rattus norvegicus	28-31
23989004-6	2013	By means of mutational analysis, a key role for a stimulating protein-1 (SP1)/guanosine cytidine box in mediating the effect of extracellular thiamine level on SLC19A3 promoter was established.	Thiamine	142-150	Sp1 transcription factor	Homo sapiens	50-71
23989004-6	2013	By means of mutational analysis, a key role for a stimulating protein-1 (SP1)/guanosine cytidine box in mediating the effect of extracellular thiamine level on SLC19A3 promoter was established.	Thiamine	142-150	solute carrier family 19 member 3	Homo sapiens	160-167
23989004-7	2013	Furthermore, extracellular level of thiamine was found to affect SP1 protein expression and binding pattern to the thiamine level-responsive region of SLC19A3 promoter in Caco-2 cells as shown by Western blotting and electrophoretic mobility shift assay analysis, respectively.	Thiamine	36-44	solute carrier family 19 member 3	Homo sapiens	151-158
23989004-7	2013	Furthermore, extracellular level of thiamine was found to affect SP1 protein expression and binding pattern to the thiamine level-responsive region of SLC19A3 promoter in Caco-2 cells as shown by Western blotting and electrophoretic mobility shift assay analysis, respectively.	Thiamine	115-123	solute carrier family 19 member 3	Homo sapiens	151-158
23989004-8	2013	These studies demonstrate that the human intestinal thiamine uptake is adaptively regulated by the extracellular substrate level via transcriptional regulation of the THTR-2 system, and report that SP1 transcriptional factor is involved in this regulation.	Thiamine	52-60	solute carrier family 19 member 3	Homo sapiens	167-173
23715873-9	2013	CONCLUSION/INTERPRETATION: Supplementation with high-dose thiamine may prevent deterioration in fasting glucose and insulin, and improve glucose tolerance in patients with hyperglycemia.	Thiamine	58-66	insulin	Homo sapiens	116-123
23989004-0	2013	Adaptive regulation of human intestinal thiamine uptake by extracellular substrate level: a role for THTR-2 transcriptional regulation.	Thiamine	40-48	solute carrier family 19 member 3	Homo sapiens	101-107
23989004-5	2013	Using 5"-truncated promoter-luciferase constructs, we identified the thiamine level-responsive region in the SLC19A3 promoter to be between -77 and -29 (using transcriptional start site as +1).	Thiamine	69-77	solute carrier family 19 member 3	Homo sapiens	109-116
23707715-9	2013	CONCLUSIONS: The specificity for ThTP is linked to a stacking interaction between the thiazole heterocycle of thiamine and a tryptophan residue.	Thiamine	110-118	thiamine triphosphatase	Homo sapiens	33-37
23462281-5	2013	Multiple studies have evaluated the connection between thiamine and PD pathology, and candidate pathways involve the transcription factor Sp1, p53, Bcl-2, caspase-3, tyrosine hydroxylase, glycogen synthase kinase-3beta, vascular endothelial growth factor, advanced glycation end products, nuclear factor kappa B, mitogen-activated protein kinase, and the reduced form of nicotinamide adenine dinucleotide phosphate.	Thiamine	55-63	tumor protein p53	Homo sapiens	143-146
24072090-0	2013	Novel mutation in the SLC19A2 gene in an Iranian family with thiamine-responsive megaloblastic anemia: a series of three cases.	Thiamine	61-69	solute carrier family 19 member 2	Homo sapiens	22-29
23642734-5	2013	Intracellular availability of thiamine is facilitated by the activity of thiamine transporters and thiamine pyrophosphokinase-1 (TPK-1).	Thiamine	30-38	thiamin pyrophosphokinase 1	Homo sapiens	99-127
23642734-5	2013	Intracellular availability of thiamine is facilitated by the activity of thiamine transporters and thiamine pyrophosphokinase-1 (TPK-1).	Thiamine	30-38	thiamin pyrophosphokinase 1	Homo sapiens	129-134
23289844-0	2013	Thiamine responsive megaloblastic anemia: a novel SLC19A2 compound heterozygous mutation in two siblings.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	50-57
23289844-1	2013	Thiamine responsive megaloblastic anemia (TRMA) is an autosomal recessive disease caused by loss of function mutations in the SLC19A2 gene.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	126-133
23960051-0	2013	The effect of magnesium administration on erythrocyte transketolase activity in alcoholic patients treated with thiamine.	Thiamine	112-120	transketolase	Homo sapiens	54-67
23960051-4	2013	We describe the effect of concurrent thiamine and magnesium administration on the activity of the thiamine-dependent enzyme erythrocyte transketolase in a cohort of chronic alcoholic patients.	Thiamine	37-45	transketolase	Homo sapiens	136-149
23960051-4	2013	We describe the effect of concurrent thiamine and magnesium administration on the activity of the thiamine-dependent enzyme erythrocyte transketolase in a cohort of chronic alcoholic patients.	Thiamine	98-106	transketolase	Homo sapiens	136-149
23816351-7	2013	Collectively, these results show that ThiM homologs are the main source of THZ kinase activity in plants and are consequently crucial for thiamin salvage.	Thiamine	138-145	hydroxyethylthiazole kinase	Zea mays	38-42
24298824-3	2013	The biological exploration of vitamin B1 status is based on the measurement of thiamine pyrophosphate concentration or of the activity of a thiamine-dependent enzyme, transketolase, in erythrocytes.	Thiamine	30-40	transketolase	Homo sapiens	167-180
23462281-5	2013	Multiple studies have evaluated the connection between thiamine and PD pathology, and candidate pathways involve the transcription factor Sp1, p53, Bcl-2, caspase-3, tyrosine hydroxylase, glycogen synthase kinase-3beta, vascular endothelial growth factor, advanced glycation end products, nuclear factor kappa B, mitogen-activated protein kinase, and the reduced form of nicotinamide adenine dinucleotide phosphate.	Thiamine	55-63	vascular endothelial growth factor A	Homo sapiens	220-254
22982063-7	2013	In animal models, thiamine deficiency exacerbates plaque formation, promotes phosphorylation of tau and impairs memory.	Thiamine	18-26	microtubule associated protein tau	Homo sapiens	96-99
23893925-5	2013	Thiamine has also been implicated in cancer through its effects on matrix metalloproteinases, prostaglandins, cyclooxygenase-2, reactive oxygen species, and nitric oxide synthase.	Thiamine	0-8	prostaglandin-endoperoxide synthase 2	Homo sapiens	110-126
22982063-8	2013	In contrast, treatment of mouse models of AD with the thiamine derivative benfotiamine diminishes plaques, decreases phosphorylation of tau and reverses memory deficits.	Thiamine	54-62	microtubule associated protein tau	Homo sapiens	136-139
22982063-11	2013	In diabetes, benfotiamine induces key thiamine-dependent enzymes of the pentose shunt to reduce accumulation of toxic metabolites including advanced glycation end products (AGE).	Thiamine	38-46	renin binding protein	Homo sapiens	173-176
23423671-6	2013	In vivo overexpression of wild-type SLC19A3 showed an increased thiamine uptake, whereas overexpression of mutant SLC19A3 did not, confirming that the mutation results in an absent or non-functional protein.	Thiamine	64-72	solute carrier family 19 member 3	Homo sapiens	36-43
23357554-9	2013	Transketolase activity was significantly reduced in red blood cells, liver, lung, kidney and spleen tissue after two weeks of thiamine deficient diet.	Thiamine	126-134	transketolase	Rattus norvegicus	0-13
23555166-14	2013	High intakes of carbohydrate, vitamin B1, and vitamin E may decrease the risk of RUNX3 methylation in gastric cancer tissue, particularly in CagA- or H. pylori-negative infection, with OR of 0.41 (0.19-0.90), 0.42 (0.20-0.89), and 0.29 (0.13-0.62), respectively.	Thiamine	30-40	RUNX family transcription factor 3	Homo sapiens	81-86
23555166-14	2013	High intakes of carbohydrate, vitamin B1, and vitamin E may decrease the risk of RUNX3 methylation in gastric cancer tissue, particularly in CagA- or H. pylori-negative infection, with OR of 0.41 (0.19-0.90), 0.42 (0.20-0.89), and 0.29 (0.13-0.62), respectively.	Thiamine	30-40	S100 calcium binding protein A8	Homo sapiens	141-145
23512295-0	2013	Thiamine responsive megaloblastic anemia with a novel SLC19A2 mutation presenting with myeloid maturational arrest.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	54-61
23454484-0	2013	Identification of a SLC19A2 nonsense mutation in Persian families with thiamine-responsive megaloblastic anemia.	Thiamine	71-79	solute carrier family 19 member 2	Homo sapiens	20-27
23454484-1	2013	Thiamine-responsive megaloblastic anemia (TRMA) is an autosomal recessive syndrome characterized by early-onset anemia, diabetes, and hearing loss caused by mutations in the SLC19A2 gene.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	42-46
23454484-1	2013	Thiamine-responsive megaloblastic anemia (TRMA) is an autosomal recessive syndrome characterized by early-onset anemia, diabetes, and hearing loss caused by mutations in the SLC19A2 gene.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	174-181
23274124-3	2013	Thiamine also affects HIV through non-genomic factors, i.e., matrix metalloproteinase, vascular endothelial growth factor, heme oxygenase 1, the prostaglandins, cyclooxygenase 2, reactive oxygen species, and nitric oxide.	Thiamine	0-8	vascular endothelial growth factor A	Homo sapiens	87-121
23274124-3	2013	Thiamine also affects HIV through non-genomic factors, i.e., matrix metalloproteinase, vascular endothelial growth factor, heme oxygenase 1, the prostaglandins, cyclooxygenase 2, reactive oxygen species, and nitric oxide.	Thiamine	0-8	heme oxygenase 1	Homo sapiens	123-139
23274124-3	2013	Thiamine also affects HIV through non-genomic factors, i.e., matrix metalloproteinase, vascular endothelial growth factor, heme oxygenase 1, the prostaglandins, cyclooxygenase 2, reactive oxygen species, and nitric oxide.	Thiamine	0-8	prostaglandin-endoperoxide synthase 2	Homo sapiens	161-177
23506878-3	2013	SLC19A2 and SLC19A3 transport thiamine but not folates.	Thiamine	30-38	solute carrier family 19 member 2	Homo sapiens	0-7
23506878-3	2013	SLC19A2 and SLC19A3 transport thiamine but not folates.	Thiamine	30-38	solute carrier family 19 member 3	Homo sapiens	12-19
23506878-4	2013	SLC19A1 and SLC19A2 deliver their substrates to systemic tissues; SLC19A3 mediates intestinal thiamine absorption.	Thiamine	94-102	solute carrier family 19 member 1	Homo sapiens	0-7
23506878-4	2013	SLC19A1 and SLC19A2 deliver their substrates to systemic tissues; SLC19A3 mediates intestinal thiamine absorption.	Thiamine	94-102	solute carrier family 19 member 3	Homo sapiens	66-73
23506878-8	2013	There are autosomal recessive disorders associated with mutations in genes encoded for SLC46A1 (hereditary folate malabsorption), FOLR1 (cerebral folate deficiency), SLC19A2 (thiamine-responsive megaloblastic anemia), and SLC19A3 (biotin-responsive basal ganglia disease).	Thiamine	175-183	solute carrier family 46 member 1	Homo sapiens	87-94
23506878-8	2013	There are autosomal recessive disorders associated with mutations in genes encoded for SLC46A1 (hereditary folate malabsorption), FOLR1 (cerebral folate deficiency), SLC19A2 (thiamine-responsive megaloblastic anemia), and SLC19A3 (biotin-responsive basal ganglia disease).	Thiamine	175-183	solute carrier family 19 member 2	Homo sapiens	166-173
23506878-8	2013	There are autosomal recessive disorders associated with mutations in genes encoded for SLC46A1 (hereditary folate malabsorption), FOLR1 (cerebral folate deficiency), SLC19A2 (thiamine-responsive megaloblastic anemia), and SLC19A3 (biotin-responsive basal ganglia disease).	Thiamine	175-183	solute carrier family 19 member 3	Homo sapiens	222-229
23280001-1	2013	PURPOSE: The goal of the present study was to investigate whether the antioxidants vitamin E, vitamin C and vitamin B1 can reduce the transforming growth factor-beta2 (TGF-beta2)-induced gene expressions in cultured human optic nerve head (ONH) astrocytes.	Thiamine	108-118	transforming growth factor beta 2	Homo sapiens	134-166
23280001-1	2013	PURPOSE: The goal of the present study was to investigate whether the antioxidants vitamin E, vitamin C and vitamin B1 can reduce the transforming growth factor-beta2 (TGF-beta2)-induced gene expressions in cultured human optic nerve head (ONH) astrocytes.	Thiamine	108-118	transforming growth factor beta 2	Homo sapiens	168-177
23280001-5	2013	Pretreatment with different concentrations of vitamin E, vitamin C and vitamin B1 reduced the TGF-beta2-stimulated gene expressions.	Thiamine	71-81	transforming growth factor beta 2	Homo sapiens	94-103
23280001-6	2013	CONCLUSION: In cultured human ONH astrocytes, the TGF-beta2-stimulated gene expressions could be reduced by pretreatment with vitamin E, vitamin C and vitamin B1.	Thiamine	151-161	transforming growth factor beta 2	Homo sapiens	50-59
23423671-14	2013	Our data shows that SLC19A3 is a new candidate for mutation screening in patients with Leigh syndrome, who might benefit from high doses of thiamine and/or biotin.	Thiamine	140-148	solute carrier family 19 member 3	Homo sapiens	20-27
23804074-3	2013	Overexpression of thiamine pyrophosphokinase (the enzyme that converts thiamine into its active form, thiamine pyrophosphate) hypersensitizes parasites to oxythiamine by up to 1,700-fold, consistent with oxythiamine being a substrate for thiamine pyrophosphokinase and its conversion into an antimetabolite.	Thiamine	18-26	thiamine pyrophosphokinase	Mus musculus	238-264
23022222-9	2013	In addition, THD and kindlin-3 cooperatively augmented protease-activated receptor 1-induced alpha(IIb)beta(3) activation.	Thiamine	13-16	coagulation factor II thrombin receptor	Homo sapiens	55-84
24114639-1	2013	INTRODUCTION: The activity of erythrocyte transketolase induced by thiamine pyrophosphate and normalized to age of the patient is a marker of thiamine metabolism disturbances with pathological consequences in the central and peripheral nervous system.	Thiamine	67-75	transketolase	Homo sapiens	42-55
24114639-2	2013	The measurement of erythrocyte transketolase activity enables evaluation of the thiamine status and therapeutic decisions in the disorders of the nervous system related to its deficiency.	Thiamine	80-88	transketolase	Homo sapiens	31-44
24114639-14	2013	Abnormalities in transketolase activity, when expressed in three modalities: basal activity, normalized transketolase activity ratio and the activity after the stimulation with thiamine pyrophosphate may be differentiated as thiamine-dependent or resulting from posttranslational modification.	Thiamine	177-185	transketolase	Homo sapiens	17-30
23220278-1	2013	Transketolase is a convenient model system to study enzymatic thiamin catalysis.	Thiamine	62-69	transketolase	Homo sapiens	0-13
24846908-0	2013	HIF1-alpha-mediated gene expression induced by vitamin B1 deficiency.	Thiamine	47-57	hypoxia inducible factor 1 subunit alpha	Homo sapiens	0-10
24846908-6	2013	Similar to cells exposed to hypoxia, there was a corresponding increase in HIF-1alpha stabilization and activation of target gene expression during thiamine deficiency, including glucose transporter-1 (GLUT1), vascular endothelial growth factor (VEGF), and aldolase A.	Thiamine	148-156	hypoxia inducible factor 1 subunit alpha	Homo sapiens	75-85
24846908-6	2013	Similar to cells exposed to hypoxia, there was a corresponding increase in HIF-1alpha stabilization and activation of target gene expression during thiamine deficiency, including glucose transporter-1 (GLUT1), vascular endothelial growth factor (VEGF), and aldolase A.	Thiamine	148-156	solute carrier family 2 member 1	Homo sapiens	179-200
24846908-7	2013	Both hypoxia and thiamine deficiency exposure resulted in an increase in the expression of the thiamine transporter SLC19A3.	Thiamine	17-25	solute carrier family 19 member 3	Homo sapiens	116-123
24846908-8	2013	These results indicate thiamine deficiency induces HIF-1alpha-mediated gene expression similar to that observed in hypoxic stress, and may provide evidence for a central transcriptional response associated with the clinical manifestations of thiamine deficiency.	Thiamine	23-31	hypoxia inducible factor 1 subunit alpha	Homo sapiens	51-61
24846908-8	2013	These results indicate thiamine deficiency induces HIF-1alpha-mediated gene expression similar to that observed in hypoxic stress, and may provide evidence for a central transcriptional response associated with the clinical manifestations of thiamine deficiency.	Thiamine	242-250	hypoxia inducible factor 1 subunit alpha	Homo sapiens	51-61
22107884-2	2012	In this study, we aim to assess blood and urine thiamine status by high performance liquid chromatography (HPLC) in patients with DM Type 1 and Type 2 (DMT1, DMT2) and to identify associations with markers of incipient nephropathy and kidney dysfunction.	Thiamine	48-56	charged multivesicular body protein 2B	Homo sapiens	152-156
23341335-4	2013	Our results show that thiamin biosynthesis is largely regulated by the circadian clock via the activity of the THIAMIN C SYNTHASE (THIC) promoter, while the riboswitch located at the 3" untranslated region of this gene controls overall thiamin biosynthesis.	Thiamine	22-29	thiaminC	Arabidopsis thaliana	111-129
23341335-4	2013	Our results show that thiamin biosynthesis is largely regulated by the circadian clock via the activity of the THIAMIN C SYNTHASE (THIC) promoter, while the riboswitch located at the 3" untranslated region of this gene controls overall thiamin biosynthesis.	Thiamine	22-29	thiaminC	Arabidopsis thaliana	131-135
23341335-6	2013	Our model suggests that in Arabidopsis, the THIC promoter and the thiamin-pyrophosphate riboswitch act simultaneously to tightly regulate thiamin biosynthesis in a circadian manner and consequently sense and control vital points of core cellular metabolism.	Thiamine	66-73	thiaminC	Arabidopsis thaliana	44-48
22107884-7	2012	RESULTS: Blood thiamine concentrations (ng 1-1) were decreased by 75.7% and 49.6% in patients with DMT1 and DMT2, respectively [controls (54.8+/-11.4); DMT1 (41.5+/-17.9); DMT2 (27.2+/-12.7), p&lt;0.001].	Thiamine	15-23	charged multivesicular body protein 2B	Homo sapiens	99-103
22107884-7	2012	RESULTS: Blood thiamine concentrations (ng 1-1) were decreased by 75.7% and 49.6% in patients with DMT1 and DMT2, respectively [controls (54.8+/-11.4); DMT1 (41.5+/-17.9); DMT2 (27.2+/-12.7), p&lt;0.001].	Thiamine	15-23	charged multivesicular body protein 2B	Homo sapiens	152-156
22107884-8	2012	Among those with normo-albuminuria, urinary excretion of thiamine was significantly increased to 390.1 microg/ml and 1212.4 microg/ml in DMT1 and DMT2 respectively, as compared to controls (326.4 microg/ml).	Thiamine	57-65	charged multivesicular body protein 2B	Homo sapiens	137-141
22107884-9	2012	DMT1 and DMT2 patients with micro- albuminuria on the other hand had 2.5- and 3.4-fold increase in urinary excretion of thiamine compared to controls.	Thiamine	120-128	charged multivesicular body protein 2B	Homo sapiens	0-4
22107884-10	2012	CONCLUSION: Low levels of blood thiamine are present in patients with DMT1 and DMT2, and are associated with increased thiamine clearance.	Thiamine	32-40	charged multivesicular body protein 2B	Homo sapiens	70-74
22727569-8	2012	Only two patients with mutations in the BCKDHB and DBT genes were thiamine-responsive and presented a better clinical outcome.	Thiamine	66-74	branched chain keto acid dehydrogenase E1 subunit beta	Homo sapiens	40-46
23091473-2	2012	Cobalamin (B(12)) and thiamine (B(1)) auxotrophy are widespread throughout eukaryotic phytoplankton, with over 50% of cultured isolates requiring B(12) and 20% requiring B(1).	Thiamine	22-30	immunoglobulin kappa variable 7-3 (pseudogene)	Homo sapiens	31-36
22449018-4	2012	Our analyses on the gene expression and enzymatic activity levels generally showed an increased production of thiamine biosynthesis enzymes (THI4 and THI6/THI6), a TDP synthesizing enzyme (THI80/THI80) and a TDP-requiring enzyme, transketolase (TKL1/TKL) by yeast subjected to oxidative (1 mM hydrogen peroxide) and osmotic (1 M sorbitol) stress.	Thiamine	110-118	thiamine thiazole synthase	Saccharomyces cerevisiae S288C	141-145
22449018-4	2012	Our analyses on the gene expression and enzymatic activity levels generally showed an increased production of thiamine biosynthesis enzymes (THI4 and THI6/THI6), a TDP synthesizing enzyme (THI80/THI80) and a TDP-requiring enzyme, transketolase (TKL1/TKL) by yeast subjected to oxidative (1 mM hydrogen peroxide) and osmotic (1 M sorbitol) stress.	Thiamine	110-118	bifunctional hydroxyethylthiazole kinase/thiamine-phosphate diphosphorylase	Saccharomyces cerevisiae S288C	150-154
22449018-4	2012	Our analyses on the gene expression and enzymatic activity levels generally showed an increased production of thiamine biosynthesis enzymes (THI4 and THI6/THI6), a TDP synthesizing enzyme (THI80/THI80) and a TDP-requiring enzyme, transketolase (TKL1/TKL) by yeast subjected to oxidative (1 mM hydrogen peroxide) and osmotic (1 M sorbitol) stress.	Thiamine	110-118	bifunctional hydroxyethylthiazole kinase/thiamine-phosphate diphosphorylase	Saccharomyces cerevisiae S288C	155-159
23151240-8	2012	A core set of 46 proteins, encompassing 2.2% of the total pan-plasmid (2,095 CDS), conserved among all LPP-1 plasmid sequences, includes those required for thiamine and pigment biosynthesis.	Thiamine	156-164	phospholipid phosphatase 1	Homo sapiens	103-108
22659053-1	2012	Thiamin pyrophosphokinase (TPK) converts thiamin to its active form, thiamin diphosphate.	Thiamine	41-48	thiamin pyrophosphokinase 1	Oncorhynchus mykiss	0-25
22659053-1	2012	Thiamin pyrophosphokinase (TPK) converts thiamin to its active form, thiamin diphosphate.	Thiamine	41-48	thiamin pyrophosphokinase 1	Oncorhynchus mykiss	27-30
22659053-2	2012	In humans, TPK expression is down-regulated in some thiamin deficiency related syndrome, and enhanced during pregnancy.	Thiamine	52-59	thiamin pyrophosphokinase 1	Oncorhynchus mykiss	11-14
22659053-9	2012	Moreover, decimated tpk expression in a hepatoma cell line relative to hepatic and gonadal cell lines appears to be consistent with previously reported down-regulation of thiamin metabolism in cancer.	Thiamine	171-178	thiamin pyrophosphokinase 1	Oncorhynchus mykiss	20-23
22727569-8	2012	Only two patients with mutations in the BCKDHB and DBT genes were thiamine-responsive and presented a better clinical outcome.	Thiamine	66-74	dihydrolipoamide branched chain transacylase E2	Homo sapiens	51-54
22674684-3	2012	Two of the thiamine biosynthesis regulatory genes, THI2 and THI3, were disrupted in the S. cerevisiae parent strain FMME-002.	Thiamine	11-19	Thi2p	Saccharomyces cerevisiae S288C	51-55
21984258-7	2012	In comparison, thiamine (200 muM) increased overall glucose metabolism but did not change glucose oxidation.	Thiamine	15-23	latexin	Homo sapiens	29-32
22369132-0	2012	Recessive SLC19A2 mutations are a cause of neonatal diabetes mellitus in thiamine-responsive megaloblastic anaemia.	Thiamine	73-81	solute carrier family 19 member 2	Homo sapiens	10-17
22369132-3	2012	Thiamine-responsive megaloblastic anaemia (TRMA), due to mutations in the thiamine transporter SLC19A2, is associated with the classical clinical triad of diabetes, deafness, and megaloblastic anaemia.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	95-102
22507301-0	2012	Thiamine deficiency degrades the link between spatial behavior and hippocampal synapsin I and phosphorylated synapsin I protein levels.	Thiamine	0-8	synapsin I	Rattus norvegicus	79-89
22507301-0	2012	Thiamine deficiency degrades the link between spatial behavior and hippocampal synapsin I and phosphorylated synapsin I protein levels.	Thiamine	0-8	synapsin I	Rattus norvegicus	109-119
22719800-1	2012	Thiamine acts as a coenzyme for transketolase (Tk) and for the pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes, enzymes which play a fundamental role for intracellular glucose metabolism.	Thiamine	0-8	transketolase	Homo sapiens	32-45
22719800-1	2012	Thiamine acts as a coenzyme for transketolase (Tk) and for the pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complexes, enzymes which play a fundamental role for intracellular glucose metabolism.	Thiamine	0-8	transketolase	Homo sapiens	47-49
22719800-4	2012	Genetic studies provide opportunity to link the relationship between thiamine and DM (such as Tk, SLC19A2 gene, transcription factor Sp1, alpha-1-antitrypsin, and p53).	Thiamine	69-77	solute carrier family 19 member 2	Homo sapiens	98-105
22674684-3	2012	Two of the thiamine biosynthesis regulatory genes, THI2 and THI3, were disrupted in the S. cerevisiae parent strain FMME-002.	Thiamine	11-19	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	60-64
22385680-5	2012	Thiamine has also been implicated in PD through its effects on L-type voltage-sensitive calcium channels (L-VSCC), matrix metalloproteinases (MMPs), prostaglandins (PGs), cyclooxygenase-2 (COX-2), reactive oxygen species (ROS), and nitric oxide synthase (NOS).	Thiamine	0-8	prostaglandin-endoperoxide synthase 2	Homo sapiens	171-187
22385680-5	2012	Thiamine has also been implicated in PD through its effects on L-type voltage-sensitive calcium channels (L-VSCC), matrix metalloproteinases (MMPs), prostaglandins (PGs), cyclooxygenase-2 (COX-2), reactive oxygen species (ROS), and nitric oxide synthase (NOS).	Thiamine	0-8	prostaglandin-endoperoxide synthase 2	Homo sapiens	189-194
22385680-5	2012	Thiamine has also been implicated in PD through its effects on L-type voltage-sensitive calcium channels (L-VSCC), matrix metalloproteinases (MMPs), prostaglandins (PGs), cyclooxygenase-2 (COX-2), reactive oxygen species (ROS), and nitric oxide synthase (NOS).	Thiamine	0-8	nitric oxide synthase 2	Homo sapiens	232-253
22194418-6	2012	Using gene-specific siRNA against mouse THTR-1 and THTR-2, we observed a significant inhibition in carrier-mediated thiamin uptake by 266-6 cells in both cases.	Thiamine	116-123	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	40-46
22387857-4	2012	In conclusion, our results are compatible with the possibility of thiamine being transported not only by ThTr1 and/or ThTr2, but also by members of the OCT family of transporters (most probably OCT1 and/or OCT3), thus sharing the same transporters with several other organic cations at the small intestinal level.	Thiamine	66-74	solute carrier family 19 member 2	Homo sapiens	105-110
22387857-4	2012	In conclusion, our results are compatible with the possibility of thiamine being transported not only by ThTr1 and/or ThTr2, but also by members of the OCT family of transporters (most probably OCT1 and/or OCT3), thus sharing the same transporters with several other organic cations at the small intestinal level.	Thiamine	66-74	solute carrier family 19 member 3	Homo sapiens	118-123
22387857-4	2012	In conclusion, our results are compatible with the possibility of thiamine being transported not only by ThTr1 and/or ThTr2, but also by members of the OCT family of transporters (most probably OCT1 and/or OCT3), thus sharing the same transporters with several other organic cations at the small intestinal level.	Thiamine	66-74	solute carrier family 22 member 1	Homo sapiens	194-198
22387857-4	2012	In conclusion, our results are compatible with the possibility of thiamine being transported not only by ThTr1 and/or ThTr2, but also by members of the OCT family of transporters (most probably OCT1 and/or OCT3), thus sharing the same transporters with several other organic cations at the small intestinal level.	Thiamine	66-74	solute carrier family 22 member 3	Homo sapiens	206-210
22404710-0	2012	Facilitated recruitment of Pdc2p, a yeast transcriptional activator, in response to thiamin starvation.	Thiamine	84-91	Pdc2p	Saccharomyces cerevisiae S288C	27-32
22404710-1	2012	In Saccharomyces cerevisiae, genes involved in thiamin pyrophosphate (TPP) synthesis (THI genes) and the pyruvate decarboxylase structural gene PDC5 are transcriptionally induced in response to thiamin starvation.	Thiamine	47-54	indolepyruvate decarboxylase 5	Saccharomyces cerevisiae S288C	144-148
22404710-7	2012	The association of Pdc2p or Thi2p with THI gene promoters was enhanced by thiamin starvation, suggesting that Pdc2p and Thi2p assist each other in their recruitment to the THI promoters via interaction with Thi3p.	Thiamine	74-81	Pdc2p	Saccharomyces cerevisiae S288C	19-24
22404710-7	2012	The association of Pdc2p or Thi2p with THI gene promoters was enhanced by thiamin starvation, suggesting that Pdc2p and Thi2p assist each other in their recruitment to the THI promoters via interaction with Thi3p.	Thiamine	74-81	Thi2p	Saccharomyces cerevisiae S288C	28-33
22404710-7	2012	The association of Pdc2p or Thi2p with THI gene promoters was enhanced by thiamin starvation, suggesting that Pdc2p and Thi2p assist each other in their recruitment to the THI promoters via interaction with Thi3p.	Thiamine	74-81	Pdc2p	Saccharomyces cerevisiae S288C	110-115
22404710-7	2012	The association of Pdc2p or Thi2p with THI gene promoters was enhanced by thiamin starvation, suggesting that Pdc2p and Thi2p assist each other in their recruitment to the THI promoters via interaction with Thi3p.	Thiamine	74-81	Thi2p	Saccharomyces cerevisiae S288C	120-125
22404710-7	2012	The association of Pdc2p or Thi2p with THI gene promoters was enhanced by thiamin starvation, suggesting that Pdc2p and Thi2p assist each other in their recruitment to the THI promoters via interaction with Thi3p.	Thiamine	74-81	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	207-212
22404710-8	2012	It is highly likely that, under thiamin-deprived conditions, a ternary Thi2p/Thi3p/Pdc2p complex is formed and transactivates THI genes in yeast cells.	Thiamine	32-39	Thi2p	Saccharomyces cerevisiae S288C	71-76
22404710-8	2012	It is highly likely that, under thiamin-deprived conditions, a ternary Thi2p/Thi3p/Pdc2p complex is formed and transactivates THI genes in yeast cells.	Thiamine	32-39	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	77-82
22404710-8	2012	It is highly likely that, under thiamin-deprived conditions, a ternary Thi2p/Thi3p/Pdc2p complex is formed and transactivates THI genes in yeast cells.	Thiamine	32-39	Pdc2p	Saccharomyces cerevisiae S288C	83-88
22194418-6	2012	Using gene-specific siRNA against mouse THTR-1 and THTR-2, we observed a significant inhibition in carrier-mediated thiamin uptake by 266-6 cells in both cases.	Thiamine	116-123	solute carrier family 19, member 3	Mus musculus	51-57
22194418-7	2012	Similarly, thiamin uptake by freshly isolated primary pancreatic acinar cells of the Slc19a2 and Slc19a3 knockout mice was significantly lower than uptake by acinar cells of the respective littermates; the degree of inhibition observed in the former knockout model was greater than that of the latter.	Thiamine	11-18	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	85-92
22194418-7	2012	Similarly, thiamin uptake by freshly isolated primary pancreatic acinar cells of the Slc19a2 and Slc19a3 knockout mice was significantly lower than uptake by acinar cells of the respective littermates; the degree of inhibition observed in the former knockout model was greater than that of the latter.	Thiamine	11-18	solute carrier family 19, member 3	Mus musculus	97-104
22194418-8	2012	These findings demonstrate, for the first time, that both mTHTR-1 and mTHTR-2 are involved in carrier-mediated thiamin uptake by pancreatic acinar cells.	Thiamine	111-118	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	58-65
22194418-8	2012	These findings demonstrate, for the first time, that both mTHTR-1 and mTHTR-2 are involved in carrier-mediated thiamin uptake by pancreatic acinar cells.	Thiamine	111-118	solute carrier family 19, member 3	Mus musculus	70-77
22192411-3	2012	In this review, we discuss the anatomical, neurochemical and behavioral changes that occur during the acute and chronic phases of thiamine deficiency and describe how rodent models of Wernicke-Korsakoff Syndrome aid in developing a more detailed picture of brain structures involved in learning and memory.	Thiamine	130-138	activation induced cytidine deaminase	Homo sapiens	212-215
22876572-1	2012	The thiamine-responsive megaloblastic anemia syndrome (TRMA) is an autosomal recessive disorder characterized by diabetes mellitus, megaloblastic anemia and sensorineural hearing loss due to mutations in SLC 19A2 that encodes a thiamine transporter protein.	Thiamine	4-12	solute carrier family 19 member 2	Homo sapiens	204-212
22238076-4	2012	Mice lacking the gene for the high-affinity thiamine transporter (Slc19a2) have normal cochlear structure and function when fed a regular (thiamine-rich) diet.	Thiamine	44-52	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	66-73
22226368-10	2012	Furthermore, the finding of unexplained thiamine deficiency in a patient with Wolfram syndrome suggests a potential link between WFS1 biology and thiamine metabolism that has implications for the clinical management of Wolfram syndrome patients.	Thiamine	40-48	wolframin ER transmembrane glycoprotein	Homo sapiens	129-133
22226368-10	2012	Furthermore, the finding of unexplained thiamine deficiency in a patient with Wolfram syndrome suggests a potential link between WFS1 biology and thiamine metabolism that has implications for the clinical management of Wolfram syndrome patients.	Thiamine	146-154	wolframin ER transmembrane glycoprotein	Homo sapiens	129-133
22214485-7	2012	The changes in these gene transcript levels were further found to correlate with increases in thiamine and its diphosphate ester content in seedlings, as well as with the enhancement of gene expression for enzymes which require thiamine diphosphate as a cofactor, mainly alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase and transketolase.	Thiamine	94-102	Transketolase	Arabidopsis thaliana	333-346
22645655-4	2012	An invariant residue of the TKT consensus sequence required for thiamine cofactor binding is mutated in TBTKT; yet its catalytic activities are unaffected, and the 2.5 A resolution structure of full-length TBTKT provides an explanation for this.	Thiamine	64-72	transketolase	Homo sapiens	28-31
22672899-10	2012	The alteration of calprotectin and RBP4 was found to be specific to THD rather than trichloroethylene exposure.	Thiamine	68-71	retinol binding protein 4	Homo sapiens	35-39
23209439-9	2012	In addition, CQ completely inhibited a human thiamine transporter (SLC19A3) expressed in yeast and significantly inhibited thiamine uptake in cultured human cell lines.	Thiamine	45-53	solute carrier family 19 member 3	Homo sapiens	67-74
23119057-0	2012	Prostatic acid phosphatase is required for the antinociceptive effects of thiamine and benfotiamine.	Thiamine	74-82	acid phosphatase 3	Homo sapiens	0-26
23119057-6	2012	However, we found that the antinociceptive effects of BT, thiamine monophosphate (TMP) and thiamine-a compound that is not phosphorylated-were entirely dependent on PAP at the spinal level.	Thiamine	58-66	acid phosphatase 3	Homo sapiens	165-168
23119057-8	2012	Taken together, our study highlights an obligatory role for PAP in the antinociceptive effects of thiamine and phosphorylated thiamine analogs, and suggests a novel phosphatase-independent function for PAP.	Thiamine	98-106	acid phosphatase 3	Homo sapiens	60-63
23118983-1	2012	Besides transketolase (TKT), a thiamin-dependent enzyme of the pentose phosphate pathway, the human genome encodes for two closely related transketolase-like proteins, which share a high sequence identity with TKT.	Thiamine	31-38	transketolase	Homo sapiens	8-21
23118983-1	2012	Besides transketolase (TKT), a thiamin-dependent enzyme of the pentose phosphate pathway, the human genome encodes for two closely related transketolase-like proteins, which share a high sequence identity with TKT.	Thiamine	31-38	transketolase	Homo sapiens	139-152
23119057-8	2012	Taken together, our study highlights an obligatory role for PAP in the antinociceptive effects of thiamine and phosphorylated thiamine analogs, and suggests a novel phosphatase-independent function for PAP.	Thiamine	126-134	acid phosphatase 3	Homo sapiens	60-63
21784107-5	2011	Furthermore, both developmental thiamine deficiencies and ethanol exposure produce two waves of neurofunctional alterations, peaking at P15 (postnatal day 15) and P25, respectively.	Thiamine	32-40	tubulin polymerization promoting protein	Homo sapiens	163-166
21836059-1	2011	The human thiamine transporter-1 (hTHTR-1) contributes to intestinal thiamine uptake, and its function is regulated at both the transcriptional and posttranscriptional levels.	Thiamine	10-18	solute carrier family 19 member 2	Homo sapiens	34-41
21836059-9	2011	This finding was also confirmed at the functional level when a significantly higher thiamine uptake was observed in cycloheximide-treated (6 h) cells expressing hTHTR-1 together with hTspan-1 compared with those expressing hTHTR-1 alone.	Thiamine	84-92	solute carrier family 19 member 2	Homo sapiens	161-168
21836059-9	2011	This finding was also confirmed at the functional level when a significantly higher thiamine uptake was observed in cycloheximide-treated (6 h) cells expressing hTHTR-1 together with hTspan-1 compared with those expressing hTHTR-1 alone.	Thiamine	84-92	tetraspanin 1	Homo sapiens	183-191
21836059-9	2011	This finding was also confirmed at the functional level when a significantly higher thiamine uptake was observed in cycloheximide-treated (6 h) cells expressing hTHTR-1 together with hTspan-1 compared with those expressing hTHTR-1 alone.	Thiamine	84-92	solute carrier family 19 member 2	Homo sapiens	223-230
21868632-5	2011	Chronic exposure (96 h) of AR42J cells to alcohol also led to a significant decreased carrier-mediated thiamin uptake, an effect that was associated with a significant decrease in the activity of the human SLC19A2 and SLC19A3 promoters expressed in these cells.	Thiamine	103-110	solute carrier family 19 member 3	Homo sapiens	218-225
21965752-0	2011	Thiamine supplementation attenuated hepatocellular carcinoma in the Atp7b mouse model of Wilson"s disease.	Thiamine	0-8	ATPase, Cu++ transporting, beta polypeptide	Mus musculus	68-73
21965752-2	2011	Exposure of HepG2 cells, and livers of Atp7b mutant mice to toxic Cu(2+) resulted in oxidation, (KGDH) and (PDH) enzyme inhibition, and death that was attenuated by thiamine.	Thiamine	165-173	ATPase copper transporting beta	Homo sapiens	39-44
21965752-3	2011	MATERIALS AND METHODS: The effect of oral thiamine supplementation (2%) on hepatocellular carcinoma induced by Cu(2+) accumulation in the livers of Atp7b animals at 4, 6, 9, 12, 16, and 21 months was demonstrated using gross morphology and multi-nucleate analysis.	Thiamine	42-50	ATPase, Cu++ transporting, beta polypeptide	Mus musculus	148-153
21965752-5	2011	At 16 months the livers of thiamine treated Atp7b mice were <130% the weight of controls and <30% cancerous, and at 21 months the mice were still active.	Thiamine	27-35	ATPase, Cu++ transporting, beta polypeptide	Mus musculus	44-49
21904031-7	2011	The TenA domain of THI20 possesses some features of both classes, consistent with its ability to hydrolyze both thiamin and the thiamin-degradation product 2-methyl-4-amino-5-aminomethylpyrimidine.	Thiamine	112-119	trifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase/thiaminase	Saccharomyces cerevisiae S288C	19-24
21904031-7	2011	The TenA domain of THI20 possesses some features of both classes, consistent with its ability to hydrolyze both thiamin and the thiamin-degradation product 2-methyl-4-amino-5-aminomethylpyrimidine.	Thiamine	128-135	trifunctional hydroxymethylpyrimidine kinase/phosphomethylpyrimidine kinase/thiaminase	Saccharomyces cerevisiae S288C	19-24
21725571-4	2011	This allows us to utilize the H(2)O(2)-thiamine fluorescent system for the quantitative analysis of thrombin.	Thiamine	39-47	coagulation factor II, thrombin	Homo sapiens	100-108
21612515-4	2011	Thiamine is converted to thiamine diphosphate (TDP) by thiamine diphosphokinase (TDPK).	Thiamine	0-8	thiamin pyrophosphokinase 1	Homo sapiens	55-79
21612515-4	2011	Thiamine is converted to thiamine diphosphate (TDP) by thiamine diphosphokinase (TDPK).	Thiamine	0-8	thiamin pyrophosphokinase 1	Homo sapiens	81-85
21612515-8	2011	Molecular modeling studies showed that ALT-711 fits into the thiamine-binding pocket of TDPK, and there are three interactions between the thiazolium ring and the enzyme, as well as parallel stacking between the phenyl ring and the indole ring of Trp222B.	Thiamine	61-69	thiamin pyrophosphokinase 1	Homo sapiens	88-92
21149507-10	2011	However, expressions of both folate (RFC and PCFT) and thiamin (THTR-1, THTR-2) transporters were markedly reduced in the small intestine, heart, liver and brain of the CKD animals.	Thiamine	55-62	solute carrier family 19 member 2	Homo sapiens	64-70
21149507-10	2011	However, expressions of both folate (RFC and PCFT) and thiamin (THTR-1, THTR-2) transporters were markedly reduced in the small intestine, heart, liver and brain of the CKD animals.	Thiamine	55-62	solute carrier family 19 member 3	Homo sapiens	72-78
20652275-9	2011	CONCLUSIONS: Thiamine administration for 1 month decreased glucose and leptin concentrations in drug-naive patients with T2DM.	Thiamine	13-21	leptin	Homo sapiens	71-77
20930543-2	2010	Using a real time PCR array strategy to further characterize changes in transporter expression within a chronic hypoxia breast cancer cell line model (BT474), we have found a 31 fold increase in the expression of the thiamine transporter, SLC19A3.	Thiamine	217-225	solute carrier family 19 member 3	Homo sapiens	239-246
21285901-2	2011	The disease is caused by mutations in the gene, SLC19A2, encoding a high-affinity thiamine transporter, which disturbs the active thiamine uptake into cells.	Thiamine	82-90	solute carrier family 19 member 2	Homo sapiens	48-55
21068344-7	2011	RESULTS: Low blood thiamine concentrations upon admission were detected in 57 patients (28.2%) and were shown to be independently associated with C-reactive protein concentrations &gt;20 mg/dL (odds ratio: 2.17; 95% CI: 1.13, 4.17; P = 0.02) but not with malnutrition.	Thiamine	19-27	C-reactive protein	Homo sapiens	146-164
21364976-1	2011	BACKGROUND: Infantile beriberi is a potentially lethal manifestation of thiamin deficiency, associated with traditional post-partum maternal food avoidance, which persists in the Lao PDR (Laos).	Thiamine	72-79	interleukin 4 induced 1	Homo sapiens	179-182
19233513-2	2011	In this study, we analyzed the relationship between thiamine deficiency (TD) and amyloid precursor protein (APP) processing in both cellular and animal models of TD.	Thiamine	52-60	amyloid beta precursor protein	Homo sapiens	81-106
22205947-13	2011	Blood samples taken from 16 cases prior to treatment showed increased levels of erythrocyte transketolase activation coefficient, consistent with thiamine deficiency.	Thiamine	146-154	transketolase	Homo sapiens	92-105
21176162-8	2010	CONCLUSION: Our cases broaden the phenotypic spectrum of disorders associated with SLC19A3 mutations and highlight the potential benefit of biotin and/or thiamin treatments and the need to assess the clinical efficacy of these treatments.	Thiamine	154-161	solute carrier family 19 member 3	Homo sapiens	83-90
20816907-0	2010	Up-regulation of caveolin-1 and blood-brain barrier breakdown are attenuated by N-acetylcysteine in thiamine deficiency.	Thiamine	100-108	caveolin 1, caveolae protein	Mus musculus	17-27
20816907-6	2010	A significant and focal increase in both caveolin-1 gene and protein expression was detected in the thalamus of thiamine-deficient mice, concomitant with IgG extravasation.	Thiamine	112-120	caveolin 1, caveolae protein	Mus musculus	41-51
20835854-1	2010	Thiamine-responsive megaloblastic anemia (TRMA) syndrome usually associated with diabetes mellitus, anemia and deafness, due to mutations in SLC19A2, encoding a thiamine transporter protein.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	42-46
21110885-0	2010	ADAR2-dependent RNA editing of GluR2 is involved in thiamine deficiency-induced alteration of calcium dynamics.	Thiamine	52-60	adenosine deaminase RNA specific B1	Homo sapiens	0-5
21110885-0	2010	ADAR2-dependent RNA editing of GluR2 is involved in thiamine deficiency-induced alteration of calcium dynamics.	Thiamine	52-60	glutamate ionotropic receptor AMPA type subunit 2	Homo sapiens	31-36
20835854-1	2010	Thiamine-responsive megaloblastic anemia (TRMA) syndrome usually associated with diabetes mellitus, anemia and deafness, due to mutations in SLC19A2, encoding a thiamine transporter protein.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	141-148
20219672-6	2010	Benfotiamine suppresses oxidative stress-induced NF-kappaB activation and prevents bacterial endotoxin-induced inflammation, indicating that vitamin B1 supplementation could be beneficial in the treatment of inflammatory diseases.	Thiamine	141-151	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	49-58
20674425-2	2010	Confirming thiamine deficiency is problematic and relies on demonstrating reduced red blood cells transketolase activity, or indirect methods including urinary organic acid analysis and dietary analysis.	Thiamine	11-19	transketolase	Homo sapiens	98-111
20971897-5	2010	Positional cloning of blk1-R identified a predicted missense mutation in a highly conserved amino acid encoded by thiamine biosynthesis2 (thi2).	Thiamine	114-122	thiamine thiazole synthase 2, chloroplastic	Zea mays	22-26
20971897-5	2010	Positional cloning of blk1-R identified a predicted missense mutation in a highly conserved amino acid encoded by thiamine biosynthesis2 (thi2).	Thiamine	114-122	thiamine thiazole synthase 2, chloroplastic	Zea mays	138-142
20971897-6	2010	Consistent with chromosome dosage studies suggesting that blk1-R is a null mutation, biochemical analyses confirm that the wild-type THI2 enzyme copurifies with a thiazole precursor to thiamine, whereas the mutant enzyme does not.	Thiamine	185-193	thiamine thiazole synthase 2, chloroplastic	Zea mays	133-137
20971897-8	2010	All blk1-R mutant phenotypes are rescued by exogenous thiamine supplementation, suggesting that blk1-R is a thiamine auxotroph.	Thiamine	54-62	thiamine thiazole synthase 2, chloroplastic	Zea mays	4-8
20971897-8	2010	All blk1-R mutant phenotypes are rescued by exogenous thiamine supplementation, suggesting that blk1-R is a thiamine auxotroph.	Thiamine	54-62	thiamine thiazole synthase 2, chloroplastic	Zea mays	96-100
20971897-8	2010	All blk1-R mutant phenotypes are rescued by exogenous thiamine supplementation, suggesting that blk1-R is a thiamine auxotroph.	Thiamine	108-116	thiamine thiazole synthase 2, chloroplastic	Zea mays	4-8
20971897-8	2010	All blk1-R mutant phenotypes are rescued by exogenous thiamine supplementation, suggesting that blk1-R is a thiamine auxotroph.	Thiamine	108-116	thiamine thiazole synthase 2, chloroplastic	Zea mays	96-100
19404565-4	2010	We aimed at verifying the effects of thiamine and benfotiamine on MMP-2, MMP-9 and TIMP expression and activity in human vascular cells with high glucose.	Thiamine	37-45	matrix metallopeptidase 2	Homo sapiens	66-71
19404565-4	2010	We aimed at verifying the effects of thiamine and benfotiamine on MMP-2, MMP-9 and TIMP expression and activity in human vascular cells with high glucose.	Thiamine	37-45	matrix metallopeptidase 9	Homo sapiens	73-78
19404565-4	2010	We aimed at verifying the effects of thiamine and benfotiamine on MMP-2, MMP-9 and TIMP expression and activity in human vascular cells with high glucose.	Thiamine	37-45	TIMP metallopeptidase inhibitor 1	Homo sapiens	83-87
19404565-5	2010	In HRP, MMP-2 activity, though not expression, increased with high glucose and decreased with thiamine and benfotiamine; TIMP-1 expression increased with high glucose plus thiamine and benfotiamine; MMP-9 was not expressed.	Thiamine	94-102	matrix metallopeptidase 2	Homo sapiens	8-13
19404565-5	2010	In HRP, MMP-2 activity, though not expression, increased with high glucose and decreased with thiamine and benfotiamine; TIMP-1 expression increased with high glucose plus thiamine and benfotiamine; MMP-9 was not expressed.	Thiamine	172-180	TIMP metallopeptidase inhibitor 1	Homo sapiens	121-127
20439498-3	2010	Both of these HDACs associate with a distal region of the affected THI gene promoters that does not overlap with a previously defined enhancer region bound by the thiamine-responsive Thi2/Thi3/Pdc2 transcriptional activators.	Thiamine	163-171	Thi2p	Saccharomyces cerevisiae S288C	183-187
20439498-3	2010	Both of these HDACs associate with a distal region of the affected THI gene promoters that does not overlap with a previously defined enhancer region bound by the thiamine-responsive Thi2/Thi3/Pdc2 transcriptional activators.	Thiamine	163-171	branched-chain-2-oxoacid decarboxylase THI3	Saccharomyces cerevisiae S288C	188-192
20439498-3	2010	Both of these HDACs associate with a distal region of the affected THI gene promoters that does not overlap with a previously defined enhancer region bound by the thiamine-responsive Thi2/Thi3/Pdc2 transcriptional activators.	Thiamine	163-171	Pdc2p	Saccharomyces cerevisiae S288C	193-197
20439498-6	2010	Importantly, lowering the NAD(+) concentration and inhibiting the Hst1/Sum1 HDAC complex elevated the intracellular thiamine concentration due to increased thiamine biosynthesis and transport, implicating NAD(+) in the control of thiamine homeostasis.	Thiamine	116-124	Sum1p	Saccharomyces cerevisiae S288C	71-75
20439498-6	2010	Importantly, lowering the NAD(+) concentration and inhibiting the Hst1/Sum1 HDAC complex elevated the intracellular thiamine concentration due to increased thiamine biosynthesis and transport, implicating NAD(+) in the control of thiamine homeostasis.	Thiamine	156-164	Sum1p	Saccharomyces cerevisiae S288C	71-75
20439498-6	2010	Importantly, lowering the NAD(+) concentration and inhibiting the Hst1/Sum1 HDAC complex elevated the intracellular thiamine concentration due to increased thiamine biosynthesis and transport, implicating NAD(+) in the control of thiamine homeostasis.	Thiamine	156-164	Sum1p	Saccharomyces cerevisiae S288C	71-75
19404565-10	2010	Thiamine and benfotiamine correct the increase in MMP-2 activity due to high glucose in HRP, while increasing TIMP-1.	Thiamine	0-8	matrix metallopeptidase 2	Homo sapiens	50-55
19404565-10	2010	Thiamine and benfotiamine correct the increase in MMP-2 activity due to high glucose in HRP, while increasing TIMP-1.	Thiamine	0-8	TIMP metallopeptidase inhibitor 1	Homo sapiens	110-116
19830429-1	2010	PURPOSE: We have previously shown that the expression of the thiamine transporter THTR2 is decreased sevenfold in breast cancer, which may leave breast cancer cells vulnerable to acute thiamine starvation.	Thiamine	61-69	solute carrier family 19 member 3	Homo sapiens	82-87
20107192-0	2010	Vitamin B1 analog benfotiamine prevents diabetes-induced diastolic dysfunction and heart failure through Akt/Pim-1-mediated survival pathway.	Thiamine	0-10	thymoma viral proto-oncogene 1	Mus musculus	105-108
19879271-1	2010	BACKGROUND &amp; AIMS: Intestinal thiamin uptake process is vital for maintaining normal body homeostasis of the vitamin; in vitro studies suggest that both thiamin transporter-1 (THTR-1) and -2 (THTR-2) are involved.	Thiamine	34-41	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	180-194
19879271-1	2010	BACKGROUND &amp; AIMS: Intestinal thiamin uptake process is vital for maintaining normal body homeostasis of the vitamin; in vitro studies suggest that both thiamin transporter-1 (THTR-1) and -2 (THTR-2) are involved.	Thiamine	34-41	solute carrier family 19, member 3	Mus musculus	196-202
19879271-2	2010	Mutations in THTR-1 cause thiamin-responsive megaloblastic anemia, a tissue-specific disease associated with diabetes mellitus, megaloblastic anemia, and sensorineural deafness.	Thiamine	26-33	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	13-19
19879271-3	2010	However, in patients with thiamin-responsive megaloblastic anemia, plasma thiamin levels are within normal range, indicating that THTR-2 (or another carrier) could provide sufficient intestinal thiamin absorption.	Thiamine	26-33	solute carrier family 19 member 3	Homo sapiens	130-136
19879271-4	2010	We tested this possibility and examined the role of THTR-2 in uptake of thiamin in the intestine of mice.	Thiamine	72-79	solute carrier family 19, member 3	Mus musculus	52-58
19879271-5	2010	METHODS: THTR-2-deficient mice were generated by SLC19A3 gene knockout and used to examine intestinal uptake of thiamin in vitro (isolated cells) and in vivo (intact intestinal loops).	Thiamine	112-119	solute carrier family 19, member 3	Mus musculus	9-15
19879271-7	2010	RESULTS: Intestine of THTR-2-deficient mice had reduced uptake of thiamin compared with those of wild-type littermate mice (P &lt; .01); this reduction was associated with a decrease (P &lt; .01) in blood thiamin levels in THTR-2-deficient mice.	Thiamine	66-73	solute carrier family 19, member 3	Mus musculus	22-28
19879271-7	2010	RESULTS: Intestine of THTR-2-deficient mice had reduced uptake of thiamin compared with those of wild-type littermate mice (P &lt; .01); this reduction was associated with a decrease (P &lt; .01) in blood thiamin levels in THTR-2-deficient mice.	Thiamine	205-212	solute carrier family 19, member 3	Mus musculus	22-28
19879271-8	2010	However, intestinal uptake of thiamin in THTR-1-deficient mice was not significantly different from that of wild-type littermate animals.	Thiamine	30-37	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	41-47
19879271-10	2010	CONCLUSIONS: THTR-2 is required for normal uptake of thiamin in the intestine and can fulfill normal levels of uptake in conditions associated with THTR-1 dysfunction.	Thiamine	53-60	solute carrier family 19, member 3	Mus musculus	13-19
20404999-2	2010	Several IscS-interacting partners including IscU, a scaffold for Fe-S cluster assembly; TusA, the first member of a sulfur relay leading to sulfur incorporation into the wobble uridine of several tRNAs; ThiI, involved in tRNA modification and thiamine biosynthesis; and rhodanese RhdA are sulfur acceptors.	Thiamine	243-251	NFS1 cysteine desulfurase	Homo sapiens	8-12
20107192-0	2010	Vitamin B1 analog benfotiamine prevents diabetes-induced diastolic dysfunction and heart failure through Akt/Pim-1-mediated survival pathway.	Thiamine	0-10	proviral integration site 1	Mus musculus	109-114
20684226-6	2010	Further, the influence of classic thiamine antagonists (amprolium, oxythiamine and pyrithiamine) on both biological activities of TBP in SPM was studied.	Thiamine	34-42	TATA box binding protein	Rattus norvegicus	130-133
21422702-8	2010	Histological evaluation revealed that thiamine alleviated adipocyte hypertrophy, steatosis in the liver, heart, and skeletal muscle, sinusoidal fibrosis with formation of basement membranes (called pseudocapillarization) which accompanied significantly reduced expression of laminin beta1 and nidogen-1 mRNA, interstitial fibrosis in the heart and kidney, fatty degeneration in the pancreas, thickening of the basement membrane of the vasculature, and glomerulopathy and mononuclear cell infiltration in the kidney.	Thiamine	38-46	laminin subunit beta 1	Rattus norvegicus	275-288
21422702-8	2010	Histological evaluation revealed that thiamine alleviated adipocyte hypertrophy, steatosis in the liver, heart, and skeletal muscle, sinusoidal fibrosis with formation of basement membranes (called pseudocapillarization) which accompanied significantly reduced expression of laminin beta1 and nidogen-1 mRNA, interstitial fibrosis in the heart and kidney, fatty degeneration in the pancreas, thickening of the basement membrane of the vasculature, and glomerulopathy and mononuclear cell infiltration in the kidney.	Thiamine	38-46	nidogen 1	Rattus norvegicus	293-302
19563509-3	2010	After TSCI, pyrophosphate of thiamine or non-degradable cocarboxylase (NDC) enzyme was used to maintain energy levels, antioxidants such as superoxide dismutase and catalase (ANT) were used to decrease oxidative damage and methylprednisolone (MP), which has both therapeutic properties, was used as a control.	Thiamine	29-37	catalase	Rattus norvegicus	165-173
20644337-0	2010	Thiamine ameliorates diabetes-induced inhibition of pyruvate dehydrogenase (PDH) in rat heart mitochondria: investigating the discrepancy between PDH activity and PDH E1alpha phosphorylation in cardiac fibroblasts exposed to high glucose.	Thiamine	0-8	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	52-74
20644337-0	2010	Thiamine ameliorates diabetes-induced inhibition of pyruvate dehydrogenase (PDH) in rat heart mitochondria: investigating the discrepancy between PDH activity and PDH E1alpha phosphorylation in cardiac fibroblasts exposed to high glucose.	Thiamine	0-8	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	76-79
20644337-0	2010	Thiamine ameliorates diabetes-induced inhibition of pyruvate dehydrogenase (PDH) in rat heart mitochondria: investigating the discrepancy between PDH activity and PDH E1alpha phosphorylation in cardiac fibroblasts exposed to high glucose.	Thiamine	0-8	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	146-149
20644337-0	2010	Thiamine ameliorates diabetes-induced inhibition of pyruvate dehydrogenase (PDH) in rat heart mitochondria: investigating the discrepancy between PDH activity and PDH E1alpha phosphorylation in cardiac fibroblasts exposed to high glucose.	Thiamine	0-8	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	146-149
20644337-3	2010	PDH requires thiamine as a coenzyme.	Thiamine	13-21	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	0-3
20644337-5	2010	Treatment of rats with thiamine significantly, although partially, recovered streptozotocin (STZ)-induced reductions in mitochondrial PDH activity.	Thiamine	23-31	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	134-137
20644337-6	2010	Nevertheless, we found that PDH E1alpha phosphorylation in the thiamine-treated STZ group was perfectly diminished to the same level as that in the control group.	Thiamine	63-71	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	28-31
20644337-9	2010	Thiamine dramatically recovered high glucose-induced PDH inhibition.	Thiamine	0-8	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	53-56
20644337-13	2010	These results suggest that thiamine ameliorates diabetes-induced PDH inhibition by suppressing the increased expression of the O-glycosylated protein.	Thiamine	27-35	pyruvate dehydrogenase phosphatase catalytic subunit 1	Homo sapiens	65-68
20684226-12	2010	The obtained data indicate that the active sites on SPM responsible for thiamine binding and ThTPase activity have different sensitivity to thiamine antagonists.	Thiamine	140-148	thiamine triphosphatase	Rattus norvegicus	93-100
19812694-11	2009	Two classical genetic markers (PY, ALB1) were identified based on similar map locations of known genes required for thiamine (THIC) and chlorophyll (PDE166) biosynthesis.	Thiamine	116-124	ALBINA 1	Arabidopsis thaliana	35-39
19922902-1	2009	Thiamine-responsive megaloblastic anemia (TRMA) is a rare autosomal recessive disorder characterized by megaloblastic anemia, diabetes mellitus and progressive sensorineural deafness.	Thiamine	0-8	solute carrier family 19 member 2	Homo sapiens	42-46
19812694-11	2009	Two classical genetic markers (PY, ALB1) were identified based on similar map locations of known genes required for thiamine (THIC) and chlorophyll (PDE166) biosynthesis.	Thiamine	116-124	thiaminC	Arabidopsis thaliana	126-130
19628653-5	2009	Kinetic parameters of both the nanomolar (mediated by THTR-2) and the micromolar (mediated by THTR-1) saturable thiamin uptake processes were affected by EPEC infection.	Thiamine	112-119	solute carrier family 19 member 2	Homo sapiens	94-100
19628653-10	2009	These results demonstrate for the first time that EPEC infection of human intestinal epithelial cells leads to inhibition in thiamin uptake via effects on physiological and molecular parameters of hTHTR-1 and -2.	Thiamine	125-132	solute carrier family 19 member 2	Homo sapiens	197-211
18614593-0	2009	A novel mutation in the SLC19A2 gene in a Turkish female with thiamine-responsive megaloblastic anemia syndrome.	Thiamine	62-70	solute carrier family 19 member 2	Homo sapiens	24-31
19686241-0	2009	Decreased transketolase activity contributes to impaired hippocampal neurogenesis induced by thiamine deficiency.	Thiamine	93-101	transketolase	Mus musculus	10-23
19798730-2	2009	Using homozygosity mapping, a pathogenic missense mutation in the SLC25A19 gene that encodes the mitochondrial thiamine pyrophosphate transporter was identified.	Thiamine	111-119	solute carrier family 25 member 19	Homo sapiens	66-74
18614593-2	2009	Besides reporting a new mutation on the gene SLC19A2 for the first time in the literature, we highlight the recognition of this syndrome--when megaloblastic anemia and diabetes mellitus coexists--and the role of thiamine replacement for the treatment of both disorders.	Thiamine	212-220	solute carrier family 19 member 2	Homo sapiens	45-52
19423748-6	2009	Maintaining beta-TC-6 cells in the presence of a high level of thiamin led to a significant (P &lt; 0.01) decrease in thiamin uptake, which was associated with a significant downregulation in level of expression of THTR-1 and THTR-2 at the protein and mRNA levels and a decrease in transcriptional (promoter) activity.	Thiamine	63-70	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	215-221
19423748-6	2009	Maintaining beta-TC-6 cells in the presence of a high level of thiamin led to a significant (P &lt; 0.01) decrease in thiamin uptake, which was associated with a significant downregulation in level of expression of THTR-1 and THTR-2 at the protein and mRNA levels and a decrease in transcriptional (promoter) activity.	Thiamine	63-70	solute carrier family 19, member 3	Mus musculus	226-232
19423748-8	2009	Finally, confocal imaging of live beta-TC-6 cells showed that clinical mutants of THTR-1 have mixed expression phenotypes and all led to impairment in thiamin uptake.	Thiamine	151-158	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	82-88
19423748-10	2009	Furthermore, clinical mutants of THTR-1 impair thiamin uptake via different mechanisms.	Thiamine	47-54	solute carrier family 19 (thiamine transporter), member 2	Mus musculus	33-39
19409210-2	2009	Under thiamine-deficient conditions, the uptake of glutamate into astrocytes, and the levels of proteins and mRNA expressions of glutamate aspartate transporter of astrocytes significantly decreased.	Thiamine	6-14	solute carrier family 1 member 3	Rattus norvegicus	129-160
19817279-2	2009	Mutations in the SLC19A2 gene, encoding a high-affinity thiamine transporter protein, THTR-1, are responsible for the clinical features associated with thiamine-responsive megaloblastic anemia syndrome in which treatment with pharmacological doses of thiamine correct the megaloblastic anemia and diabetes mellitus.	Thiamine	56-64	solute carrier family 19 member 2	Homo sapiens	17-24
19817279-2	2009	Mutations in the SLC19A2 gene, encoding a high-affinity thiamine transporter protein, THTR-1, are responsible for the clinical features associated with thiamine-responsive megaloblastic anemia syndrome in which treatment with pharmacological doses of thiamine correct the megaloblastic anemia and diabetes mellitus.	Thiamine	56-64	solute carrier family 19 member 2	Homo sapiens	86-92
19817279-2	2009	Mutations in the SLC19A2 gene, encoding a high-affinity thiamine transporter protein, THTR-1, are responsible for the clinical features associated with thiamine-responsive megaloblastic anemia syndrome in which treatment with pharmacological doses of thiamine correct the megaloblastic anemia and diabetes mellitus.	Thiamine	152-160	solute carrier family 19 member 2	Homo sapiens	17-24
19817279-2	2009	Mutations in the SLC19A2 gene, encoding a high-affinity thiamine transporter protein, THTR-1, are responsible for the clinical features associated with thiamine-responsive megaloblastic anemia syndrome in which treatment with pharmacological doses of thiamine correct the megaloblastic anemia and diabetes mellitus.	Thiamine	152-160	solute carrier family 19 member 2	Homo sapiens	42-76
19817279-2	2009	Mutations in the SLC19A2 gene, encoding a high-affinity thiamine transporter protein, THTR-1, are responsible for the clinical features associated with thiamine-responsive megaloblastic anemia syndrome in which treatment with pharmacological doses of thiamine correct the megaloblastic anemia and diabetes mellitus.	Thiamine	152-160	solute carrier family 19 member 2	Homo sapiens	86-92
18490188-5	2009	Abnormal transketolase expression and/or activity have been implicated in a number of diseases where thiamin availability is low, including Wernicke-Korsakoff"s Syndrome and alcoholism.	Thiamine	101-108	transketolase	Homo sapiens	9-22