PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
20960050-3	2011	Likewise, vitamin B2 was modestly inversely associated among individuals with the MTHFR c.665CC (rs1801133) genotype (RR = 0.66; p (trend) = 0.08), but with a significant reduced risk when <= 1 rare allele occurred in the combination of folate metabolizing enzymes MTHFR, MTRR and MTR (RR = 0.30; p (trend) = 0.005).	Riboflavin	10-20	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	275-279
20888556-0	2011	Polymorphisms in MTHFR and MTRR genes associated with blood plasma homocysteine concentration and sperm counts.	Homocysteine	67-79	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	27-31
20888556-1	2011	OBJECTIVE: To investigate the relationship between MTHFR and MTRR genetic variants with respect to both blood plasma homocysteine concentration and sperm counts.	Homocysteine	117-129	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	61-65
21070756-7	2011	CONCLUSION: Our findings provide support for the synergistic effects of polymorphisms in the folate metabolic pathway genes in PD susceptibility; the increased PD risk would be more significant in carriers with the polymorphisms of MTHFR, MTR, and MTRR genes.	Folic Acid	93-99	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	248-252
20634897-2	2010	MsrB1 is a selenocysteine-containing cytosolic/nuclear Msr with high expression in liver and kidney.	Selenocysteine	11-25	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
20411324-1	2010	Methionine synthase reductase (MTRR) is one of the important enzymes involved in the folate metabolic pathway and its functional genetic polymorphisms may be associated with breast cancer risk.	Folic Acid	85-91	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
20411324-1	2010	Methionine synthase reductase (MTRR) is one of the important enzymes involved in the folate metabolic pathway and its functional genetic polymorphisms may be associated with breast cancer risk.	Folic Acid	85-91	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
20544798-10	2010	In African Americans, folate derivative levels were associated with smoking, B(12), and polymorphisms in MTR, TYMS, methionine synthase reductase (MTRR), and reduced folate carrier1 (RFC1).	Folic Acid	22-28	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	116-145
20544798-10	2010	In African Americans, folate derivative levels were associated with smoking, B(12), and polymorphisms in MTR, TYMS, methionine synthase reductase (MTRR), and reduced folate carrier1 (RFC1).	Folic Acid	22-28	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	147-151
20404551-7	2010	Using these Msr enzymes in combination with peptide mapping, we were able to detect and differentiate diastereomers of methionine sulfoxide within the highly conserved heavy chain of an IgG2 that had been photo-oxidized, as well as those in an IgG1 oxidized with peroxide.	methionine sulfoxide	119-139	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	12-15
20386493-4	2010	RESULTS: RBC folate concentrations were significantly associated with MTHFR 677C>T (P=0.002), MTRR 66A>G (P<0.0001), MTHFD1 1958G>A (P=0.001) and SHMT 1420C>T (P=0.012), whereas no association of these polymorphisms with disease activity was observed.	Folic Acid	13-19	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	97-101
20096994-6	2010	The MSR(s) decrement was lower for BS than for SS probably due to stronger affinity of PHE on organic matter in BS than in SS, which cause lower efficiency of soil washing than estimated by intrinsic sorption of PHE.	phenanthrene	87-90	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-7
20096994-6	2010	The MSR(s) decrement was lower for BS than for SS probably due to stronger affinity of PHE on organic matter in BS than in SS, which cause lower efficiency of soil washing than estimated by intrinsic sorption of PHE.	phenanthrene	212-215	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-7
20404551-7	2010	Using these Msr enzymes in combination with peptide mapping, we were able to detect and differentiate diastereomers of methionine sulfoxide within the highly conserved heavy chain of an IgG2 that had been photo-oxidized, as well as those in an IgG1 oxidized with peroxide.	Peroxides	263-271	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	12-15
20404551-8	2010	The rapid identification of the stereospecificity of methionine oxidation by Msr enzymes not only definitively differentiates Met(O) diastereomers, which previously has been indistinguishable using traditional techniques, but also provides an important tool that may contribute to understanding of the mechanisms of protein oxidation and development of new formulation strategies to stabilize protein therapeutics.	Methionine	53-63	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	77-80
20218727-2	2010	Methionine is one of the most readily oxidized amino acids, and its oxidative state is regulated in vivo by the methionine sulfoxide reductases (Msr).	Methionine	0-10	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	112-143
20218727-2	2010	Methionine is one of the most readily oxidized amino acids, and its oxidative state is regulated in vivo by the methionine sulfoxide reductases (Msr).	Methionine	0-10	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	145-148
21045269-1	2010	This study aimed to investigate the role of maternal polymorphisms, as well as their risk genotypes combinations of MTR A2756G, MTRR A66G, CBS 844ins68, and RFC A80G, involved in folate/homocysteine metabolism, as possible risk factors for Down syndrome (DS) in Southern Brazil.	Folic Acid	179-185	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	128-132
19243433-0	2009	Cobalamin uptake and reactivation occurs through specific protein interactions in the methionine synthase-methionine synthase reductase complex.	Vitamin B 12	0-9	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	106-135
19558554-2	2009	It is readily oxidized to methionine-S-sulphoxide and methionine-R-sulphoxide, which can be reduced by methionine sulphoxide reductase (MSR) A and B, respectively.	methionine-s-sulphoxide	26-49	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	103-134
19558554-2	2009	It is readily oxidized to methionine-S-sulphoxide and methionine-R-sulphoxide, which can be reduced by methionine sulphoxide reductase (MSR) A and B, respectively.	methionine-r-sulphoxide	54-77	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	103-134
19348062-2	2009	Methionine Synthase Reductase (MTRR) is one of several key enzymes in the homocysteine metabolic pathway and its mutant forms have been implicated in abnormal homocysteine accumulation.	Homocysteine	74-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
19348062-2	2009	Methionine Synthase Reductase (MTRR) is one of several key enzymes in the homocysteine metabolic pathway and its mutant forms have been implicated in abnormal homocysteine accumulation.	Homocysteine	74-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
18682255-8	2009	Smaller effects were also seen for one-carbon metabolism genes choline dehydrogenase (CHDH) (rs9001, rs7626693) and 5-methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) (rs1801394) and genes involved in reduction reactions, glutaredoxin (GLRX) (rs3822751) and peroxiredoxin 2 (PRDX2) (rs10427027, rs12151144).	Carbon	39-45	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	154-181
18682255-8	2009	Smaller effects were also seen for one-carbon metabolism genes choline dehydrogenase (CHDH) (rs9001, rs7626693) and 5-methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) (rs1801394) and genes involved in reduction reactions, glutaredoxin (GLRX) (rs3822751) and peroxiredoxin 2 (PRDX2) (rs10427027, rs12151144).	Carbon	39-45	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	183-187
19394322-4	2009	RESULTS: MTHFR 677T, MTRR 66A, GCPII 1561T, male gender, alcohol intake, smoking, diabetes, creatinine and hypertension were found to influence tHcy.	thcy	144-148	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	21-25
19339913-2	2009	Methionine synthase reductase is the only human enzyme that is able to reverse the oxidation of vitamin B12, which also occurs naturally by reactive oxygen species.	Vitamin B 12	96-107	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
19339913-2	2009	Methionine synthase reductase is the only human enzyme that is able to reverse the oxidation of vitamin B12, which also occurs naturally by reactive oxygen species.	Reactive Oxygen Species	140-163	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
19243433-2	2009	Recently, it was also reported that MSR enhances uptake of cobalamin by apo-MS, a role associated with the MSR-catalysed reduction of exogenous aquacob(III)alamin to cob(II)alamin [Yamada K, Gravel RA, TorayaT & Matthews RG (2006) Proc Natl Acad Sci USA103, 9476-9481].	Vitamin B 12	59-68	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-39
19243433-2	2009	Recently, it was also reported that MSR enhances uptake of cobalamin by apo-MS, a role associated with the MSR-catalysed reduction of exogenous aquacob(III)alamin to cob(II)alamin [Yamada K, Gravel RA, TorayaT & Matthews RG (2006) Proc Natl Acad Sci USA103, 9476-9481].	Vitamin B 12	59-68	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	107-110
19243433-6	2009	Despite the ability of all three enzymes to reduce aquacob(III)alamin, only MSR (the full-length form or the isolated FMN domain) enhanced the uptake of cobalamin by apo-MS. MSR was also the only diflavin reductase to reactivate the inert cob(II)alamin form of purified human MS (K(act) of 107 nm) isolated from Pichia pastoris.	Vitamin B 12	153-162	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	76-79
19243433-6	2009	Despite the ability of all three enzymes to reduce aquacob(III)alamin, only MSR (the full-length form or the isolated FMN domain) enhanced the uptake of cobalamin by apo-MS. MSR was also the only diflavin reductase to reactivate the inert cob(II)alamin form of purified human MS (K(act) of 107 nm) isolated from Pichia pastoris.	Vitamin B 12	153-162	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	174-177
19243433-1	2009	Human methionine synthase reductase (MSR), a diflavin enzyme, restores the activity of human methionine synthase through reductive methylation of methionine synthase (MS)-bound cob(II)alamin.	diflavin	45-53	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	6-35
19243433-1	2009	Human methionine synthase reductase (MSR), a diflavin enzyme, restores the activity of human methionine synthase through reductive methylation of methionine synthase (MS)-bound cob(II)alamin.	diflavin	45-53	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-40
19243433-1	2009	Human methionine synthase reductase (MSR), a diflavin enzyme, restores the activity of human methionine synthase through reductive methylation of methionine synthase (MS)-bound cob(II)alamin.	cob(II)alamin	177-190	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	6-35
19243433-1	2009	Human methionine synthase reductase (MSR), a diflavin enzyme, restores the activity of human methionine synthase through reductive methylation of methionine synthase (MS)-bound cob(II)alamin.	cob(II)alamin	177-190	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-40
18715149-6	2009	Our results indicate that overexpression of the Msr enzymes, due to their antioxidant properties, counteracts the pro-oxidant effects of zinc treatment, which lead to a cellular protection against protein oxidative damage and cell death, by reducing the production of reactive oxygen species.	Reactive Oxygen Species	268-291	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	48-51
18602821-10	2009	The study shows a strong influence of folate status on Mtrr transcription in HepG2 cells.	Folic Acid	38-44	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	55-59
19823697-1	2009	Methionine oxidation by reactive oxygen species and reduction mediated by the methionine sulfoxide reductase (Msr) system may attenuate protein function in signal transduction pathways.	Methionine	0-10	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	78-108
19823697-1	2009	Methionine oxidation by reactive oxygen species and reduction mediated by the methionine sulfoxide reductase (Msr) system may attenuate protein function in signal transduction pathways.	Methionine	0-10	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	110-113
19823697-8	2009	Thus, the roles of oxidized-methionine residues and their reduction, by the Msr system, are discussed as potential regulators of cellular immune response.	Methionine	28-38	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	76-79
18980384-0	2008	Impeded electron transfer from a pathogenic FMN domain mutant of methionine synthase reductase and its responsiveness to flavin supplementation.	4,6-dinitro-o-cresol	121-127	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	65-94
19852428-5	2009	Molecular analysis of 12 genetic polymorphisms involved in the folate metabolism revealed that the mother is heterozygous for the MTHFR C677T and TC2 A67G polymorphisms, and homozygous for the mutant MTRR A66G polymorphism.	Folic Acid	63-69	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	200-204
18980384-1	2008	Methionine synthase reductase (MSR) is a diflavin oxidoreductase that transfers electrons from NADPH to oxidized cobalamin and plays a vital role in repairing inactive cobalamin-dependent methionine synthase.	NADP	95-100	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
18980384-1	2008	Methionine synthase reductase (MSR) is a diflavin oxidoreductase that transfers electrons from NADPH to oxidized cobalamin and plays a vital role in repairing inactive cobalamin-dependent methionine synthase.	NADP	95-100	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-34
18980384-5	2008	The A129T MSR mutant transfers electrons to ferricyanide as efficiently as wild type MSR but the rate of cytochrome c, 2,6-dichloroindophenol, and menadione reduction is decreased 10-15 fold.	hexacyanoferrate III	44-56	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	10-13
18980384-5	2008	The A129T MSR mutant transfers electrons to ferricyanide as efficiently as wild type MSR but the rate of cytochrome c, 2,6-dichloroindophenol, and menadione reduction is decreased 10-15 fold.	2,6-Dichloroindophenol	119-141	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	10-13
18980384-5	2008	The A129T MSR mutant transfers electrons to ferricyanide as efficiently as wild type MSR but the rate of cytochrome c, 2,6-dichloroindophenol, and menadione reduction is decreased 10-15 fold.	Vitamin K 3	147-156	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	10-13
18980384-9	2008	Together, our results reveal that the primary biochemical penalty associated with the A129T MSR mutant is its lower FMN content, provide insights into the distinct roles of the FAD and FMN centers in human MSR for delivering electrons to various electron acceptors, and suggest that patients harboring the A129T mutation may be responsive to riboflavin therapy.	Riboflavin	342-352	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	92-95
18792976-1	2008	Polymorphisms in the methylenetetrahydrofolate reductase (MTHFR), methionine synthase reductase (MTRR) and cystathionine beta-synthase (CBS) genes, involved in the intracellular metabolism of homocysteine (Hcy), can result in hyperhomocysteinemia.	Homocysteine	192-204	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	66-95
18792976-1	2008	Polymorphisms in the methylenetetrahydrofolate reductase (MTHFR), methionine synthase reductase (MTRR) and cystathionine beta-synthase (CBS) genes, involved in the intracellular metabolism of homocysteine (Hcy), can result in hyperhomocysteinemia.	Homocysteine	192-204	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	97-101
18792976-1	2008	Polymorphisms in the methylenetetrahydrofolate reductase (MTHFR), methionine synthase reductase (MTRR) and cystathionine beta-synthase (CBS) genes, involved in the intracellular metabolism of homocysteine (Hcy), can result in hyperhomocysteinemia.	Homocysteine	206-209	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	66-95
18792976-1	2008	Polymorphisms in the methylenetetrahydrofolate reductase (MTHFR), methionine synthase reductase (MTRR) and cystathionine beta-synthase (CBS) genes, involved in the intracellular metabolism of homocysteine (Hcy), can result in hyperhomocysteinemia.	Homocysteine	206-209	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	97-101
18034637-1	2008	BACKGROUND: The rationale behind this study was to examine the relationship between polymorphisms in genes that regulate remethylation of homocysteine to methionine, i.e., methionine synthase (MTR A2756G) and methionine synthase reductase (MTRR A66G), and risk of deep vein thrombosis (DVT) in a South Indian cohort (163 DVT cases and 163 controls), as elevated homocysteine has been documented as an independent risk factor for DVT in the same cohort.	Homocysteine	138-150	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	209-238
18843018-7	2008	In stratified analysis, effect of alcohol consumption on pancreatic cancer was observed in individuals with the MTHFR 667 CC, MTR 2756 AA, or MTRR 66 G allele.	Alcohols	34-41	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	142-146
18557976-12	2008	Our best hypothesis is that the presence of ROS-destroying enzymes such as peroxiredoxins and a lower dissolved O2 concentration in those msr-lacking organisms grown at high temperatures might account for the successful survival of these organisms under oxidative stress.	Reactive Oxygen Species	44-47	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	138-141
18557976-12	2008	Our best hypothesis is that the presence of ROS-destroying enzymes such as peroxiredoxins and a lower dissolved O2 concentration in those msr-lacking organisms grown at high temperatures might account for the successful survival of these organisms under oxidative stress.	Oxygen	112-114	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	138-141
17522601-0	2008	Association between decreased vitamin levels and MTHFR, MTR and MTRR gene polymorphisms as determinants for elevated total homocysteine concentrations in pregnant women.	Homocysteine	123-135	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	64-68
17522601-12	2008	The interaction between low levels of serum Cbl and MTHFR (C677T or A1298C) or MTRR A66G gene polymorphisms was associated with increased tHcy.	thcy	138-142	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	79-83
18174236-9	2008	In addition, interaction between the MTRR A66G polymorphism and folate intake for risk of postmenopausal breast cancer was observed (interaction P = 0.008).	Folic Acid	64-70	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-41
18515090-8	2008	Stable transfectants of the risk haplotype MTRR cDNA showed significantly elevated homocysteine levels in a culture medium, a lower level of the LINE-1 methylation, and a lower expression of the MTRR protein than did the transfectants with the wild-type haplotype cDNA.	Homocysteine	83-95	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	43-47
18515090-9	2008	CONCLUSIONS: Our study suggested a common missense SNP of the MTRR gene as a novel pancreatic cancer susceptibility factor with a functional significance in folate-related metabolism and the genome-wide methylation status.	Folic Acid	157-163	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	62-66
18774994-8	2008	The MTRR 66GG and MTHFR 1298 CC genotypes may confer protection against early nephropathy, possibly because they are associated with lower tHcy.	thcy	139-143	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-8
18614746-9	2008	We found a significant interaction between MTHFR 677C-->T and MTRR 66A-->G on serum homocysteine concentrations among non-Hispanic whites.	Homocysteine	90-102	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	65-69
18302927-2	2008	Methionine sulfoxide reductases (Msr) are ubiquitous enzymes, which catalyze the reduction of the sulfoxide function of the oxidized methionine residues.	sulfoxide	11-20	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	33-36
18302927-2	2008	Methionine sulfoxide reductases (Msr) are ubiquitous enzymes, which catalyze the reduction of the sulfoxide function of the oxidized methionine residues.	Methionine	133-143	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-31
18302927-2	2008	Methionine sulfoxide reductases (Msr) are ubiquitous enzymes, which catalyze the reduction of the sulfoxide function of the oxidized methionine residues.	Methionine	133-143	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	33-36
18226574-13	2008	In conclusion, MTRR 66 GG and TC 776 GG genotypes in mothers and children may contribute to the risk of CHDs, particularly when the maternal vitamin B12 status is low.	Vitamin B 12	141-152	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	15-19
18034637-1	2008	BACKGROUND: The rationale behind this study was to examine the relationship between polymorphisms in genes that regulate remethylation of homocysteine to methionine, i.e., methionine synthase (MTR A2756G) and methionine synthase reductase (MTRR A66G), and risk of deep vein thrombosis (DVT) in a South Indian cohort (163 DVT cases and 163 controls), as elevated homocysteine has been documented as an independent risk factor for DVT in the same cohort.	Homocysteine	138-150	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	240-244
18034637-8	2008	A positive association was observed between plasma homocysteine and the MTRR G allele, and the MTR G allele was shown to have an additive effect.	Homocysteine	51-63	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	72-76
17376725-4	2007	We further evaluated whether homocysteine levels differed between cases and controls for MTRR and BHMT genotypes.	Homocysteine	29-41	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	89-93
18050048-1	2007	INTRODUCTION: Defects of methionine synthase or methionine synthase reductase result in an impaired remethylation of homocysteine to methionine.	Homocysteine	117-129	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	48-77
17892308-2	2007	MSR contains one FAD and one FMN cofactor per polypeptide and functions in the sequential transfer of reducing equivalents from NADPH to MS via its flavin centers.	Flavin-Adenine Dinucleotide	17-20	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
17892308-2	2007	MSR contains one FAD and one FMN cofactor per polypeptide and functions in the sequential transfer of reducing equivalents from NADPH to MS via its flavin centers.	NADP	128-133	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
17892308-2	2007	MSR contains one FAD and one FMN cofactor per polypeptide and functions in the sequential transfer of reducing equivalents from NADPH to MS via its flavin centers.	4,6-dinitro-o-cresol	148-154	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
17892308-3	2007	We report the 1.9 A crystal structure of the NADP+-bound FNR-like module of MSR that spans the NADP(H)-binding domain, the FAD-binding domain, the connecting domain, and part of the extended hinge region, a feature unique to MSR.	NADP	45-50	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	76-79
17892308-3	2007	We report the 1.9 A crystal structure of the NADP+-bound FNR-like module of MSR that spans the NADP(H)-binding domain, the FAD-binding domain, the connecting domain, and part of the extended hinge region, a feature unique to MSR.	NADP	45-50	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	225-228
17892308-3	2007	We report the 1.9 A crystal structure of the NADP+-bound FNR-like module of MSR that spans the NADP(H)-binding domain, the FAD-binding domain, the connecting domain, and part of the extended hinge region, a feature unique to MSR.	NADP	95-102	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	76-79
17892308-5	2007	However, the extended hinge region of MSR, which is positioned between the NADP(H)/FAD- and FMN-binding domains, is in an unexpected orientation with potential implications for the mechanism of electron transfer.	NADP	75-82	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	38-41
17892308-5	2007	However, the extended hinge region of MSR, which is positioned between the NADP(H)/FAD- and FMN-binding domains, is in an unexpected orientation with potential implications for the mechanism of electron transfer.	Flavin-Adenine Dinucleotide	83-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	38-41
17892308-8	2007	Isothermal titration calorimetry reveals a binding constant of 37 and 2 microM for binding of NADP+ and 2",5"-ADP, respectively, for the ligand-protein complex formed with full-length MSR or the isolated FNR module.	NADP	94-99	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	184-187
17892308-8	2007	Isothermal titration calorimetry reveals a binding constant of 37 and 2 microM for binding of NADP+ and 2",5"-ADP, respectively, for the ligand-protein complex formed with full-length MSR or the isolated FNR module.	adenosine 2',5'-diphosphate	104-113	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	184-187
17892308-10	2007	The relatively weaker binding of NADP+ to MSR compared with other members of the diflavin oxidoreductase family might arise from unique electrostatic repulsive forces near the 5"-pyrophosphate moiety and/or increased hydrophobic stacking between Trp697 and the re face of the FAD isoalloxazine ring.	NADP	33-37	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	42-45
17892308-10	2007	The relatively weaker binding of NADP+ to MSR compared with other members of the diflavin oxidoreductase family might arise from unique electrostatic repulsive forces near the 5"-pyrophosphate moiety and/or increased hydrophobic stacking between Trp697 and the re face of the FAD isoalloxazine ring.	5"-pyrophosphate	176-192	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	42-45
17892308-10	2007	The relatively weaker binding of NADP+ to MSR compared with other members of the diflavin oxidoreductase family might arise from unique electrostatic repulsive forces near the 5"-pyrophosphate moiety and/or increased hydrophobic stacking between Trp697 and the re face of the FAD isoalloxazine ring.	fad isoalloxazine	276-293	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	42-45
17892308-12	2007	The biological implications of an attenuated mechanism of MS reactivation by MSR on methionine and folate metabolism are discussed.	Methionine	84-94	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	77-80
17892308-12	2007	The biological implications of an attenuated mechanism of MS reactivation by MSR on methionine and folate metabolism are discussed.	Folic Acid	99-105	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	77-80
17596206-2	2007	Functional polymorphisms in genes encoding one-carbon metabolism enzymes, such as methylenetetrahydrofolate reductase (MTHFR C677T and A1298C), methionine synthase (MTR A2756G), methionine synthase reductase (MTRR A66G) and thymidylate synthase (TS), influence folate metabolism and thus might impact on HNSCC risk.	Carbon	47-53	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	178-207
17611986-0	2007	2756GG genotype of methionine synthase reductase gene is more prevalent in rheumatoid arthritis patients treated with methotrexate and is associated with methotrexate-induced nodulosis.	Methotrexate	118-130	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	19-48
17611986-0	2007	2756GG genotype of methionine synthase reductase gene is more prevalent in rheumatoid arthritis patients treated with methotrexate and is associated with methotrexate-induced nodulosis.	Methotrexate	154-166	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	19-48
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	Methotrexate	174-186	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	77-106
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	Methotrexate	174-186	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	108-111
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	Methotrexate	188-191	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	77-106
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	Methotrexate	188-191	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	108-111
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	Homocysteine	309-321	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	77-106
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	Homocysteine	309-321	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	108-111
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	thcy	323-327	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	77-106
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	thcy	323-327	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	108-111
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	Folic Acid	336-342	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	77-106
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	Folic Acid	336-342	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	108-111
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	Vitamin B 12	347-358	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	77-106
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	Vitamin B 12	347-358	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	108-111
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	Methotrexate	389-392	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	77-106
17611986-1	2007	OBJECTIVE: To investigate the distribution of the A2756G polymorphism of the methionine synthase reductase (MTR) gene in patients with rheumatoid arthritis (RA) treated with methotrexate (MTX) compared with a healthy control group; and to examine the relationships among the A2756G polymorphism, plasma total homocysteine (tHcy), serum folate and vitamin B12 levels, disease activity, and MTX toxicity in patients with RA.	Methotrexate	389-392	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	108-111
17611986-11	2007	CONCLUSION: In our population of MTX-treated RA patients the 2756GG genotype of the MTR gene was more common than expected and was associated with MIARN.	Methotrexate	33-36	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	84-87
17938273-2	2008	Two stable diastereomers of Met sulfoxide [Met-(O)] may be formed [Met-S-(O) and Met-R-(O)], but these can be reduced by two classes of Methionine-sulfoxide-reductase (Msr) enzymes: MsrA, which reduces the S, and MsrB, which reduces the R sulfoxide.	methionine sulfoxide	28-41	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	136-166
17938273-2	2008	Two stable diastereomers of Met sulfoxide [Met-(O)] may be formed [Met-S-(O) and Met-R-(O)], but these can be reduced by two classes of Methionine-sulfoxide-reductase (Msr) enzymes: MsrA, which reduces the S, and MsrB, which reduces the R sulfoxide.	methionine sulfoxide	28-41	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	168-171
17938273-2	2008	Two stable diastereomers of Met sulfoxide [Met-(O)] may be formed [Met-S-(O) and Met-R-(O)], but these can be reduced by two classes of Methionine-sulfoxide-reductase (Msr) enzymes: MsrA, which reduces the S, and MsrB, which reduces the R sulfoxide.	sulfoxide	32-41	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	136-166
17938273-2	2008	Two stable diastereomers of Met sulfoxide [Met-(O)] may be formed [Met-S-(O) and Met-R-(O)], but these can be reduced by two classes of Methionine-sulfoxide-reductase (Msr) enzymes: MsrA, which reduces the S, and MsrB, which reduces the R sulfoxide.	sulfoxide	32-41	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	168-171
17883856-2	2007	Zn homeostasis influences development and function of immune cells, activity of stress-related and antioxidant proteins [metallothioneins (MT), chaperones, ApoJ, Poly(ADP-Ribose) polymerase-1 (PARP-1) and Methionione Sulfoxide Reductase (Msr), Superoxide Dismutase (SOD)], and helps to maintain genomic integrity and stability.	Zinc	0-2	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	205-236
17883856-2	2007	Zn homeostasis influences development and function of immune cells, activity of stress-related and antioxidant proteins [metallothioneins (MT), chaperones, ApoJ, Poly(ADP-Ribose) polymerase-1 (PARP-1) and Methionione Sulfoxide Reductase (Msr), Superoxide Dismutase (SOD)], and helps to maintain genomic integrity and stability.	Zinc	0-2	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	238-241
17636160-11	2007	This was twice the total genetic contribution of 4.56%, and only the C1763T SNP of MTRR showed significant association with homocysteine.	Homocysteine	124-136	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	83-87
17389618-6	2007	In addition, the methionine synthase reductase (MTRR) Arg415Cys and MTRR Ser284Thr variant carriers, also in the vitamin B(12) pathway, have suggestive associations with advanced colorectal adenoma (defined as being larger than 1 cm, villous, tubular-villous or carcinoma in situ histology).	Niacinamide	113-122	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	17-46
17389618-6	2007	In addition, the methionine synthase reductase (MTRR) Arg415Cys and MTRR Ser284Thr variant carriers, also in the vitamin B(12) pathway, have suggestive associations with advanced colorectal adenoma (defined as being larger than 1 cm, villous, tubular-villous or carcinoma in situ histology).	Niacinamide	113-122	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	48-52
17389618-6	2007	In addition, the methionine synthase reductase (MTRR) Arg415Cys and MTRR Ser284Thr variant carriers, also in the vitamin B(12) pathway, have suggestive associations with advanced colorectal adenoma (defined as being larger than 1 cm, villous, tubular-villous or carcinoma in situ histology).	Niacinamide	113-122	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	68-72
17477549-4	2007	The C-terminal activation domain also interacts with methionine synthase reductase (MSR), a NADPH-dependent diflavin oxidoreductase required for the reductive regeneration of catalytically inert cob(II)alamin (which is formed every 200-1000 catalytic cycles of MS) to cob(I)alamin.	Vitamin B 12	268-280	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	53-82
17477549-4	2007	The C-terminal activation domain also interacts with methionine synthase reductase (MSR), a NADPH-dependent diflavin oxidoreductase required for the reductive regeneration of catalytically inert cob(II)alamin (which is formed every 200-1000 catalytic cycles of MS) to cob(I)alamin.	Vitamin B 12	268-280	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	84-87
17477549-5	2007	We have investigated complex formation between the (i) MS activation domain and MSR and (ii) MS activation domain and the isolated FMN-binding domain of MSR.	Flavin Mononucleotide	131-134	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	153-156
17144657-1	2006	Methionines can play an important role in modulating protein-protein interactions associated with intracellular signaling, and their reversible oxidation to form methionine sulfoxides [Met(O)] in calmodulin (CaM) and other signaling proteins has been suggested to couple cellular redox changes to protein functional changes through the action of methionine sulfoxide reductases (Msr).	Methionine	0-11	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	346-377
17113603-3	2007	Methionine synthase reductase (MTRR) is an enzyme that catalyzes the remethylation of homocysteine (Hcy) to methionine via cobalamin and folate dependant reactions.	Homocysteine	86-98	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
17113603-3	2007	Methionine synthase reductase (MTRR) is an enzyme that catalyzes the remethylation of homocysteine (Hcy) to methionine via cobalamin and folate dependant reactions.	Homocysteine	86-98	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
17113603-3	2007	Methionine synthase reductase (MTRR) is an enzyme that catalyzes the remethylation of homocysteine (Hcy) to methionine via cobalamin and folate dependant reactions.	Homocysteine	100-103	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
17113603-3	2007	Methionine synthase reductase (MTRR) is an enzyme that catalyzes the remethylation of homocysteine (Hcy) to methionine via cobalamin and folate dependant reactions.	Homocysteine	100-103	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
17113603-3	2007	Methionine synthase reductase (MTRR) is an enzyme that catalyzes the remethylation of homocysteine (Hcy) to methionine via cobalamin and folate dependant reactions.	Methionine	108-118	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
17113603-3	2007	Methionine synthase reductase (MTRR) is an enzyme that catalyzes the remethylation of homocysteine (Hcy) to methionine via cobalamin and folate dependant reactions.	Methionine	108-118	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
17113603-3	2007	Methionine synthase reductase (MTRR) is an enzyme that catalyzes the remethylation of homocysteine (Hcy) to methionine via cobalamin and folate dependant reactions.	Vitamin B 12	123-132	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
17113603-3	2007	Methionine synthase reductase (MTRR) is an enzyme that catalyzes the remethylation of homocysteine (Hcy) to methionine via cobalamin and folate dependant reactions.	Vitamin B 12	123-132	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
17113603-3	2007	Methionine synthase reductase (MTRR) is an enzyme that catalyzes the remethylation of homocysteine (Hcy) to methionine via cobalamin and folate dependant reactions.	Folic Acid	137-143	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
17113603-3	2007	Methionine synthase reductase (MTRR) is an enzyme that catalyzes the remethylation of homocysteine (Hcy) to methionine via cobalamin and folate dependant reactions.	Folic Acid	137-143	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
17144657-1	2006	Methionines can play an important role in modulating protein-protein interactions associated with intracellular signaling, and their reversible oxidation to form methionine sulfoxides [Met(O)] in calmodulin (CaM) and other signaling proteins has been suggested to couple cellular redox changes to protein functional changes through the action of methionine sulfoxide reductases (Msr).	Methionine	0-11	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	379-382
17144657-1	2006	Methionines can play an important role in modulating protein-protein interactions associated with intracellular signaling, and their reversible oxidation to form methionine sulfoxides [Met(O)] in calmodulin (CaM) and other signaling proteins has been suggested to couple cellular redox changes to protein functional changes through the action of methionine sulfoxide reductases (Msr).	methionine sulfoxide	162-183	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	346-377
17144657-1	2006	Methionines can play an important role in modulating protein-protein interactions associated with intracellular signaling, and their reversible oxidation to form methionine sulfoxides [Met(O)] in calmodulin (CaM) and other signaling proteins has been suggested to couple cellular redox changes to protein functional changes through the action of methionine sulfoxide reductases (Msr).	methionine sulfoxide	162-183	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	379-382
16861746-1	2006	BACKGROUND: Three typical folate metabolism enzymes-i.e. methylenetetrahydrofolate reductase (MTHFR), methionine synthase (MS) and MS reductase (MTRR) in the folate cycle-play a critical role in DNA synthesis and methylation reactions.	Folic Acid	26-32	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	145-149
16985020-5	2006	Furthermore, a significant reduction in recurrence risk was seen in MTRR A66G heterozygotes who received folate supplements but not in those who did not receive folate.	Folic Acid	105-111	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	68-72
17024475-1	2006	The methionine synthase reductase (MTRR) enzyme restores methionine synthase (MTR) enzyme activity and therefore plays an essential role in homocysteine remethylation.	Homocysteine	140-152	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-33
17024475-1	2006	The methionine synthase reductase (MTRR) enzyme restores methionine synthase (MTR) enzyme activity and therefore plays an essential role in homocysteine remethylation.	Homocysteine	140-152	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-39
17024475-10	2006	Moreover, we demonstrate a possible interaction between the MTRR 66GG genotype and high plasma MMA levels (OR 5.5, 95% CI 2.2-13.5).	Methylmalonic Acid	95-98	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	60-64
17024475-12	2006	These data show that the MTRR 66GG genotype is a maternal risk factor for spina bifida especially when intracellular vitamin B12 status is low.	Vitamin B 12	117-128	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	25-29
17079868-2	2006	Methionine synthase reductase (MTRR) is an enzyme involved in the conversion of Hcy to methionine.	Homocysteine	80-83	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
17079868-2	2006	Methionine synthase reductase (MTRR) is an enzyme involved in the conversion of Hcy to methionine.	Homocysteine	80-83	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
17079868-2	2006	Methionine synthase reductase (MTRR) is an enzyme involved in the conversion of Hcy to methionine.	Methionine	87-97	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
17079868-2	2006	Methionine synthase reductase (MTRR) is an enzyme involved in the conversion of Hcy to methionine.	Methionine	87-97	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
16769880-10	2006	Apoenzyme alone is quite unstable at 37 degrees C. MSR also is able to reduce aquacobalamin to cob(II)alamin in the presence of NADPH, and this reduction leads to stimulation of the conversion of apoMS and aquacobalamin to MS holoenzyme.	cob(II)alamin	95-108	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	51-54
16774207-3	2006	Recent investigations on the Msr mechanism have clearly shown that a sulfenic acid intermediate is formed on the catalytic cysteine of the active site concomitantly to the methionine product.	Sulfenic Acids	69-82	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	29-32
16774207-3	2006	Recent investigations on the Msr mechanism have clearly shown that a sulfenic acid intermediate is formed on the catalytic cysteine of the active site concomitantly to the methionine product.	Cysteine	123-131	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	29-32
16774207-3	2006	Recent investigations on the Msr mechanism have clearly shown that a sulfenic acid intermediate is formed on the catalytic cysteine of the active site concomitantly to the methionine product.	Methionine	172-182	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	29-32
16846473-5	2006	Inborn errors of cobalamin metabolism affect its absorption, (intrinsic factor deficiency, Imerslund-Grasbeck syndrome) and transport (transcobalamin deficiency) as well as its intracellular metabolism affecting adenosylcobalamin synthesis (cblA and cblB), methionine synthase function (cblE and cblG) or both (cblC, cblD and cblF).	Vitamin B 12	17-26	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	287-291
16769880-10	2006	Apoenzyme alone is quite unstable at 37 degrees C. MSR also is able to reduce aquacobalamin to cob(II)alamin in the presence of NADPH, and this reduction leads to stimulation of the conversion of apoMS and aquacobalamin to MS holoenzyme.	NADP	128-133	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	51-54
16485733-0	2006	Influence of methionine synthase (A2756G) and methionine synthase reductase (A66G) polymorphisms on plasma homocysteine levels and relation to risk of coronary artery disease.	Homocysteine	107-119	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	46-75
16735467-7	2006	The results indicate that thionein (T), which is formed when the zinc is removed from Zn-MT, can function as a reducing system for the Msr proteins because of its high content of cysteine residues and that Trx can reduce oxidized T.	Cysteine	179-187	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	135-138
16735467-1	2006	It has been generally accepted, primarily from studies on methionine sulfoxide reductase (Msr) A, that the biological reducing agent for the members of the Msr family is reduced thioredoxin (Trx), although high levels of DTT can be used as the reductant in vitro.	Dithiothreitol	221-224	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	156-159
16735467-7	2006	The results indicate that thionein (T), which is formed when the zinc is removed from Zn-MT, can function as a reducing system for the Msr proteins because of its high content of cysteine residues and that Trx can reduce oxidized T.	Lys-Cys-Thr-Cys-Cys-Ala	26-34	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	135-138
16485733-12	2006	This study provides evidence that the MTR A2756G and MTRR A66G polymorphisms significantly influence the circulating homocysteine concentration.	Homocysteine	117-129	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	53-57
15797993-5	2005	Patients with the MTHFR 1298AC variant or the MTRR 66 G-allele showed decreased in vitro MTX sensitivity measured under both test conditions.	Methotrexate	89-92	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	46-50
16169148-1	2006	Altered maternal folate status and homozygous mutation in the methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) genes can promote chromosomal instability and non-dysjunction resulting in fetal trisomy 21.	Folic Acid	17-23	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	141-145
17087642-2	2006	The methionine synthase reductase (MTRR) enzyme restores methionine synthase (MTR) enzyme activity and therefore plays an essential role in the folate- and vitamin B(12)-dependent remethylation of homocysteine to methionine.	Folic Acid	144-150	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-33
17087642-2	2006	The methionine synthase reductase (MTRR) enzyme restores methionine synthase (MTR) enzyme activity and therefore plays an essential role in the folate- and vitamin B(12)-dependent remethylation of homocysteine to methionine.	Folic Acid	144-150	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-39
17087642-2	2006	The methionine synthase reductase (MTRR) enzyme restores methionine synthase (MTR) enzyme activity and therefore plays an essential role in the folate- and vitamin B(12)-dependent remethylation of homocysteine to methionine.	Niacinamide	156-165	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-33
17087642-2	2006	The methionine synthase reductase (MTRR) enzyme restores methionine synthase (MTR) enzyme activity and therefore plays an essential role in the folate- and vitamin B(12)-dependent remethylation of homocysteine to methionine.	Niacinamide	156-165	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-39
17087642-2	2006	The methionine synthase reductase (MTRR) enzyme restores methionine synthase (MTR) enzyme activity and therefore plays an essential role in the folate- and vitamin B(12)-dependent remethylation of homocysteine to methionine.	Homocysteine	197-209	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-33
17087642-2	2006	The methionine synthase reductase (MTRR) enzyme restores methionine synthase (MTR) enzyme activity and therefore plays an essential role in the folate- and vitamin B(12)-dependent remethylation of homocysteine to methionine.	Homocysteine	197-209	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-39
17087642-2	2006	The methionine synthase reductase (MTRR) enzyme restores methionine synthase (MTR) enzyme activity and therefore plays an essential role in the folate- and vitamin B(12)-dependent remethylation of homocysteine to methionine.	Methionine	4-14	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-39
17087642-11	2006	Maternal MTRR 66GG genotype with compromised vitamin B(12) status may possibly result in increased CHD risk.	Niacinamide	45-54	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	9-13
17101561-1	2006	The MTRR gene codes for methionine synthase reductase, one of the enzymes involved in the conversion of homocysteine to methionine.	Homocysteine	104-116	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-8
17101561-1	2006	The MTRR gene codes for methionine synthase reductase, one of the enzymes involved in the conversion of homocysteine to methionine.	Homocysteine	104-116	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	24-53
17101561-1	2006	The MTRR gene codes for methionine synthase reductase, one of the enzymes involved in the conversion of homocysteine to methionine.	Methionine	24-34	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-8
16257642-3	2005	Repair is limited to the reversion of a few modifications such as the reduction of methionine oxidation by the methionine sulfoxide reductase (Msr) system.	Methionine	83-93	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	111-141
16257642-3	2005	Repair is limited to the reversion of a few modifications such as the reduction of methionine oxidation by the methionine sulfoxide reductase (Msr) system.	Methionine	83-93	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	143-146
15797993-7	2005	In conclusion, polymorphisms in the folate-related genes MTHFR, MTRR, and SHMT1 are related to MTX resistance in pediatric patients with ALL.	Methotrexate	95-98	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	64-68
15612980-6	2005	MTRR A66G was also correlated with serum folate.	Folic Acid	41-47	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-4
15931548-1	2005	BACKGROUND: Isolated functional methionine synthase deficiency occurs in the cblE and cblG defects of methylcobalamin metabolism and is one of a number of causes of severely elevated plasma homocysteine.	mecobalamin	102-117	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	77-81
15680231-1	2005	The methionine sulfoxide reductase (Msr) family is composed of two structurally unrelated classes of monomeric enzymes named MsrA and MsrB, which display opposite stereo-selectivities towards the sulfoxide function.	sulfoxide	15-24	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-39
15680231-3	2005	The mechanism includes three steps with (1) formation of a sulfenic acid intermediate with a concomitant release of 1 mol of methionine per mol of enzyme; (2) formation of an intramonomeric disulfide Msr bond followed by; (3) reduction of the oxidized Msr by thioredoxin (Trx).	Sulfenic Acids	59-72	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	200-203
15680231-3	2005	The mechanism includes three steps with (1) formation of a sulfenic acid intermediate with a concomitant release of 1 mol of methionine per mol of enzyme; (2) formation of an intramonomeric disulfide Msr bond followed by; (3) reduction of the oxidized Msr by thioredoxin (Trx).	Sulfenic Acids	59-72	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	252-255
15680231-3	2005	The mechanism includes three steps with (1) formation of a sulfenic acid intermediate with a concomitant release of 1 mol of methionine per mol of enzyme; (2) formation of an intramonomeric disulfide Msr bond followed by; (3) reduction of the oxidized Msr by thioredoxin (Trx).	Methionine	125-135	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	200-203
15680231-3	2005	The mechanism includes three steps with (1) formation of a sulfenic acid intermediate with a concomitant release of 1 mol of methionine per mol of enzyme; (2) formation of an intramonomeric disulfide Msr bond followed by; (3) reduction of the oxidized Msr by thioredoxin (Trx).	Methionine	125-135	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	252-255
15680231-3	2005	The mechanism includes three steps with (1) formation of a sulfenic acid intermediate with a concomitant release of 1 mol of methionine per mol of enzyme; (2) formation of an intramonomeric disulfide Msr bond followed by; (3) reduction of the oxidized Msr by thioredoxin (Trx).	Disulfides	190-199	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	200-203
15680231-3	2005	The mechanism includes three steps with (1) formation of a sulfenic acid intermediate with a concomitant release of 1 mol of methionine per mol of enzyme; (2) formation of an intramonomeric disulfide Msr bond followed by; (3) reduction of the oxidized Msr by thioredoxin (Trx).	Disulfides	190-199	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	252-255
15652901-8	2005	RESULT(S): Prolactin release in response to fenfluramine was significantly greater in the HSR group compared with the MSR or SS groups.	Fenfluramine	44-56	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	118-121
15979034-1	2005	Methionine synthase reductase (MTRR) regenerates methylated cobalamin levels from the oxidised cob(II)alamin form and in so doing plays a crucial role in maintaining the active state of methionine synthase (MTR).	Vitamin B 12	60-69	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
15979034-1	2005	Methionine synthase reductase (MTRR) regenerates methylated cobalamin levels from the oxidised cob(II)alamin form and in so doing plays a crucial role in maintaining the active state of methionine synthase (MTR).	Vitamin B 12	60-69	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
15979034-1	2005	Methionine synthase reductase (MTRR) regenerates methylated cobalamin levels from the oxidised cob(II)alamin form and in so doing plays a crucial role in maintaining the active state of methionine synthase (MTR).	cob(II)alamin	95-108	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
15979034-1	2005	Methionine synthase reductase (MTRR) regenerates methylated cobalamin levels from the oxidised cob(II)alamin form and in so doing plays a crucial role in maintaining the active state of methionine synthase (MTR).	cob(II)alamin	95-108	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
15979034-3	2005	Single nucleotide polymorphisms (SNPs) within the MTRR gene may potentially compromise MTR activity leading to elevated homocysteine levels, a known risk factor for neural tube defects (NTDs).	Homocysteine	120-132	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	50-54
15714522-10	2005	Importantly, transfection of fibroblasts of cblE patients with a wild-type MTRR minigene expression construct resulted in a significant approximately four-fold increase of methionine synthesis, indicating correction of the enzyme defect.	Methionine	172-182	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	44-48
15714522-10	2005	Importantly, transfection of fibroblasts of cblE patients with a wild-type MTRR minigene expression construct resulted in a significant approximately four-fold increase of methionine synthesis, indicating correction of the enzyme defect.	Methionine	172-182	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	75-79
15735045-6	2005	The ratio of MS to MSR varied over a 5-fold range in the different cell types, which may modulate methionine synthesis.	Methionine	98-108	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	19-22
15680219-4	2005	In vivo, methionine sulfoxide is subject to reduction by the methionine sulfoxide reductase (Msr) system, suggesting that some methionine sulfoxide residues may only be transiently involved in the deactivation of proteins through reactive oxygen species (ROS).	methionine sulfoxide	9-29	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	61-91
15680219-4	2005	In vivo, methionine sulfoxide is subject to reduction by the methionine sulfoxide reductase (Msr) system, suggesting that some methionine sulfoxide residues may only be transiently involved in the deactivation of proteins through reactive oxygen species (ROS).	methionine sulfoxide	9-29	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	93-96
15680219-4	2005	In vivo, methionine sulfoxide is subject to reduction by the methionine sulfoxide reductase (Msr) system, suggesting that some methionine sulfoxide residues may only be transiently involved in the deactivation of proteins through reactive oxygen species (ROS).	methionine sulfoxide	61-81	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	93-96
15680219-4	2005	In vivo, methionine sulfoxide is subject to reduction by the methionine sulfoxide reductase (Msr) system, suggesting that some methionine sulfoxide residues may only be transiently involved in the deactivation of proteins through reactive oxygen species (ROS).	Reactive Oxygen Species	230-253	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	61-91
15680219-4	2005	In vivo, methionine sulfoxide is subject to reduction by the methionine sulfoxide reductase (Msr) system, suggesting that some methionine sulfoxide residues may only be transiently involved in the deactivation of proteins through reactive oxygen species (ROS).	Reactive Oxygen Species	230-253	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	93-96
15680219-4	2005	In vivo, methionine sulfoxide is subject to reduction by the methionine sulfoxide reductase (Msr) system, suggesting that some methionine sulfoxide residues may only be transiently involved in the deactivation of proteins through reactive oxygen species (ROS).	Reactive Oxygen Species	255-258	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	61-91
15680219-4	2005	In vivo, methionine sulfoxide is subject to reduction by the methionine sulfoxide reductase (Msr) system, suggesting that some methionine sulfoxide residues may only be transiently involved in the deactivation of proteins through reactive oxygen species (ROS).	Reactive Oxygen Species	255-258	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	93-96
15680219-5	2005	Other methionine sulfoxide residues may accumulate, depending on the accessibility to Msr.	methionine sulfoxide	6-26	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	86-89
15680219-6	2005	Moreover, methionine sulfoxide levels may increase as a result of a lower abundance of active Msr and/or the required cofactors as a consequence of pathologies and biological aging.	methionine sulfoxide	10-30	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	94-97
16351505-9	2005	MTRR polymorphism interacted with the association of folate (P for interaction = 0.04) or vitamin (P for interaction = 0.02) with colorectal cancer, although the other polymorphisms did not interact with any nutrient intake.	Folic Acid	53-59	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-4
15612980-9	2005	Differences in cobalamin and folate levels with the MTRR A66G and MS A2756G polymorphisms were noted.	Vitamin B 12	15-24	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	52-56
15612980-9	2005	Differences in cobalamin and folate levels with the MTRR A66G and MS A2756G polymorphisms were noted.	Folic Acid	29-35	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	52-56
15347655-6	2004	Investigations also showed that purified recombinant human methionine synthase reductase (MSR) in combination with purified ATR can convert cob(II)alamin to AdoCbl in vitro.	cob(II)alamin	140-153	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	59-88
15347655-9	2004	The finding that MSR reduced cob(II)alamin to cob(I)alamin for AdoCbl synthesis (in conjunction with the prior finding that MSR reduced cob(II)alamin for the activation of methionine synthase) indicates a dual physiological role for MSR.	cob(II)alamin	29-42	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	17-20
15347655-9	2004	The finding that MSR reduced cob(II)alamin to cob(I)alamin for AdoCbl synthesis (in conjunction with the prior finding that MSR reduced cob(II)alamin for the activation of methionine synthase) indicates a dual physiological role for MSR.	Vitamin B 12	46-58	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	17-20
15347655-6	2004	Investigations also showed that purified recombinant human methionine synthase reductase (MSR) in combination with purified ATR can convert cob(II)alamin to AdoCbl in vitro.	cob(II)alamin	140-153	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	90-93
15347655-9	2004	The finding that MSR reduced cob(II)alamin to cob(I)alamin for AdoCbl synthesis (in conjunction with the prior finding that MSR reduced cob(II)alamin for the activation of methionine synthase) indicates a dual physiological role for MSR.	cob(II)alamin	136-149	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	124-127
15347655-9	2004	The finding that MSR reduced cob(II)alamin to cob(I)alamin for AdoCbl synthesis (in conjunction with the prior finding that MSR reduced cob(II)alamin for the activation of methionine synthase) indicates a dual physiological role for MSR.	cob(II)alamin	136-149	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	124-127
15514263-0	2004	Methionine synthase reductase 66A->G polymorphism is associated with increased plasma homocysteine concentration when combined with the homozygous methylenetetrahydrofolate reductase 677C->T variant.	Homocysteine	89-101	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
15514263-1	2004	Methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) are important for homocysteine remethylation.	Homocysteine	103-115	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	48-77
15182370-2	2004	This is replaced by Trp676 in human cytochrome P450 reductase, a tryptophan in related diflavin reductases (e.g. methionine synthase reductase and novel reductase 1), and tyrosine in plant ferredoxin-NADP(+) reductase.	Tryptophan	65-75	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	113-142
15514263-1	2004	Methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) are important for homocysteine remethylation.	Homocysteine	103-115	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	79-83
15514263-5	2004	Women with the MTHFR 677 TT/MTRR 66 AG genotype had higher (P < 0.05) plasma homocysteine than all other genotype combinations except the TT/AA and TT/GG genotypes.	Homocysteine	80-92	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	28-32
15514263-9	2004	The potential negative effect of combined polymorphisms of the MTHFR and MTRR genes on plasma homocysteine in at-risk population groups with low folate and/or vitamin B-12 status, such as women of reproductive potential, deserves further investigation.	Homocysteine	94-106	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	73-77
14967039-1	2004	Human methionine synthase reductase (MSR) is a protein containing both FAD and FMN, and it reactivates methionine synthase that has lost activity due to oxidation of cob(I)alamin to cob(II)alamin.	Flavin-Adenine Dinucleotide	71-74	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	6-35
15135249-1	2004	The association of variants of the gene encoding methionine synthase reductase (MTRR) with hyperhomocysteinemia, folate and Vitamin B(12) status in kidney graft recipients is unknown.	Folic Acid	113-119	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	49-78
15135249-1	2004	The association of variants of the gene encoding methionine synthase reductase (MTRR) with hyperhomocysteinemia, folate and Vitamin B(12) status in kidney graft recipients is unknown.	Folic Acid	113-119	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	80-84
15135249-1	2004	The association of variants of the gene encoding methionine synthase reductase (MTRR) with hyperhomocysteinemia, folate and Vitamin B(12) status in kidney graft recipients is unknown.	Niacinamide	124-133	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	49-78
15135249-1	2004	The association of variants of the gene encoding methionine synthase reductase (MTRR) with hyperhomocysteinemia, folate and Vitamin B(12) status in kidney graft recipients is unknown.	Niacinamide	124-133	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	80-84
15154797-8	2004	DFT is used to explore surface intermediates and the transition state in the methanol synthesis reaction (MSR).	Methanol	77-85	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	106-109
15154797-20	2004	The rearrangement of trans-HCOH (carbon bound) to CH(2)O (oxygen bound) on ZnO(0001) was calculated to be the overall barrier of the MSR reaction.	trans-hcoh	21-31	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	133-136
15154797-20	2004	The rearrangement of trans-HCOH (carbon bound) to CH(2)O (oxygen bound) on ZnO(0001) was calculated to be the overall barrier of the MSR reaction.	Carbon	33-39	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	133-136
15154797-20	2004	The rearrangement of trans-HCOH (carbon bound) to CH(2)O (oxygen bound) on ZnO(0001) was calculated to be the overall barrier of the MSR reaction.	Oxygen	58-64	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	133-136
15154797-20	2004	The rearrangement of trans-HCOH (carbon bound) to CH(2)O (oxygen bound) on ZnO(0001) was calculated to be the overall barrier of the MSR reaction.	Zinc Oxide	75-78	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	133-136
14967039-1	2004	Human methionine synthase reductase (MSR) is a protein containing both FAD and FMN, and it reactivates methionine synthase that has lost activity due to oxidation of cob(I)alamin to cob(II)alamin.	Flavin-Adenine Dinucleotide	71-74	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-40
14967039-1	2004	Human methionine synthase reductase (MSR) is a protein containing both FAD and FMN, and it reactivates methionine synthase that has lost activity due to oxidation of cob(I)alamin to cob(II)alamin.	Vitamin B 12	166-178	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	6-35
14967039-1	2004	Human methionine synthase reductase (MSR) is a protein containing both FAD and FMN, and it reactivates methionine synthase that has lost activity due to oxidation of cob(I)alamin to cob(II)alamin.	Vitamin B 12	166-178	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-40
14967039-1	2004	Human methionine synthase reductase (MSR) is a protein containing both FAD and FMN, and it reactivates methionine synthase that has lost activity due to oxidation of cob(I)alamin to cob(II)alamin.	cob(II)alamin	182-195	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	6-35
14967039-1	2004	Human methionine synthase reductase (MSR) is a protein containing both FAD and FMN, and it reactivates methionine synthase that has lost activity due to oxidation of cob(I)alamin to cob(II)alamin.	cob(II)alamin	182-195	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-40
14967039-2	2004	In this study, anaerobic redox titrations were employed to determine the midpoint reduction potentials for the flavin cofactors in two highly prevalent polymorphic variants of MSR, I22/L175 and M22/S175.	4,6-dinitro-o-cresol	111-117	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	176-179
14967039-6	2004	In MSR I22/L175, the FMN potentials are -103 mV (oxidized/semiquinone) and -175 mV (semiquinone/hydroquinone) at pH 7.0 and 25 degrees C, and the corresponding FAD potentials are -252 and -285 mV, respectively.	semiquinone	58-69	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	3-6
14967039-6	2004	In MSR I22/L175, the FMN potentials are -103 mV (oxidized/semiquinone) and -175 mV (semiquinone/hydroquinone) at pH 7.0 and 25 degrees C, and the corresponding FAD potentials are -252 and -285 mV, respectively.	hydroquinone	96-108	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	3-6
15354395-3	2004	Objective of this study was to analyze the impact of CAG repeats, polymorphisms of various homocysteine metabolizing enzymes, like CBS, Methyltetrahydrofolate Reductase (MTHTR), Methionine Synthase Reductase (MSR) and methionine synthase (MS) on HD onset in 171 patients.	Homocysteine	91-103	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	209-212
14717604-1	2004	Human methionine synthase reductase (MSR) is a key enzyme in folate and methionine metabolism as it reactivates the catalytically inert cob(II)alamin form of methionine synthase (MS).	Folic Acid	61-67	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	6-35
14717604-1	2004	Human methionine synthase reductase (MSR) is a key enzyme in folate and methionine metabolism as it reactivates the catalytically inert cob(II)alamin form of methionine synthase (MS).	Folic Acid	61-67	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-40
14717604-1	2004	Human methionine synthase reductase (MSR) is a key enzyme in folate and methionine metabolism as it reactivates the catalytically inert cob(II)alamin form of methionine synthase (MS).	Methionine	6-16	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-40
14717604-1	2004	Human methionine synthase reductase (MSR) is a key enzyme in folate and methionine metabolism as it reactivates the catalytically inert cob(II)alamin form of methionine synthase (MS).	cob(II)alamin	136-149	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	6-35
14717604-1	2004	Human methionine synthase reductase (MSR) is a key enzyme in folate and methionine metabolism as it reactivates the catalytically inert cob(II)alamin form of methionine synthase (MS).	cob(II)alamin	136-149	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-40
14717604-3	2004	MSR contains stoichiometric amounts of FAD and FMN, which shuttle NADPH-derived electrons to the MS cob(II)alamin cofactor.	Flavin-Adenine Dinucleotide	39-42	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
14717604-3	2004	MSR contains stoichiometric amounts of FAD and FMN, which shuttle NADPH-derived electrons to the MS cob(II)alamin cofactor.	NADP	66-71	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
14717604-3	2004	MSR contains stoichiometric amounts of FAD and FMN, which shuttle NADPH-derived electrons to the MS cob(II)alamin cofactor.	cob(II)alamin	100-113	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
14717604-5	2004	Photodiode array and single-wavelength spectroscopy performed on both full-length MSR and the isolated FAD domain enabled assignment of observed kinetic phases to mechanistic steps in reduction of the flavins.	Flavins	201-208	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	82-85
14717604-7	2004	These two kinetic phases are also observed for reduction of full-length MSR by NADPH, and are followed by two slower and additional kinetic phases (0.2 and 0.016 s(-1)) involving electron transfer between FAD and FMN (thus yielding the disemiquinoid form of MSR) and further reduction of MSR by a second molecule of NADPH.	NADP	79-84	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	72-75
14717604-7	2004	These two kinetic phases are also observed for reduction of full-length MSR by NADPH, and are followed by two slower and additional kinetic phases (0.2 and 0.016 s(-1)) involving electron transfer between FAD and FMN (thus yielding the disemiquinoid form of MSR) and further reduction of MSR by a second molecule of NADPH.	NADP	79-84	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	258-261
14717604-7	2004	These two kinetic phases are also observed for reduction of full-length MSR by NADPH, and are followed by two slower and additional kinetic phases (0.2 and 0.016 s(-1)) involving electron transfer between FAD and FMN (thus yielding the disemiquinoid form of MSR) and further reduction of MSR by a second molecule of NADPH.	NADP	79-84	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	258-261
14717604-7	2004	These two kinetic phases are also observed for reduction of full-length MSR by NADPH, and are followed by two slower and additional kinetic phases (0.2 and 0.016 s(-1)) involving electron transfer between FAD and FMN (thus yielding the disemiquinoid form of MSR) and further reduction of MSR by a second molecule of NADPH.	Flavin-Adenine Dinucleotide	205-208	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	72-75
14717604-7	2004	These two kinetic phases are also observed for reduction of full-length MSR by NADPH, and are followed by two slower and additional kinetic phases (0.2 and 0.016 s(-1)) involving electron transfer between FAD and FMN (thus yielding the disemiquinoid form of MSR) and further reduction of MSR by a second molecule of NADPH.	Flavin-Adenine Dinucleotide	205-208	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	258-261
14717604-7	2004	These two kinetic phases are also observed for reduction of full-length MSR by NADPH, and are followed by two slower and additional kinetic phases (0.2 and 0.016 s(-1)) involving electron transfer between FAD and FMN (thus yielding the disemiquinoid form of MSR) and further reduction of MSR by a second molecule of NADPH.	Flavin-Adenine Dinucleotide	205-208	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	258-261
14717604-7	2004	These two kinetic phases are also observed for reduction of full-length MSR by NADPH, and are followed by two slower and additional kinetic phases (0.2 and 0.016 s(-1)) involving electron transfer between FAD and FMN (thus yielding the disemiquinoid form of MSR) and further reduction of MSR by a second molecule of NADPH.	disemiquinoid	236-249	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	72-75
14717604-7	2004	These two kinetic phases are also observed for reduction of full-length MSR by NADPH, and are followed by two slower and additional kinetic phases (0.2 and 0.016 s(-1)) involving electron transfer between FAD and FMN (thus yielding the disemiquinoid form of MSR) and further reduction of MSR by a second molecule of NADPH.	disemiquinoid	236-249	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	258-261
14717604-7	2004	These two kinetic phases are also observed for reduction of full-length MSR by NADPH, and are followed by two slower and additional kinetic phases (0.2 and 0.016 s(-1)) involving electron transfer between FAD and FMN (thus yielding the disemiquinoid form of MSR) and further reduction of MSR by a second molecule of NADPH.	disemiquinoid	236-249	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	258-261
14717604-7	2004	These two kinetic phases are also observed for reduction of full-length MSR by NADPH, and are followed by two slower and additional kinetic phases (0.2 and 0.016 s(-1)) involving electron transfer between FAD and FMN (thus yielding the disemiquinoid form of MSR) and further reduction of MSR by a second molecule of NADPH.	NADP	316-321	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	72-75
14717604-8	2004	The observed rate constants associated with flavin reduction are dependent hyperbolically on NADPH and [4(R)-2H]NADPH concentration, and the observed primary kinetic isotope effect on this step is 2.2 and 1.7 for the isolated FAD domain and full-length MSR, respectively.	4,6-dinitro-o-cresol	44-50	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	253-256
14717604-8	2004	The observed rate constants associated with flavin reduction are dependent hyperbolically on NADPH and [4(R)-2H]NADPH concentration, and the observed primary kinetic isotope effect on this step is 2.2 and 1.7 for the isolated FAD domain and full-length MSR, respectively.	NADP	93-98	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	253-256
14717604-9	2004	Both full-length MSR and the separated FAD domain that have been reduced with dithionite catalyze the reduction of NADP+.	Dithionite	78-88	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	17-20
14717604-9	2004	Both full-length MSR and the separated FAD domain that have been reduced with dithionite catalyze the reduction of NADP+.	NADP	115-120	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	17-20
14717604-11	2004	The stopped-flow kinetic data, in conjunction with the reported redox potentials of the flavin cofactors for MSR [Wolthers, K. R., Basran, J., Munro, A. W., and Scrutton, N. S. (2003) Biochemistry, 42, 3911-3920], are used to define the mechanism of electron transfer for the reductive half-reaction of MSR.	4,6-dinitro-o-cresol	88-94	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	109-112
12871938-3	2003	Genetic and biochemical studies have demonstrated that the soluble dual flavoprotein oxidoreductase, methionine synthase reductase, serves as a redox partner for methionine synthase in an NADPH-dependent reaction.	NADP	188-193	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	101-130
14656028-1	2003	One-carbon metabolism is under the influence of folate, vitamin B12 and genetic polymorphisms of methylenetetrahydrofolate reductase (MTHFR 677 C --> T and 1298 A --> C), of methionine synthase (MTR 2756 C --> G), methionine synthase reductase (MTRR 66 A --> G) and transcobalamin (TCN 776 C --> G).	Carbon	4-10	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	223-252
14656028-1	2003	One-carbon metabolism is under the influence of folate, vitamin B12 and genetic polymorphisms of methylenetetrahydrofolate reductase (MTHFR 677 C --> T and 1298 A --> C), of methionine synthase (MTR 2756 C --> G), methionine synthase reductase (MTRR 66 A --> G) and transcobalamin (TCN 776 C --> G).	Carbon	4-10	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	254-258
12871939-2	2003	Though the targets of the related NADPH-dependent flavoprotein reductases, cytochrome P450 reductase, methionine synthase reductase, and nitric oxide synthase, are known, the cellular function of Nr1 is not clear.	NADP	34-39	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	102-131
12855226-7	2003	In MS/MSR, homocysteine distribution is not significantly affected in TE subjects, but approaches significance in non-TE individuals (p=0.062).	Homocysteine	11-23	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	6-9
14580313-2	2003	However, unlike the ROS-dependent oxidation of other amino acid residues of proteins (except cysteine residues), the oxidation of Met residues is readily reversed by the action of methionine sulfoxide reductase (Msr) that catalyzes the thioredoxin-dependent reduction of MetO residues of proteins back to Met.	Reactive Oxygen Species	20-23	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	180-210
14580313-2	2003	However, unlike the ROS-dependent oxidation of other amino acid residues of proteins (except cysteine residues), the oxidation of Met residues is readily reversed by the action of methionine sulfoxide reductase (Msr) that catalyzes the thioredoxin-dependent reduction of MetO residues of proteins back to Met.	Reactive Oxygen Species	20-23	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	212-215
14580313-2	2003	However, unlike the ROS-dependent oxidation of other amino acid residues of proteins (except cysteine residues), the oxidation of Met residues is readily reversed by the action of methionine sulfoxide reductase (Msr) that catalyzes the thioredoxin-dependent reduction of MetO residues of proteins back to Met.	Cysteine	93-101	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	180-210
14580313-2	2003	However, unlike the ROS-dependent oxidation of other amino acid residues of proteins (except cysteine residues), the oxidation of Met residues is readily reversed by the action of methionine sulfoxide reductase (Msr) that catalyzes the thioredoxin-dependent reduction of MetO residues of proteins back to Met.	Cysteine	93-101	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	212-215
15692239-4	2003	A number of common polymorphisms in genes coding for methylenetetrahydrofolate reductase(MTHFR), methionine-synthase, methionine-synthase reductase and cysthationine beta-synthase (CBS) have been explored for their association with homocysteine levels, fasting and post-methionine load, and with thrombotic diseases.	Homocysteine	232-244	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	118-147
12855226-8	2003	However, the increased power obtained when all subjects are analysed demonstrates a significant influence of MS/MSR upon homocysteine distribution (p=0.008).	Homocysteine	121-133	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	112-115
12855226-9	2003	Other significant influences of MS/MSR were on total cellular 5-methyl-H4folate in non-TE subjects (p=0.042) and vitamin B12 in TE subjects (p=0.018).	5-methyl-h4folate	62-79	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-38
12855226-9	2003	Other significant influences of MS/MSR were on total cellular 5-methyl-H4folate in non-TE subjects (p=0.042) and vitamin B12 in TE subjects (p=0.018).	Vitamin B 12	113-124	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-38
12855226-13	2003	This may be related to variation in activity of the functional enzymes coded for by polymorphic forms of compound MS/MSR, resulting in altered catalytic cycling of methylcobalamin/cob(I)alamin, which in turn influences Hcy (and total 5-methyl-H4folate).	Homocysteine	219-222	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	117-120
12855226-13	2003	This may be related to variation in activity of the functional enzymes coded for by polymorphic forms of compound MS/MSR, resulting in altered catalytic cycling of methylcobalamin/cob(I)alamin, which in turn influences Hcy (and total 5-methyl-H4folate).	-methyl-h4folate	235-251	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	117-120
12801615-0	2003	Methylenetetrahydrofolate reductase (MTHFR) 677C>T and methionine synthase reductase (MTRR) 66A>G polymorphisms: association with serum homocysteine and angiographic coronary artery disease in the era of flour products fortified with folic acid.	Homocysteine	142-154	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	58-87
12801615-0	2003	Methylenetetrahydrofolate reductase (MTHFR) 677C>T and methionine synthase reductase (MTRR) 66A>G polymorphisms: association with serum homocysteine and angiographic coronary artery disease in the era of flour products fortified with folic acid.	Homocysteine	142-154	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	89-93
12801615-0	2003	Methylenetetrahydrofolate reductase (MTHFR) 677C>T and methionine synthase reductase (MTRR) 66A>G polymorphisms: association with serum homocysteine and angiographic coronary artery disease in the era of flour products fortified with folic acid.	Folic Acid	240-250	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	89-93
12801615-1	2003	We analyzed the association between the methylenetetrahydrofolate reductase (MTHFR) 677C>T and methionine synthase reductase (MTRR) 66A>G polymorphisms with serum homocysteine and with coronary artery disease (CAD) in 504 patients undergoing clinically-indicated angiography between July 1998 and January 1999.	Homocysteine	169-181	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	98-127
12801615-1	2003	We analyzed the association between the methylenetetrahydrofolate reductase (MTHFR) 677C>T and methionine synthase reductase (MTRR) 66A>G polymorphisms with serum homocysteine and with coronary artery disease (CAD) in 504 patients undergoing clinically-indicated angiography between July 1998 and January 1999.	Homocysteine	169-181	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	129-133
12482550-4	2003	Methionine synthase catalyzes the remethylation of homocysteine to form methionine and methionine synthase reductase is required for the reductive activation of the cobalamin-dependent methionine synthase.	Homocysteine	51-63	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	87-116
12667082-0	2003	Molecular dissection of human methionine synthase reductase: determination of the flavin redox potentials in full-length enzyme and isolated flavin-binding domains.	4,6-dinitro-o-cresol	82-88	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	30-59
12667082-0	2003	Molecular dissection of human methionine synthase reductase: determination of the flavin redox potentials in full-length enzyme and isolated flavin-binding domains.	4,6-dinitro-o-cresol	141-147	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	30-59
12667082-1	2003	Human methionine synthase reductase (MSR) catalyzes the NADPH-dependent reductive methylation of methionine synthase.	NADP	56-61	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	6-35
12667082-1	2003	Human methionine synthase reductase (MSR) catalyzes the NADPH-dependent reductive methylation of methionine synthase.	NADP	56-61	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-40
12667082-3	2003	MSR and its individual flavin-binding domains were cloned as GST-tagged fusion proteins for expression and purification from Escherichia coli.	4,6-dinitro-o-cresol	23-29	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
12667082-4	2003	The isolated flavin domains of MSR retain UV-visible and secondary structural properties indicative of correctly folded flavoproteins.	4,6-dinitro-o-cresol	13-19	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-34
12626825-4	2003	Based on evidence that abnormal folate and methyl metabolism can lead to DNA hypomethylation and abnormal chromosomal segregation, researchers have observed that mothers with mutation in MTHFR (C677T) and MTRR (A66G) gene have elevated levels of plasma homocysteine.	Folic Acid	32-38	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	205-209
12626825-4	2003	Based on evidence that abnormal folate and methyl metabolism can lead to DNA hypomethylation and abnormal chromosomal segregation, researchers have observed that mothers with mutation in MTHFR (C677T) and MTRR (A66G) gene have elevated levels of plasma homocysteine.	Homocysteine	253-265	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	205-209
12482550-6	2003	The methionine synthase reductase gene (MTRR) mutation is an A to G substitution, 66A-->G, that converts an isoleucine to a methionine residue.	Isoleucine	111-121	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-33
12482550-6	2003	The methionine synthase reductase gene (MTRR) mutation is an A to G substitution, 66A-->G, that converts an isoleucine to a methionine residue.	Isoleucine	111-121	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	40-44
12482550-6	2003	The methionine synthase reductase gene (MTRR) mutation is an A to G substitution, 66A-->G, that converts an isoleucine to a methionine residue.	Methionine	4-14	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	40-44
14633777-23	2003	Two disorders of cobalamin metabolism, cblG and cblE, are now known to arise from mutations of the methionine synthase and methionine synthase reductase genes, respectively.	Vitamin B 12	17-26	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	48-52
14633777-23	2003	Two disorders of cobalamin metabolism, cblG and cblE, are now known to arise from mutations of the methionine synthase and methionine synthase reductase genes, respectively.	Vitamin B 12	17-26	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	123-152
12020105-1	2002	OBJECTIVE: This population-based case-control study was designed to investigate the interrelationships between polymorphisms in the methylenetetrahydrofolate (MTHFR C677T and A1298C) gene and other genes (MTR A2756G; MTRR A66G and CBS 844ins68), intake of B-vitamins and colorectal cancer risk (CRC).	5,10-methylenetetrahydrofolic acid	132-157	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	217-221
12971424-7	2003	Enzymatic analysis, complementation studies and clearly reduced production of methylcobalamin from 57Co-labelled cyanocobalamin indicated functional methionine synthase reductase deficiency due to the cblE defect.	mecobalamin	78-93	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	201-205
12971424-7	2003	Enzymatic analysis, complementation studies and clearly reduced production of methylcobalamin from 57Co-labelled cyanocobalamin indicated functional methionine synthase reductase deficiency due to the cblE defect.	Vitamin B 12	113-127	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	201-205
12971424-8	2003	Genetic analysis confirmed that both patients are homozygous for a novel mutation c.1361C>T in the methionine synthase reductase gene leading to a replacement of serine by leucine (S454L) in a highly conserved FAD-binding domain.	Serine	165-171	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	102-131
12971424-8	2003	Genetic analysis confirmed that both patients are homozygous for a novel mutation c.1361C>T in the methionine synthase reductase gene leading to a replacement of serine by leucine (S454L) in a highly conserved FAD-binding domain.	Leucine	175-182	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	102-131
12971424-8	2003	Genetic analysis confirmed that both patients are homozygous for a novel mutation c.1361C>T in the methionine synthase reductase gene leading to a replacement of serine by leucine (S454L) in a highly conserved FAD-binding domain.	Flavin-Adenine Dinucleotide	213-216	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	102-131
12810987-5	2002	Ones of those are genes of metabolism of folic acid as MTHFR, MTR, MTRR, CBS, MTHFD, folic acid receptors (FR) regulator genes from PAX family, T, PDGFRA and BRCA1 genes.	Folic Acid	41-51	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	67-71
12482398-9	2002	These two loci harbor the methylenetetrahydrofolate dehydrogenase (MTHFD1) and 5"-methyltetrahdrofolate-homocysteine methyltransferase reductase (MTRR) genes, both of which are involved in folate metabolism.	Folic Acid	45-51	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	117-144
12482398-9	2002	These two loci harbor the methylenetetrahydrofolate dehydrogenase (MTHFD1) and 5"-methyltetrahdrofolate-homocysteine methyltransferase reductase (MTRR) genes, both of which are involved in folate metabolism.	Folic Acid	45-51	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	146-150
11466310-0	2001	Human methionine synthase reductase, a soluble P-450 reductase-like dual flavoprotein, is sufficient for NADPH-dependent methionine synthase activation.	NADP	105-110	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	6-35
11807890-1	2002	Polymorphisms in genes encoding the folate metabolizing enzymes methylenetetrahydrofolate reductase (MTHFR C677T) and methionine synthase reductase (MTRR A66G) have been linked to the etiology of Down syndrome.	Folic Acid	36-42	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	118-147
11807890-1	2002	Polymorphisms in genes encoding the folate metabolizing enzymes methylenetetrahydrofolate reductase (MTHFR C677T) and methionine synthase reductase (MTRR A66G) have been linked to the etiology of Down syndrome.	Folic Acid	36-42	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	149-153
11466310-12	2001	In this study, we have cloned and expressed the cDNA encoding human methionine synthase reductase and demonstrate that it is sufficient for supporting NADPH-dependent activity of methionine synthase at a level that is comparable with that seen in the in vitro assay that utilizes artificial reductants.	NADP	151-156	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	68-97
11466310-16	2001	Methionine synthase reductase reduces cytochrome c in an NADPH-dependent reaction at a rate (0.44 micromol min(-1) mg(-1) at 25 degrees C) that is comparable with that reported for NR1, a soluble dual flavoprotein of unknown function, but is approximately 100-fold slower than that of P-450 reductase.	NADP	57-62	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
11466310-17	2001	The K(m) for NADPH is 2.6 +/- 0.5 microm, and the K(act) for methionine synthase reductase is 80.7 +/- 13.7 nm for NADPH-dependent activity of methionine synthase.	NADP	13-18	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	61-90
11466310-17	2001	The K(m) for NADPH is 2.6 +/- 0.5 microm, and the K(act) for methionine synthase reductase is 80.7 +/- 13.7 nm for NADPH-dependent activity of methionine synthase.	NADP	115-120	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	61-90
11472746-0	2001	The methionine synthase reductase (MTRR) A66G polymorphism is a novel genetic determinant of plasma homocysteine concentrations.	Homocysteine	100-112	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-33
11472746-0	2001	The methionine synthase reductase (MTRR) A66G polymorphism is a novel genetic determinant of plasma homocysteine concentrations.	Homocysteine	100-112	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-39
11472746-3	2001	One such enzyme, methionine synthase reductase (MTRR), maintains adequate levels of methylcob(III)alamin, the activated cofactor for methionine synthase, which catalyzes the remethylation of homocysteine to methionine.	Homocysteine	191-203	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	17-46
11472746-3	2001	One such enzyme, methionine synthase reductase (MTRR), maintains adequate levels of methylcob(III)alamin, the activated cofactor for methionine synthase, which catalyzes the remethylation of homocysteine to methionine.	Homocysteine	191-203	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	48-52
11472746-3	2001	One such enzyme, methionine synthase reductase (MTRR), maintains adequate levels of methylcob(III)alamin, the activated cofactor for methionine synthase, which catalyzes the remethylation of homocysteine to methionine.	Methionine	17-27	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	48-52
11472746-4	2001	A common MTRR polymorphism, i.e. a 66 A-->G substitution specifying an isoleucine to methionine substitution (I22M), was recently identified.	Isoleucine	74-84	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	9-13
11472746-4	2001	A common MTRR polymorphism, i.e. a 66 A-->G substitution specifying an isoleucine to methionine substitution (I22M), was recently identified.	Methionine	88-98	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	9-13
11472746-10	2001	This study provides the first evidence that the MTRR A66G polymorphism significantly influences the circulating tHcy concentration.	thcy	112-116	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	48-52
10930360-6	2000	Methionine synthase reductase (MTRR) is another enzyme essential for normal folate metabolism.	Folic Acid	76-82	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
11443546-2	2001	Thus, recent reports linking Down syndrome to maternal polymorphisms at either of two folate metabolism enzymes, methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR), have generated considerable interest.	Folic Acid	86-92	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	161-190
11443546-2	2001	Thus, recent reports linking Down syndrome to maternal polymorphisms at either of two folate metabolism enzymes, methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR), have generated considerable interest.	Folic Acid	86-92	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	192-196
10930360-6	2000	Methionine synthase reductase (MTRR) is another enzyme essential for normal folate metabolism.	Folic Acid	76-82	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
10837198-0	2000	Gonorrhea among men who have sex with men: outbreak caused by a single genotype of erythromycin-resistant Neisseria gonorrhoeae with a single-base pair deletion in the mtrR promoter region.	Erythromycin	83-95	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	168-172
11006889-1	2000	BACKGROUND: Methionine synthase reductase (MTRR) catalyzes the regeneration of methylcobalamin, a cofactor of methionine synthase, an enzyme essential for maintaining adequate intracellular pools of methionine and tetrahydrofolate, as well as for maintaining homocysteine concentrations at nontoxic levels.	Methionine	110-120	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	12-41
11006889-1	2000	BACKGROUND: Methionine synthase reductase (MTRR) catalyzes the regeneration of methylcobalamin, a cofactor of methionine synthase, an enzyme essential for maintaining adequate intracellular pools of methionine and tetrahydrofolate, as well as for maintaining homocysteine concentrations at nontoxic levels.	Methionine	110-120	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	43-47
11006889-1	2000	BACKGROUND: Methionine synthase reductase (MTRR) catalyzes the regeneration of methylcobalamin, a cofactor of methionine synthase, an enzyme essential for maintaining adequate intracellular pools of methionine and tetrahydrofolate, as well as for maintaining homocysteine concentrations at nontoxic levels.	5,6,7,8-tetrahydrofolic acid	214-230	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	12-41
11006889-1	2000	BACKGROUND: Methionine synthase reductase (MTRR) catalyzes the regeneration of methylcobalamin, a cofactor of methionine synthase, an enzyme essential for maintaining adequate intracellular pools of methionine and tetrahydrofolate, as well as for maintaining homocysteine concentrations at nontoxic levels.	5,6,7,8-tetrahydrofolic acid	214-230	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	43-47
11006889-1	2000	BACKGROUND: Methionine synthase reductase (MTRR) catalyzes the regeneration of methylcobalamin, a cofactor of methionine synthase, an enzyme essential for maintaining adequate intracellular pools of methionine and tetrahydrofolate, as well as for maintaining homocysteine concentrations at nontoxic levels.	Homocysteine	259-271	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	12-41
11006889-1	2000	BACKGROUND: Methionine synthase reductase (MTRR) catalyzes the regeneration of methylcobalamin, a cofactor of methionine synthase, an enzyme essential for maintaining adequate intracellular pools of methionine and tetrahydrofolate, as well as for maintaining homocysteine concentrations at nontoxic levels.	Homocysteine	259-271	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	43-47
2093214-5	1990	However, strychnine, a glycine antagonist which blocks post-synaptic inhibition, did alter both the facilitation and inhibition of the MSR by conditioning pulses.	Strychnine	9-19	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	135-138
9323567-0	1997	Cobalamin E (cblE) disease: a severe neurological disorder with megaloblastic anaemia, homocystinuria and low serum methionine.	Methionine	116-126	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-11
9323567-0	1997	Cobalamin E (cblE) disease: a severe neurological disorder with megaloblastic anaemia, homocystinuria and low serum methionine.	Methionine	116-126	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	13-17
1516297-1	1992	Several of the inborn errors of vitamin B12 (cobalamin, Cbl) metabolism (cblC, cblD, cblE, cblF, cblG) are associated with homocystinuria and hypomethioninemia due to a functional deficiency of the cytoplasmic enzyme methionine synthase which requires methylcobalamin (MeCbl) as a cofactor.	Vitamin B 12	32-43	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	85-89
1516297-1	1992	Several of the inborn errors of vitamin B12 (cobalamin, Cbl) metabolism (cblC, cblD, cblE, cblF, cblG) are associated with homocystinuria and hypomethioninemia due to a functional deficiency of the cytoplasmic enzyme methionine synthase which requires methylcobalamin (MeCbl) as a cofactor.	mecobalamin	252-267	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	85-89
1516297-1	1992	Several of the inborn errors of vitamin B12 (cobalamin, Cbl) metabolism (cblC, cblD, cblE, cblF, cblG) are associated with homocystinuria and hypomethioninemia due to a functional deficiency of the cytoplasmic enzyme methionine synthase which requires methylcobalamin (MeCbl) as a cofactor.	mecobalamin	269-274	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	85-89
1516297-2	1992	We compared the growth of cultured fibroblasts from controls, from patients with a selective deficiency of MeCbl (cblE and cblG), with those with a defect in both MeCbl and adenosylcobalamin (AdoCbl) (cblC, cblD and cblF), in methionine and folic acid-free media to their growth in fully supplemented medium.	mecobalamin	107-112	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	114-118
1542401-2	1992	It was found previously that 0.8 mg/kg physostigmine facilitated the MSR and 2.0 mg/kg initially depressed and then facilitated the MSR.	Physostigmine	39-52	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	69-72
1542401-2	1992	It was found previously that 0.8 mg/kg physostigmine facilitated the MSR and 2.0 mg/kg initially depressed and then facilitated the MSR.	Physostigmine	39-52	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	132-135
1542401-5	1992	It was found that both strychnine and bicuculline blocked the facilitation produced by the small dose of physostigmine, while bicuculline alone blocked the depression of the MSR produced by the large dose of physostigmine.	Strychnine	23-33	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	174-177
1542401-5	1992	It was found that both strychnine and bicuculline blocked the facilitation produced by the small dose of physostigmine, while bicuculline alone blocked the depression of the MSR produced by the large dose of physostigmine.	Physostigmine	105-118	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	174-177
1542401-5	1992	It was found that both strychnine and bicuculline blocked the facilitation produced by the small dose of physostigmine, while bicuculline alone blocked the depression of the MSR produced by the large dose of physostigmine.	Bicuculline	126-137	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	174-177
1542401-5	1992	It was found that both strychnine and bicuculline blocked the facilitation produced by the small dose of physostigmine, while bicuculline alone blocked the depression of the MSR produced by the large dose of physostigmine.	Physostigmine	208-221	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	174-177
1542401-7	1992	These data suggest that the depression of the MSR was the result of a GABA-mediated pathway, while the facilitation of MSR involved both glycine and GABA.	gamma-Aminobutyric Acid	70-74	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	46-49
1542401-7	1992	These data suggest that the depression of the MSR was the result of a GABA-mediated pathway, while the facilitation of MSR involved both glycine and GABA.	Glycine	137-144	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	119-122
1542401-7	1992	These data suggest that the depression of the MSR was the result of a GABA-mediated pathway, while the facilitation of MSR involved both glycine and GABA.	gamma-Aminobutyric Acid	149-153	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	119-122
10484769-0	1999	Molecular basis for methionine synthase reductase deficiency in patients belonging to the cblE complementation group of disorders in folate/cobalamin metabolism.	Folic Acid	133-139	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	90-94
10484769-0	1999	Molecular basis for methionine synthase reductase deficiency in patients belonging to the cblE complementation group of disorders in folate/cobalamin metabolism.	Vitamin B 12	140-149	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	90-94
10484769-1	1999	Methionine synthase reductase (MSR) deficiency is an autosomal recessive disorder of folate/cobalamin metabolism leading to hyperhomocysteinemia, hypo- methioninemia and megaloblastic anemia.	Folic Acid	85-91	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
10484769-1	1999	Methionine synthase reductase (MSR) deficiency is an autosomal recessive disorder of folate/cobalamin metabolism leading to hyperhomocysteinemia, hypo- methioninemia and megaloblastic anemia.	Folic Acid	85-91	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-34
10484769-1	1999	Methionine synthase reductase (MSR) deficiency is an autosomal recessive disorder of folate/cobalamin metabolism leading to hyperhomocysteinemia, hypo- methioninemia and megaloblastic anemia.	Vitamin B 12	92-101	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
10484769-1	1999	Methionine synthase reductase (MSR) deficiency is an autosomal recessive disorder of folate/cobalamin metabolism leading to hyperhomocysteinemia, hypo- methioninemia and megaloblastic anemia.	Vitamin B 12	92-101	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-34
10484769-5	1999	We have used RT-PCR, heteroduplex, single-strand conformation poly- morphism (SSCP) and DNA sequence analyses to reveal 11 mutations in eight patients from seven families belonging to the cblE complementation group of patients of cobalamin metabolism that is defective in the MSR protein.	Vitamin B 12	230-239	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	188-192
10444342-0	1999	A common variant in methionine synthase reductase combined with low cobalamin (vitamin B12) increases risk for spina bifida.	Vitamin B 12	68-77	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	20-49
10444342-0	1999	A common variant in methionine synthase reductase combined with low cobalamin (vitamin B12) increases risk for spina bifida.	Vitamin B 12	79-90	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	20-49
9627769-6	1998	The defect in cobalamin metabolism in MeWoLC1 was complemented in somatic cell complementation analysis by cblA, cblB, cblD, cblE and cblG fibroblasts, but not by cblC fibroblasts, strongly suggesting that the defect in this cell line affects the cblC locus.	Vitamin B 12	14-23	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	125-129
9501215-5	1998	Using consensus sequences to predicted binding sites for FMN, FAD, and NADPH, we have cloned a cDNA corresponding to the "methionine synthase reductase" reducing system required for maintenance of the methionine synthase in a functional state.	Flavin-Adenine Dinucleotide	62-65	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	122-151
9017526-3	1997	We examined the efficacy of sustained-release methylphenidate (MSR) in a sample of substance abusers with HIV-1-related cognitive impairment.	Methylphenidate	46-61	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	63-66
7849071-2	1994	By use of a glutaramyl-beta-alanyl spacer group, a hapten for the polychlorinated biphenyl, 2,2",4,4",5,5"-hexachlorobiphenyl (1), viz., 2-amino-2",4,4",5,5"-pentachlorobiphenyl (2), was successfully conjugated to carrier proteins to provide immunogens with high hapten/protein molar substitution ratios (MSR"s).	2,4,5,2',4',5'-hexachlorobiphenyl	92-125	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	305-308
7849071-3	1994	The procedure allows for the incorporation of beta-[3H]-alanine into the immunogen, thereby providing an accurate radiochemical method for the quantitative assessment of MSR.	beta-[3h]-alanine	46-63	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	170-173
1542401-1	1992	The purpose of this study was to determine which inhibitory pathway(s) mediate the alterations in the monosynaptic (MSR) and polysynaptic (PSR) reflexes after two different doses of physostigmine.	Physostigmine	182-195	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	116-119
2093214-6	1990	Strychnine enhanced the facilitation and partially blocked the inhibition of the MSR by both sural and medial gastrocnemius conditioning.	Strychnine	0-10	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	81-84
2093214-7	1990	These data show that the flexor reflex afferents and the larger diameter afferents alter the MSR solely through glycine-mediated post-synaptic inhibition.	Glycine	112-119	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	93-96
34667917-5	2021	The most important step in the FOCM pathway is the conversion of methionine to homocysteine, which is guided by the enzyme MTRR.	Methionine	65-75	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	123-127
33807684-1	2021	Methionine sulfoxide reductase (Msr) is a family of enzymes that reduces oxidized methionine and plays an important role in the survival of bacteria under oxidative stress conditions.	Methionine	82-92	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	32-35
34967850-11	2022	Highest vs. lowest quartiles of aggregated genetic risk scores from SNVs in MTHFR and MTRR were associated with 14.8% to 18.9% lower RBC folate concentrations.	Folic Acid	137-143	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	86-90
33806962-7	2021	After screening for antimicrobial resistance (AMR) genes, we found a ribosomal protection protein, Msr(D), in these highly azithromycin resistant nonpathogenic strains.	Azithromycin	123-135	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	99-102
34517051-6	2022	Lastly, Nrf2-regulated gene expression was also correlated with expression of intracellular cobalamin trafficking and processing genes, such as MMADHC and MTRR.	Vitamin B 12	92-101	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	155-159
34917626-16	2021	Moreover, our results provide preliminary evidence for MTRR genetic polymorphisms, involving folate metabolism function, may be related to the susceptibility to agitation.	Folic Acid	93-99	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	55-59
34667917-5	2021	The most important step in the FOCM pathway is the conversion of methionine to homocysteine, which is guided by the enzyme MTRR.	Homocysteine	79-91	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	123-127
35434830-2	2022	Methionine synthase reductase (MTRR) is one of the main targets of MTX in the folate metabolic pathways.	Methotrexate	67-70	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
34145481-6	2021	In the current review, we will focus on the role of MetO in specific signal transduction pathways of various organisms, with relation to their physiological contexts, and discuss the contribution of the Msr system to the regulation of the observed MetO effect.	methionine sulfoxide	248-252	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	203-206
34169999-13	2021	CONCLUSION: We reported significant association between genetic alterations of folate metabolism (MTHFR, MTRR) and DNA repair mechanism (RAD54L) genes with the histopathological characteristics of the meningioma tumors.	Folic Acid	79-85	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	105-109
34397023-0	2021	Individualized Supplement of Folic Acid Based on the Gene Polymorphisms of MTHER/MTRR Reduced the Incidence of Adverse Pregnancy Outcomes and Newborn Defects.	Folic Acid	29-39	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	81-85
34397023-9	2021	Results: Based on the genotype of MTHFR and MTRR, women were identified as five risk levels of folic acid metabolism.	Folic Acid	95-105	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	44-48
34078503-4	2022	We carried out a study examining the association of riboflavin intake and its interaction with MTRR (rs1532268) genetic variants with GC risk among 756 controls and 377 cases.	Riboflavin	52-62	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	95-99
34078503-7	2022	In the MTRR (rs1532268) genotypes analysis, the dominant model showed that the effects of riboflavin differed between the CC and CT+TT genotypes.	Riboflavin	90-100	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	7-11
35434830-2	2022	Methionine synthase reductase (MTRR) is one of the main targets of MTX in the folate metabolic pathways.	Methotrexate	67-70	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
35434830-2	2022	Methionine synthase reductase (MTRR) is one of the main targets of MTX in the folate metabolic pathways.	Folic Acid	78-84	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
35434830-2	2022	Methionine synthase reductase (MTRR) is one of the main targets of MTX in the folate metabolic pathways.	Folic Acid	78-84	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
35513407-4	2022	Here, we report a multiplex small RNA-seq library preparation method (MSR-seq) to investigate cellular small RNA and mRNA response to heat shock, hydrogen peroxide, and arsenite stress.	Hydrogen Peroxide	146-163	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	70-73
35513407-4	2022	Here, we report a multiplex small RNA-seq library preparation method (MSR-seq) to investigate cellular small RNA and mRNA response to heat shock, hydrogen peroxide, and arsenite stress.	arsenite	169-177	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	70-73
35579185-1	2022	OBJECTIVE: The methionine synthase reductase (MTRR) gene encodes the MTRR enzyme involved in the metabolic pathway of homocysteine.	Homocysteine	118-130	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	15-44
35489763-1	2022	BACKGROUND/AIM: 5-methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) is responsible for folate metabolism, and we aimed to investigate its genetic role in colorectal cancer (CRC) among Taiwanese.	Folic Acid	108-114	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	54-81
35489763-1	2022	BACKGROUND/AIM: 5-methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) is responsible for folate metabolism, and we aimed to investigate its genetic role in colorectal cancer (CRC) among Taiwanese.	Folic Acid	108-114	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	83-87
35579185-1	2022	OBJECTIVE: The methionine synthase reductase (MTRR) gene encodes the MTRR enzyme involved in the metabolic pathway of homocysteine.	Homocysteine	118-130	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	46-50
35579185-1	2022	OBJECTIVE: The methionine synthase reductase (MTRR) gene encodes the MTRR enzyme involved in the metabolic pathway of homocysteine.	Homocysteine	118-130	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	69-73
33865960-2	2021	Almost all characterized organisms possess thiol-oxidoreductases named methionine sulfoxide reductase (Msr) enzymes to reduce MetO back to Met.	methionine sulfoxide	126-130	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	71-101
35257137-2	2022	The MSR-BSA-MIPs were prepared through free radical polymerization using vinyl modified magnetic nanoparticles as substrates, bovine serum albumin (BSA), with high amino acid sequence similarity but low price compared to HSA, as the dummy template, N-(3-(dimethylamino)-propyl)-methacrylamide (DMAPMA) and N-isopropylacrylamide (NIPAm) as functional monomers with ionic strength and temperature response.	N-(3-(dimethylamino)propyl)methacrylamide	249-292	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-7
35257137-2	2022	The MSR-BSA-MIPs were prepared through free radical polymerization using vinyl modified magnetic nanoparticles as substrates, bovine serum albumin (BSA), with high amino acid sequence similarity but low price compared to HSA, as the dummy template, N-(3-(dimethylamino)-propyl)-methacrylamide (DMAPMA) and N-isopropylacrylamide (NIPAm) as functional monomers with ionic strength and temperature response.	N-(3-(dimethylamino)propyl)methacrylamide	294-300	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-7
35257137-2	2022	The MSR-BSA-MIPs were prepared through free radical polymerization using vinyl modified magnetic nanoparticles as substrates, bovine serum albumin (BSA), with high amino acid sequence similarity but low price compared to HSA, as the dummy template, N-(3-(dimethylamino)-propyl)-methacrylamide (DMAPMA) and N-isopropylacrylamide (NIPAm) as functional monomers with ionic strength and temperature response.	N-isopropylacrylamide	306-327	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-7
35257137-2	2022	The MSR-BSA-MIPs were prepared through free radical polymerization using vinyl modified magnetic nanoparticles as substrates, bovine serum albumin (BSA), with high amino acid sequence similarity but low price compared to HSA, as the dummy template, N-(3-(dimethylamino)-propyl)-methacrylamide (DMAPMA) and N-isopropylacrylamide (NIPAm) as functional monomers with ionic strength and temperature response.	N-isopropylacrylamide	329-334	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-7
33865960-2	2021	Almost all characterized organisms possess thiol-oxidoreductases named methionine sulfoxide reductase (Msr) enzymes to reduce MetO back to Met.	methionine sulfoxide	126-130	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	103-106
33921977-7	2021	The macrolide-lincosamide-streptogramin B methylase gene erm(Q), with erm(42) encoding MLSB monomethyltransferase, mph(E) encoding a macrolide efflux pump, and msr(E) encoding macrolide-inactivating phosphotransferase were present.	Macrolides	4-13	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	160-163
33964857-2	2021	The plasma concentration of homocysteine is dependent on the activities of several B vitamin-dependent enzymes, such as methylenetetrahydrofolate reductase (MTHFR), methionine synthase (MTR), methionine synthase reductase (MTRR), and cystathionine beta-synthase (CBS).	Homocysteine	28-40	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	192-221
33964857-2	2021	The plasma concentration of homocysteine is dependent on the activities of several B vitamin-dependent enzymes, such as methylenetetrahydrofolate reductase (MTHFR), methionine synthase (MTR), methionine synthase reductase (MTRR), and cystathionine beta-synthase (CBS).	Homocysteine	28-40	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	223-227
33834376-9	2022	RESULTS: A significant decrease was found for MS (p < 0.01) and MSR (p < 0.01) across tertiles of DII.	dilC18(3) dye	98-101	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	64-67
33724098-6	2021	Genetic factors may link B vitamins with stroke severity due to the impact on Hcy metabolism of polymorphism in the genes coding for methylenetetrahydrofolate reductase, methionine-synthase, methionine synthase reductase, and cystathionine beta-synthase.	Homocysteine	78-81	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	191-220
33407572-2	2021	In humans, the level of homocysteine is mainly affected by two enzymes: methylene tetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR).	Homocysteine	24-36	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	152-156
32735057-3	2021	Recently, the use of reductive enzymes such as Msr and Dms has emerged as new and alternative method to obtain enantiopure sulfoxides from racemic mixtures.	enantiopure sulfoxides	111-133	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	47-50
33407572-11	2021	Mutations in MTHFR A1298C and MTRR A66G were significantly associated with the homocysteine level.	Homocysteine	79-91	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	30-34
33179601-5	2020	The re-methylation reaction not only involves the enzymes methionine synthase and methionine synthase reductase but also depends on the cofactor cobalamin and on the provision of methyl groups from the folate cycle.	Folic Acid	202-208	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	82-111
33505124-1	2021	Methionine synthase reductase (MTRR) is an important enzyme of the folate/homocysteine pathway.	Folic Acid	67-73	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
33505124-1	2021	Methionine synthase reductase (MTRR) is an important enzyme of the folate/homocysteine pathway.	Folic Acid	67-73	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
33505124-1	2021	Methionine synthase reductase (MTRR) is an important enzyme of the folate/homocysteine pathway.	Homocysteine	74-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
33505124-1	2021	Methionine synthase reductase (MTRR) is an important enzyme of the folate/homocysteine pathway.	Homocysteine	74-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
33505124-3	2021	A common variant A66G is reported in the FMN-binding domain of the MTRR gene, which leads to substitution of isoleucine by methionine (I22M) in MTRR enzyme with reduced activity.	Isoleucine	109-119	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	67-71
33505124-3	2021	A common variant A66G is reported in the FMN-binding domain of the MTRR gene, which leads to substitution of isoleucine by methionine (I22M) in MTRR enzyme with reduced activity.	Isoleucine	109-119	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	144-148
33505124-3	2021	A common variant A66G is reported in the FMN-binding domain of the MTRR gene, which leads to substitution of isoleucine by methionine (I22M) in MTRR enzyme with reduced activity.	Methionine	123-133	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	67-71
33505124-3	2021	A common variant A66G is reported in the FMN-binding domain of the MTRR gene, which leads to substitution of isoleucine by methionine (I22M) in MTRR enzyme with reduced activity.	Methionine	123-133	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	144-148
33497043-0	2021	A Association of MTHFR C677T and MTRR A66G Gene Polymorphisms with Iranian Male Infertility and Its Effect on Seminal Folate and Vitamin B12.	Folic Acid	118-124	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	33-37
33497043-0	2021	A Association of MTHFR C677T and MTRR A66G Gene Polymorphisms with Iranian Male Infertility and Its Effect on Seminal Folate and Vitamin B12.	Vitamin B 12	129-140	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	33-37
33497043-2	2021	We aimed to determine whether 5, 10-methylenetetrahydrofolate reductase (MTHFR) C677T and methionine synthase reductase (MTRR) A66G genotypes are associated with male infertility in Iranian men and to evaluate its effect on seminal levels of folate and vitamin B12.	Vitamin B 12	253-264	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	121-125
33121283-1	2020	Objective: Although genetic variants of key enzymes in the folic acid-methionine metabolic circulation, including methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) were thought to be related to the risk of recurrent pregnancy loss (RPL), the results of recent studies have been inconsistent.	Folic Acid	59-69	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	193-197
33121283-1	2020	Objective: Although genetic variants of key enzymes in the folic acid-methionine metabolic circulation, including methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) were thought to be related to the risk of recurrent pregnancy loss (RPL), the results of recent studies have been inconsistent.	Methionine	70-80	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	193-197
32868325-10	2020	Azithromycin resistance was observed in four (15%) isolates (epidemiological cut-off); all with mutations in the mtrR promoter region.	Azithromycin	0-12	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	113-117
32811545-16	2020	Two strategies have been commonly implicated in gonococcal resistance against azithromycin: over expression of an efflux pump (due to mutations at mtrR coding region) and decreased antimicrobial affinity (due to mutations in genes encoding the 23S ribosomal subunit).	Azithromycin	78-90	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	147-151
32353563-1	2020	In eucaryotic cells, methionine synthase reductase (MSR/MTRR) is capable of dominating the folate-homocysteine metabolism as an irreplaceable partner in electron transfer for regeneration of methionine synthase.	Folic Acid	91-97	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	52-55
32238907-8	2020	Four exonic CpG-SNPs of MTHFD1, MTRR, and GGH genes were identified in folate pathway genes.	Folic Acid	71-77	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	32-36
32353563-1	2020	In eucaryotic cells, methionine synthase reductase (MSR/MTRR) is capable of dominating the folate-homocysteine metabolism as an irreplaceable partner in electron transfer for regeneration of methionine synthase.	Folic Acid	91-97	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	56-60
32353563-1	2020	In eucaryotic cells, methionine synthase reductase (MSR/MTRR) is capable of dominating the folate-homocysteine metabolism as an irreplaceable partner in electron transfer for regeneration of methionine synthase.	Homocysteine	98-110	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	52-55
32353563-1	2020	In eucaryotic cells, methionine synthase reductase (MSR/MTRR) is capable of dominating the folate-homocysteine metabolism as an irreplaceable partner in electron transfer for regeneration of methionine synthase.	Homocysteine	98-110	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	56-60
32203239-9	2020	RESULTS: MTHFD rs1950902 and MTRR rs162036, rs1801394 was associated with the folate treatment response (P = 0.000, 0.048, and 0.043, respectively).	Folic Acid	78-84	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	29-33
32353563-6	2020	Curiously, the deletion of arginine(s) of MTRR could not affect the electron relay, if only the FMN_Red domain was intact, but by degrees reduced the ability to promote MTR catalysis in methionine formation.	Arginine	27-35	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	42-46
32203239-11	2020	DNA methylation of MTHFR, MTR, and MTRR was also significantly associated with folate treatment response (P < 0.001).	Folic Acid	79-85	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-39
32353563-6	2020	Curiously, the deletion of arginine(s) of MTRR could not affect the electron relay, if only the FMN_Red domain was intact, but by degrees reduced the ability to promote MTR catalysis in methionine formation.	Methionine	186-196	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	42-46
32353563-8	2020	The tandem arginines at the end of MTRR N-terminus conferring high affinity to MTR were indispensable for stimulating methyltransferase activity perhaps via triggering allosteric effect that could be attenuated by removal of the arginine(s).	Arginine	11-20	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-39
32353563-8	2020	The tandem arginines at the end of MTRR N-terminus conferring high affinity to MTR were indispensable for stimulating methyltransferase activity perhaps via triggering allosteric effect that could be attenuated by removal of the arginine(s).	Arginine	11-19	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-39
32353563-9	2020	It was concluded that MTRR could also propel MTR enzymatic reaction relying on the tandem arginines at N-terminus more than just only implicated in electron transfer in MTR reactivation cycle.	Arginine	90-99	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	22-26
32199937-6	2020	Here we describe the case of a patient with an unusually high plasma homocysteine concentration (1562 mumol/L) which was only explained by a combination of such secondary etiologies, among them chronic renal failure, hypothyroidism, the homozygous C677T MTHFR variant, a novel heterozygous variant of the MSR gene, and a vitamin deficiency.	Homocysteine	69-81	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	305-308
32393056-2	2020	The present study aims to investigate if common polymorphisms of genes required for one-carbon metabolism (MTHFR, MTRR, MTR and RFC-1) and DNA methylation reactions (DNMT1, DNMT3A and DNMT3B) influence D-loop methylation levels.	Carbon	88-94	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	114-118
32146711-11	2020	CONCLUSION: MTR 2756A>G and MTRR 66A>G polymorphisms related to folate metabolism might be genetic markers for risk of hypertension in the Korean population.	Folic Acid	64-70	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	28-32
32456285-2	2020	This modification is regulated by MetO reduction through the evolutionarily conserved methionine sulfoxide reductase (Msr) system.	methionine sulfoxide	34-38	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	86-116
32456285-2	2020	This modification is regulated by MetO reduction through the evolutionarily conserved methionine sulfoxide reductase (Msr) system.	methionine sulfoxide	34-38	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	118-121
32266834-5	2020	Results: The study demonstrates that the genetic variants in folate cycle and methionine cycle genes such as MTHFR, MTRR, MTR, BHMT and DNMT1 are associated with the risk of aneurysm.	Folic Acid	61-67	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	116-120
32266834-5	2020	Results: The study demonstrates that the genetic variants in folate cycle and methionine cycle genes such as MTHFR, MTRR, MTR, BHMT and DNMT1 are associated with the risk of aneurysm.	Methionine	78-88	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	116-120
31452789-1	2019	The present study analyzed the mRNA expression levels of genes involved in the transport and metabolism of methotrexate (MTX) (RFC1, ABCC1, ABCB1, GGH, FPGS, ATIC, TS, MTHFR, MTRR, MS and MTHFD1) in patients with acute leukemia (AL).	Methotrexate	121-124	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	175-179
31775527-0	2019	Methionine sulfoxide reductase (Msr) dysfunction in human brain disease.	methionine sulfoxide	0-20	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	32-35
31775527-3	2019	One of these antioxidant mechanisms is the widely studied methionine sulfoxide reductase system (Msr).	methionine sulfoxide	58-78	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	97-100
31775527-4	2019	Methionine is one of the most easily oxidized amino acids and Msr can reverse this oxidation and restore protein function, with MsrA and MsrB reducing different stereoisomers.	Methionine	0-10	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	62-65
31356950-8	2019	These mass spectrometric studies also provide early information about post-translational modification as evident in one of the derivatives MTRR-pi showing N-terminal cleavage of methionine.	Methionine	178-188	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	139-143
31482954-1	2019	OBJECTIVE: To investigate the association of the genetic variants of the folate metabolism genes (MTHFR C677T; MTHFR A1298C; MTR A2756G; MTRR A66G and RFC-1 A80G) with the development of polycystic ovary syndrome (PCOS).	Folic Acid	73-79	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	137-141
30786773-4	2020	Patients with MTHFR 667TT and MTRR GG carriers showed higher serum Hcy levels (P = 0.019 and 0.018, respectively), which is associated with higher serum triacylglycerols (TAG) and total cholesterol (TC) levels (P = 0.014 and 0.044, respectively) and a higher risk for hypertriglyceridemia (OR = 1.889, 95% CI: 1.105-3.229, P = 0.020).	Homocysteine	67-70	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	30-34
30786773-4	2020	Patients with MTHFR 667TT and MTRR GG carriers showed higher serum Hcy levels (P = 0.019 and 0.018, respectively), which is associated with higher serum triacylglycerols (TAG) and total cholesterol (TC) levels (P = 0.014 and 0.044, respectively) and a higher risk for hypertriglyceridemia (OR = 1.889, 95% CI: 1.105-3.229, P = 0.020).	Triglycerides	153-169	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	30-34
30786773-4	2020	Patients with MTHFR 667TT and MTRR GG carriers showed higher serum Hcy levels (P = 0.019 and 0.018, respectively), which is associated with higher serum triacylglycerols (TAG) and total cholesterol (TC) levels (P = 0.014 and 0.044, respectively) and a higher risk for hypertriglyceridemia (OR = 1.889, 95% CI: 1.105-3.229, P = 0.020).	Cholesterol	186-197	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	30-34
30786773-4	2020	Patients with MTHFR 667TT and MTRR GG carriers showed higher serum Hcy levels (P = 0.019 and 0.018, respectively), which is associated with higher serum triacylglycerols (TAG) and total cholesterol (TC) levels (P = 0.014 and 0.044, respectively) and a higher risk for hypertriglyceridemia (OR = 1.889, 95% CI: 1.105-3.229, P = 0.020).	Technetium	199-201	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	30-34
31554631-6	2019	In overall and subgroup (defined via body mass index, exercise, and dietary-fat intake) analyses, we identified 2 SNPs (LINC00460 rs1725459 and MTRR rs722025) and lifetime cumulative exposure to estrogen (oral contraceptive use) and cigarette smoking as the most common and strongest predictive markers for CRC risk across the analyses.	Estrogens	195-203	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	144-148
31331979-5	2019	In the binding pocket of MtrR, we observed electron density that we hypothesized was N-cyclohexyl-3-aminopropanesulfonic acid (CAPS), a component of the crystallization reagent.	3-(cyclohexylamino)-1-propanesulfonic acid	85-125	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	25-29
31331979-5	2019	In the binding pocket of MtrR, we observed electron density that we hypothesized was N-cyclohexyl-3-aminopropanesulfonic acid (CAPS), a component of the crystallization reagent.	3-(cyclohexylamino)-1-propanesulfonic acid	127-131	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	25-29
31331979-6	2019	Using the MtrR-CAPS structure as an inducer-bound template, we hypothesized that bile salts, which bear significant chemical resemblance to CAPS, are physiologically relevant inducers.	Bile Acids and Salts	81-91	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	10-14
31331979-7	2019	Indeed, characterization of MtrR-chenodeoxycholate and MtrR-taurodeoxycholate interactions, both in vitro and in vivo, revealed that these bile salts, but not glyocholate or taurocholate, bind MtrR tightly and can act as bona fide inducers.	Chenodeoxycholic Acid	33-50	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	28-32
31331979-7	2019	Indeed, characterization of MtrR-chenodeoxycholate and MtrR-taurodeoxycholate interactions, both in vitro and in vivo, revealed that these bile salts, but not glyocholate or taurocholate, bind MtrR tightly and can act as bona fide inducers.	Taurodeoxycholic Acid	60-77	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	55-59
31331979-7	2019	Indeed, characterization of MtrR-chenodeoxycholate and MtrR-taurodeoxycholate interactions, both in vitro and in vivo, revealed that these bile salts, but not glyocholate or taurocholate, bind MtrR tightly and can act as bona fide inducers.	Taurodeoxycholic Acid	60-77	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	55-59
31331979-7	2019	Indeed, characterization of MtrR-chenodeoxycholate and MtrR-taurodeoxycholate interactions, both in vitro and in vivo, revealed that these bile salts, but not glyocholate or taurocholate, bind MtrR tightly and can act as bona fide inducers.	Bile Acids and Salts	139-149	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	28-32
31331979-7	2019	Indeed, characterization of MtrR-chenodeoxycholate and MtrR-taurodeoxycholate interactions, both in vitro and in vivo, revealed that these bile salts, but not glyocholate or taurocholate, bind MtrR tightly and can act as bona fide inducers.	Bile Acids and Salts	139-149	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	55-59
31331979-7	2019	Indeed, characterization of MtrR-chenodeoxycholate and MtrR-taurodeoxycholate interactions, both in vitro and in vivo, revealed that these bile salts, but not glyocholate or taurocholate, bind MtrR tightly and can act as bona fide inducers.	Bile Acids and Salts	139-149	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	55-59
31331979-12	2019	Here, we describe the structure of induced MtrR and use this structure to identify bile salts as physiological inducers of MtrR.	Bile Acids and Salts	83-93	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	43-47
31331979-12	2019	Here, we describe the structure of induced MtrR and use this structure to identify bile salts as physiological inducers of MtrR.	Bile Acids and Salts	83-93	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	123-127
31063268-8	2019	Other loci with greater rare, coding allele burdens in cases were in signaling pathways relevant to craniofacial development (WNT9B, BMP4, BMPR1B) as well as the methionine cycle (MTRR).	Methionine	162-172	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	180-184
31209768-0	2019	Associations of MTRR and TSER polymorphisms related to folate metabolism with susceptibility to metabolic syndrome.	Folic Acid	55-61	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	16-20
31209768-9	2019	MTRR polymorphism was significantly associated with a decreased risk of MetS in subjects with triglyceride level < 216.3 mg/dL (AOR 0.616, 95% CI 0.399-0.951, P = 0.029).	Triglycerides	94-106	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-4
31203192-9	2019	Furthermore, variants in MTRR, MMAB and MUT, underlying inborn errors of B12 metabolism, were nominally associated with variation in cB12.	cb12	133-137	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	25-29
31099277-2	2021	Here, polymorphisms in three genes involved in the methylation of homocysteine were examined: methionine synthase (MTR), methionine synthase reductase (MTRR), and methylenetetrahydrofolate dehydrogenase 1 (MTHFD1), each of which is involved in methionine metabolism, a component of the one-carbon metabolism process.	Homocysteine	66-78	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	121-150
31200713-2	2019	The aim of this study is to explore the effects of folate pathway gene polymorphisms (the 5-10-methylenetetrahydrofolate reductase, MTHTR C677T, MTHFR A1298C and the methionine synthase reductase, MTRR A66G) and their interactions with homocysteine on serum lipid levels in patients with RSA.	Folic Acid	51-57	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	166-195
31200713-2	2019	The aim of this study is to explore the effects of folate pathway gene polymorphisms (the 5-10-methylenetetrahydrofolate reductase, MTHTR C677T, MTHFR A1298C and the methionine synthase reductase, MTRR A66G) and their interactions with homocysteine on serum lipid levels in patients with RSA.	Folic Acid	51-57	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	197-201
31200713-10	2019	There were significant interactions between MTHFR C677T-A1298C and MTHFR A1298C-MTRR A66G in RSA group and control group, with ORs of 1.62 (95%CI: 1.28-2.04, p &lt; 0.001) and 1.55 (95%CI: 1.27-1.88, p &lt; 0.001), respectively.	rabbit sperm membrane autoantigen	93-96	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	80-84
31200713-14	2019	CONCLUSIONS: Interaction between the MTHFR C677T, A1298C and MTHFR A1298C, MTRR A66G are observed in our RSA group.	rabbit sperm membrane autoantigen	105-108	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	75-79
31200713-16	2019	MTHFR C677T and MTRR A66G gene variants had detrimental effects on serum homocysteine levels and insulin resistance status, while MTHFR C677T, A1298C and MTRR A66G gene variants had detrimental effects on certain serum lipid profiles.	Homocysteine	73-85	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	16-20
31099277-2	2021	Here, polymorphisms in three genes involved in the methylation of homocysteine were examined: methionine synthase (MTR), methionine synthase reductase (MTRR), and methylenetetrahydrofolate dehydrogenase 1 (MTHFD1), each of which is involved in methionine metabolism, a component of the one-carbon metabolism process.	Homocysteine	66-78	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	152-156
31099277-5	2021	In addition, the MTRR 66A &gt; G polymorphism was associated with increased plasma homocysteine levels (p = 0.019).	Homocysteine	83-95	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	17-21
30848279-2	2019	A key pathway of this metabolism is the vitamin B-12- and folate-dependent remethylation of homocysteine, which depends on methionine synthase (MS, encoded by MTR), methionine synthase reductase, and methylenetetrahydrofolate reductase.	Vitamin B 12	40-52	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	165-194
30848279-2	2019	A key pathway of this metabolism is the vitamin B-12- and folate-dependent remethylation of homocysteine, which depends on methionine synthase (MS, encoded by MTR), methionine synthase reductase, and methylenetetrahydrofolate reductase.	Folic Acid	58-64	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	165-194
30848279-2	2019	A key pathway of this metabolism is the vitamin B-12- and folate-dependent remethylation of homocysteine, which depends on methionine synthase (MS, encoded by MTR), methionine synthase reductase, and methylenetetrahydrofolate reductase.	Homocysteine	92-104	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	165-194
31951343-3	2019	Functional methionine synthase deficiency can be separated into two classes, cobalamin (Cbl) deficiency type E (CblE) and type G (CblG), which are the result of mutations that affect methionine synthase reductase or methionine synthase, respectively.	Vitamin B 12	77-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	112-116
31049278-5	2019	Patients with abnormality of FOLR1, DHFR, and MTRR tend to have a higher percentage of platinum resistance.	Platinum	87-95	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	46-50
31049278-7	2019	The combination of FOLR1, DHFR, and MTRR could produce an area of 0.864 under the receiver-operating characteristic curve in distinguishing platinum-resistant patients from platinum-sensitive patients (P &lt; 0.0001).	Platinum	140-148	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-40
31049278-7	2019	The combination of FOLR1, DHFR, and MTRR could produce an area of 0.864 under the receiver-operating characteristic curve in distinguishing platinum-resistant patients from platinum-sensitive patients (P &lt; 0.0001).	Platinum	173-181	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-40
31655735-3	2019	Thioredoxin-dependent peptide methionine sulfoxide reductases (MSR proteins) repair oxidized methionine residues and are found in all Domains of life.	Methionine	30-40	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	63-66
31655735-9	2019	Again, some mutants deficient in Mo-dependent sulfoxide reductases exhibit reduced virulence, and there is evidence that these Mo enzymes and some MSR systems are induced by hypochlorite produced by the innate immune system.	Hypochlorous Acid	174-186	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	147-150
31951343-3	2019	Functional methionine synthase deficiency can be separated into two classes, cobalamin (Cbl) deficiency type E (CblE) and type G (CblG), which are the result of mutations that affect methionine synthase reductase or methionine synthase, respectively.	Vitamin B 12	77-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	183-212
31951343-3	2019	Functional methionine synthase deficiency can be separated into two classes, cobalamin (Cbl) deficiency type E (CblE) and type G (CblG), which are the result of mutations that affect methionine synthase reductase or methionine synthase, respectively.	Vitamin B 12	88-91	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	112-116
31951343-3	2019	Functional methionine synthase deficiency can be separated into two classes, cobalamin (Cbl) deficiency type E (CblE) and type G (CblG), which are the result of mutations that affect methionine synthase reductase or methionine synthase, respectively.	Vitamin B 12	88-91	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	183-212
30096435-1	2018	The methionine sulfoxide reductase (Msr) system is known for its function in reducing protein-methionine sulfoxide to methionine.	methionine sulfoxide	4-24	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-39
30096435-1	2018	The methionine sulfoxide reductase (Msr) system is known for its function in reducing protein-methionine sulfoxide to methionine.	Methionine	4-14	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-39
29293099-3	2018	Methionine synthase and methionine synthase reductase (MTRR) are key regulatory enzymes involved in the metabolic pathway of homocysteine.	Homocysteine	125-137	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	24-53
31238314-8	2019	The analysis of MTHFR C677T and MTRR A66G polymorphisms has demonstrated a significant difference in vitamin B12 levels between recessive and dominant genotypes in case mothers (p &lt; 0.05).	Vitamin B 12	101-112	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	32-36
30546311-0	2018	Genetic Polymorphisms of TYMS, MTHFR, ATIC, MTR, and MTRR Are Related to the Outcome of Methotrexate Therapy for Rheumatoid Arthritis in a Chinese Population.	Methotrexate	88-100	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	53-57
29293099-3	2018	Methionine synthase and methionine synthase reductase (MTRR) are key regulatory enzymes involved in the metabolic pathway of homocysteine.	Homocysteine	125-137	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	55-59
29420254-0	2018	Methionine sulfoxide reductase B3 requires resolving cysteine residues for full activity and can act as a stereospecific methionine oxidase.	Cysteine	53-61	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-30
29421402-8	2018	Interactions between SNPs and water As on skin lesion risk were suggestive for three variants: the G allele of MTRR rs1801394 and T allele of FOLR1 rs1540087 were associated with lower odds of skin lesions with lower As (&lt;=50 mug/L), and the T allele of TYMS rs1001761 was associated with higher odds of skin lesions with higher As.	Water	30-35	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	111-115
29421402-8	2018	Interactions between SNPs and water As on skin lesion risk were suggestive for three variants: the G allele of MTRR rs1801394 and T allele of FOLR1 rs1540087 were associated with lower odds of skin lesions with lower As (&lt;=50 mug/L), and the T allele of TYMS rs1001761 was associated with higher odds of skin lesions with higher As.	Arsenic	36-38	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	111-115
29627528-4	2018	We detected 11 single nucleotide polymorphisms (SNP) of 7 one-carbon metabolism pathway genes (including MTHFR, MTR, MTRR, ALDH1L1, GART, SHMT1 and CBS) in donor livers and analyzed their association with HBV reinfection after liver transplantation.	Carbon	62-68	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	117-121
29373697-5	2018	The observed resistance was attributable to one of two different azithromycin resistance mechanisms; the 23S rRNA C2611T mutation was identified in 24% of isolates, whereas the majority of resistance (76%) was associated with a meningococcal-type mtrR variant.	Azithromycin	65-77	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	247-251
29159983-5	2018	METHODS: Association between population prevalence of 17 variants in 9 folate-related genes (MTRR, MTR, MTHFR, CBS, SHMT1, MTHFD1, RFC1, BHMT, TYMS) and the Fitzpatrick skin phototype of populations was assessed via collation of genotypic data from ALFRED (Allele Frequency Database) and 1000 Genomes databases.	Folic Acid	71-77	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	93-97
29162511-4	2018	METHODS: We investigated if major polymorphisms of folate-related genes, namely MTHFR c.677C>T, MTR c.2756A>G, MTRR c.66A>G and TYMS TSER (a 28-bp tandem repeat in the 5" promoter enhancer region of TYMS) increase the risk of pathological changes of the thymus in AChR+ MG patients.	Folic Acid	51-57	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	111-115
28598776-5	2017	Expression of genes important to the transport (SLC19A1, ABCB1, ABCC1, ABCG2), metabolism (FPGS, GGH), and mechanism of action (TYMS, MTR, MTRR) of MTX, including for the adenosine receptors ADORA1, ADORA2A, ADORA2B, ADORA3 and ADORA3variant were quantitated by real-time PCR in each nodule sample.	Methotrexate	148-151	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	139-143
29340279-0	2017	Effect of MTHFR A1298C and MTRR A66G Genetic Mutations on Homocysteine Levels in the Chinese Population: A Systematic Review and Meta-analysis.	Homocysteine	58-70	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	27-31
29340279-2	2017	Methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) are the two key regulatory enzymes in the folate/homocysteine (Hcy) metabolism.	Folic Acid	19-25	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	79-83
29340279-2	2017	Methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) are the two key regulatory enzymes in the folate/homocysteine (Hcy) metabolism.	Homocysteine	134-146	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	48-77
29340279-2	2017	Methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) are the two key regulatory enzymes in the folate/homocysteine (Hcy) metabolism.	Homocysteine	134-146	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	79-83
29340279-2	2017	Methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) are the two key regulatory enzymes in the folate/homocysteine (Hcy) metabolism.	Homocysteine	148-151	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	48-77
29340279-2	2017	Methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) are the two key regulatory enzymes in the folate/homocysteine (Hcy) metabolism.	Homocysteine	148-151	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	79-83
28537809-3	2017	Methionine synthase (MTR) and methionine synthase reductase (MTRR) are critical enzymes for the folate cycle.	Folic Acid	96-102	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	30-59
28778621-1	2017	Methionine synthase reductase (MTRR) is one of the main regulatory enzymes in the homocysteine/folate pathway.	Homocysteine	82-94	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
28778621-1	2017	Methionine synthase reductase (MTRR) is one of the main regulatory enzymes in the homocysteine/folate pathway.	Homocysteine	82-94	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
28778621-1	2017	Methionine synthase reductase (MTRR) is one of the main regulatory enzymes in the homocysteine/folate pathway.	Folic Acid	95-101	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
28778621-1	2017	Methionine synthase reductase (MTRR) is one of the main regulatory enzymes in the homocysteine/folate pathway.	Folic Acid	95-101	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
28712006-0	2017	An Inframe Trinucleotide Deletion in MTRR Exon 1 is Associated with the Risk of Spina Bifida.	trinucleotide	11-24	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-41
28712006-4	2017	A trinucleotide deletion (c.4_6delAGG) was identified in the first exon of MTRR.	trinucleotide	2-15	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	75-79
28537809-3	2017	Methionine synthase (MTR) and methionine synthase reductase (MTRR) are critical enzymes for the folate cycle.	Folic Acid	96-102	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	61-65
28702146-1	2017	BACKGROUND: The 5, 10-methyleneterahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) are two essential enzymes involved in folate metabolism.	Folic Acid	40-46	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	69-98
28702146-1	2017	BACKGROUND: The 5, 10-methyleneterahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) are two essential enzymes involved in folate metabolism.	Folic Acid	40-46	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	100-104
26950655-7	2017	The 5-methylcytosine levels were negatively associated with DNMT1 CC, DNMT3A CC, and MTRR AA genotypes, and positively with DNMT3B CC genotype.	5-Methylcytosine	4-20	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	85-89
27865735-3	2017	METHODS: We utilized Pediatric Heart Transplant Study (PHTS) data from 2010 to 2013 to analyze moderate-to-severe (ISHLT Grade 2R/3R) cellular rejection (MSR) detected only on RSB (RSBMSR).	(1S,5S,6R)-10-(benzo[d]thiazol-6-ylsulfonyl)-5-(methoxymethyl)-3-(pyridin-2-ylethyl)-3,10-diazabicyclo[4.3.1]decan-2-one	176-179	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	154-157
27865735-4	2017	RESULTS: RSB detected 280 of 343 (81.6%) episodes of MSR.	(1S,5S,6R)-10-(benzo[d]thiazol-6-ylsulfonyl)-5-(methoxymethyl)-3-(pyridin-2-ylethyl)-3,10-diazabicyclo[4.3.1]decan-2-one	9-12	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	53-56
28345611-8	2017	Disruption of the genes NUP98 (embryonic stem cell development) and MTRR (folate metabolism) was detected exclusively in RPL placentas, potentially indicative to novel loci implicated in RPL.	Folic Acid	74-80	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	68-72
28243331-1	2017	Methionine synthase reductase (MTRR) is a key regulatory enzyme involved in the folate metabolic pathway.	Folic Acid	80-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
28243331-1	2017	Methionine synthase reductase (MTRR) is a key regulatory enzyme involved in the folate metabolic pathway.	Folic Acid	80-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
28118645-1	2017	Polymorphisms in genes encoding the enzymes involved in the metabolism of homocysteine, such as methionine synthase (MTR) and methionine synthase reductase (MTRR), play an important function in the metabolism of folic acid and vitamin B12.	Homocysteine	74-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	126-155
28118645-1	2017	Polymorphisms in genes encoding the enzymes involved in the metabolism of homocysteine, such as methionine synthase (MTR) and methionine synthase reductase (MTRR), play an important function in the metabolism of folic acid and vitamin B12.	Homocysteine	74-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	157-161
28118645-1	2017	Polymorphisms in genes encoding the enzymes involved in the metabolism of homocysteine, such as methionine synthase (MTR) and methionine synthase reductase (MTRR), play an important function in the metabolism of folic acid and vitamin B12.	Folic Acid	212-222	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	126-155
28118645-1	2017	Polymorphisms in genes encoding the enzymes involved in the metabolism of homocysteine, such as methionine synthase (MTR) and methionine synthase reductase (MTRR), play an important function in the metabolism of folic acid and vitamin B12.	Folic Acid	212-222	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	157-161
28118645-1	2017	Polymorphisms in genes encoding the enzymes involved in the metabolism of homocysteine, such as methionine synthase (MTR) and methionine synthase reductase (MTRR), play an important function in the metabolism of folic acid and vitamin B12.	Vitamin B 12	227-238	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	126-155
28118645-1	2017	Polymorphisms in genes encoding the enzymes involved in the metabolism of homocysteine, such as methionine synthase (MTR) and methionine synthase reductase (MTRR), play an important function in the metabolism of folic acid and vitamin B12.	Vitamin B 12	227-238	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	157-161
27456431-10	2016	Our findings showed that the polymorphisms of MTRR 66 A &gt; G and TS 5"-UTR 3R &gt; 2R may be potential prognostic factors for GC patients receiving 5-FU.	Fluorouracil	150-154	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	46-50
27755291-7	2016	The neuro fuzzy model showed synergistic interactions between MTHFR C677T and MTRR A66G inflating homocysteine levels.	Homocysteine	98-110	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	78-82
28616555-0	2017	MTRR rs326119 polymorphism is associated with plasma concentrations of homocysteine and cobalamin, but not with congenital heart disease or coronary atherosclerosis in Brazilian patients.	Homocysteine	71-83	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-4
28616555-0	2017	MTRR rs326119 polymorphism is associated with plasma concentrations of homocysteine and cobalamin, but not with congenital heart disease or coronary atherosclerosis in Brazilian patients.	Vitamin B 12	88-97	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-4
28616555-4	2017	The primary objective of this study was to assess the influence of the MTRR rs326119 polymorphism on biochemical parameters of vitamin B12 metabolism, coronary lesions, and congenital heart disease in Brazilian subjects.	Vitamin B 12	127-138	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	71-75
28616555-10	2017	CONCLUSION: Our findings indicate that the MTRR rs326119 variant might be a genetic marker associated with homocysteine and cobalamin concentrations, but not a strong risk factor for CHD or coronary atherosclerosis in the Brazilian population.	Homocysteine	107-119	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	43-47
28616555-10	2017	CONCLUSION: Our findings indicate that the MTRR rs326119 variant might be a genetic marker associated with homocysteine and cobalamin concentrations, but not a strong risk factor for CHD or coronary atherosclerosis in the Brazilian population.	Vitamin B 12	124-133	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	43-47
27411575-1	2016	Here, we have reported a straightforward and effective synthetic strategy for synthesis of aspect-ratios-controllable mesoporous silica nanorods with hollow structure (hMSR) and its application for transcription factor (TF)-responsive drug delivery intracellular.	Silicon Dioxide	129-135	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	168-172
27411575-3	2016	Subsequently, the dense silica layer was removed by the surface-protected etching method and the hollow structure of hMSR was finally formed.	Silicon Dioxide	24-30	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	117-121
27411575-13	2016	In the presence of TF, the pores of hMSR can be unlocked by the TFs induced disassembly of TDNA, leading to the leakage of DOX.	Doxorubicin	123-126	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-40
27116987-29	2016	CONCLUSIONS: MTRR silencing significantly increase cisplatin-induced apoptosis and reduce the autophagy induced by cisplatin in SKOV3/DDP cells.	Cisplatin	51-60	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	13-17
27347936-2	2016	Vitamin B6 (B6) is a cofactor, and genetic polymorphisms of related key enzymes, such as serine hydroxymethyltransferase (SHMT), methionine synthase reductase (MTRR), and methionine synthase (MS), in FMOCM may govern the bioavailability of metabolites and play important roles in the maintenance of genomic stability and cell viability (GSACV).	gsacv	337-342	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	160-164
27347936-7	2016	The role of SHMT, MS, and MTRR genotype polymorphisms in GSACV is reduced compared with that of B6.	gsacv	57-62	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	26-30
26961134-8	2016	Four DM CpGs identified by SNPs in MTRR, MTHFR, and FTHFD were significantly associated with alcohol consumption and/or breast folate.	Alcohols	93-100	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-39
26961134-8	2016	Four DM CpGs identified by SNPs in MTRR, MTHFR, and FTHFD were significantly associated with alcohol consumption and/or breast folate.	Folic Acid	127-133	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	35-39
27116987-29	2016	CONCLUSIONS: MTRR silencing significantly increase cisplatin-induced apoptosis and reduce the autophagy induced by cisplatin in SKOV3/DDP cells.	Cisplatin	115-124	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	13-17
26874989-0	2016	Association between premature ovarian failure, polymorphisms in MTHFR and MTRR genes and serum homocysteine concentration.	Homocysteine	95-107	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	74-78
25978498-7	2016	CONCLUSION: Treatment with hydroxocobalamin in combination with betaine appears to be useful for hematological improvement and prevention of brain disabilities in CblE-affected patients.	Hydroxocobalamin	27-43	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	163-167
25978498-7	2016	CONCLUSION: Treatment with hydroxocobalamin in combination with betaine appears to be useful for hematological improvement and prevention of brain disabilities in CblE-affected patients.	Betaine	64-71	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	163-167
26874989-9	2016	In conclusion, MTHFR C667T/A1298C and MTRR A66G genotypes are not associated with POF development, but they affect the patients" serum Hcy concentrations.	Homocysteine	135-138	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	38-42
26917482-0	2016	[Biological effect of down-regulating of MTRR gene on cisplatin-resistant ovarian cancer SKOV3 cells in vitro and in vivo studies].	Cisplatin	54-63	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	41-45
26718410-2	2016	The two major Msr enzymes, MsrA and MsrB, can repair oxidative damage to proteins due to reactive oxygen species, by reducing the methionine sulfoxide in proteins back to methionine.	Reactive Oxygen Species	89-112	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	14-17
26718410-2	2016	The two major Msr enzymes, MsrA and MsrB, can repair oxidative damage to proteins due to reactive oxygen species, by reducing the methionine sulfoxide in proteins back to methionine.	methionine sulfoxide	130-150	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	14-17
26917482-1	2016	OBJECTIVE: To study the biological effects of down-regulatingof methionine synthase reductase (MTRR) gene on cisplatin resistant ovarian cancer SKOV3/DDP cell in vitro and in vivo.	Cisplatin	109-118	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	64-93
26718410-2	2016	The two major Msr enzymes, MsrA and MsrB, can repair oxidative damage to proteins due to reactive oxygen species, by reducing the methionine sulfoxide in proteins back to methionine.	Methionine	130-140	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	14-17
26917482-1	2016	OBJECTIVE: To study the biological effects of down-regulatingof methionine synthase reductase (MTRR) gene on cisplatin resistant ovarian cancer SKOV3/DDP cell in vitro and in vivo.	Cisplatin	109-118	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	95-99
26917482-29	2016	CONCLUSION: The growth and cisplatin resistance of ovarian cancer cells could be decreased by down-expressing of MTRR gene in vitro and in vivo.	Cisplatin	27-36	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	113-117
27524956-7	2016	Using workflow based exploitation of pathway databases and by integrating our metabolomics data with our gene expression data from the same patients we identified 4 deregulated phosphatidylcholine metabolism related genes (ALDH1B1, MBOAT1, MTRR and PLB1) that showed significant association with the changes in metabolite concentrations.	Phosphatidylcholines	177-196	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	240-244
26337056-11	2015	Each of four gene polymorphisms (MTHTR C677T, MTHFR A1298C, MTR A2756G and MTRR A66G) combined with low folate showed higher odds of hypertriglyceridemia (P for trend: 0.049, 0.004, 0.007 and 0.005, respectively).	Folic Acid	104-110	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	75-79
26550452-0	2015	MTRR silencing inhibits growth and cisplatin resistance of ovarian carcinoma via inducing apoptosis and reducing autophagy.	Cisplatin	35-44	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-4
26550452-1	2015	Methionine synthase reductase (MTRR) is involved in the DNA synthesis and production of S-adenosylmethionine (SAM) and plays an important role in the carcinogenesis.	S-Adenosylmethionine	88-108	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
26550452-1	2015	Methionine synthase reductase (MTRR) is involved in the DNA synthesis and production of S-adenosylmethionine (SAM) and plays an important role in the carcinogenesis.	S-Adenosylmethionine	88-108	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
26550452-5	2015	MTRR over-expression in OC tissue was correlated with pathologic type (P=0.005), grade (P=0.037), FIGO stage (P=0.001), organ metastasis (P=0.009) and platinum resistance (P=0.038).	Platinum	151-159	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-4
26550452-6	2015	MTRR silencing inhibited cell proliferation, cisplatin resistance and autophagy, and induced apoptosis of OC cells.	Cisplatin	45-54	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-4
26550452-9	2015	In summary, MTRR expression, which is increased in human OC, is related to the differentiation and cisplatin resistance of OC cells.	Cisplatin	99-108	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	12-16
26550452-10	2015	MTRR silencing inhibits cell growth and cisplatin resistance by regulating caspase expression and mTOR signaling pathway in OC cells.	Cisplatin	40-49	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-4
26334892-2	2015	Besides, methionine synthase (MTR) gene and methionine synthase reductase (MTRR) gene were folate metabolism involved genes and had been investigated in several previous studies with inconsistent results.	Folic Acid	91-97	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	44-73
25105440-2	2015	The genes MTHFR, MTR, MTRR, and TCN2 play key roles in folate metabolism.	Folic Acid	55-61	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	22-26
25526710-1	2015	BACKGROUND: The cobalamin E (cblE) (MTRR, methionine synthase reductase) and cobalamin G (cblG) (MTR, methionine synthase) defects are rare inborn errors of cobalamin metabolism leading to impairment of the remethylation of homocysteine to methionine.	Vitamin B 12	16-25	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	29-33
25526710-1	2015	BACKGROUND: The cobalamin E (cblE) (MTRR, methionine synthase reductase) and cobalamin G (cblG) (MTR, methionine synthase) defects are rare inborn errors of cobalamin metabolism leading to impairment of the remethylation of homocysteine to methionine.	Vitamin B 12	16-25	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-40
25526710-1	2015	BACKGROUND: The cobalamin E (cblE) (MTRR, methionine synthase reductase) and cobalamin G (cblG) (MTR, methionine synthase) defects are rare inborn errors of cobalamin metabolism leading to impairment of the remethylation of homocysteine to methionine.	Vitamin B 12	16-25	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	42-71
25526710-1	2015	BACKGROUND: The cobalamin E (cblE) (MTRR, methionine synthase reductase) and cobalamin G (cblG) (MTR, methionine synthase) defects are rare inborn errors of cobalamin metabolism leading to impairment of the remethylation of homocysteine to methionine.	Homocysteine	224-236	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	42-71
26334892-2	2015	Besides, methionine synthase (MTR) gene and methionine synthase reductase (MTRR) gene were folate metabolism involved genes and had been investigated in several previous studies with inconsistent results.	Folic Acid	91-97	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	75-79
26154858-2	2015	The mammalian folic acid cycle is highly complex and the enzymes, methylenetetrahydrofolate reductase (MTHFR), methionine synthase (MTR), and methionine synthase reductase (MTRR), have crucial roles in this metabolic pathway.	Folic Acid	14-24	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	142-171
26045171-3	2015	The gene encoding methionine synthase reductase (MTRR) is essential for adequate remethylation of Hcy.	Homocysteine	98-101	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	18-47
26045171-3	2015	The gene encoding methionine synthase reductase (MTRR) is essential for adequate remethylation of Hcy.	Homocysteine	98-101	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	49-53
26045171-4	2015	Previous studies have focused on the coding region of genes involved in one-carbon metabolism, but recent research demonstrates that an allelic change in a non-coding region of MTRR (rs326119) increases the risk of CHD.	Carbon	76-82	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	177-181
26154858-2	2015	The mammalian folic acid cycle is highly complex and the enzymes, methylenetetrahydrofolate reductase (MTHFR), methionine synthase (MTR), and methionine synthase reductase (MTRR), have crucial roles in this metabolic pathway.	Folic Acid	14-24	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	173-177
26252105-1	2015	OBJECTIVE: To assess the association of plasma homocysteine (Hcy) level and 66A/G and 524C/T polymorphisms of methionine synthase reductase (MSR) gene with essential hypertension (EH) in ethnic Uygurs and Hans from Xinjiang.	Homocysteine	47-59	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	141-144
25801246-3	2015	The single nucleotide polymorphisms, MTHFR C677T, A1298C, MTR A2756G, and MTRR A66G, alter plasmatic folate and homocysteine concentrations, causing problems during the repairment, synthesis, and methylation of the genetic material.	Folic Acid	101-107	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	74-78
25801246-3	2015	The single nucleotide polymorphisms, MTHFR C677T, A1298C, MTR A2756G, and MTRR A66G, alter plasmatic folate and homocysteine concentrations, causing problems during the repairment, synthesis, and methylation of the genetic material.	Homocysteine	112-124	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	74-78
26252105-1	2015	OBJECTIVE: To assess the association of plasma homocysteine (Hcy) level and 66A/G and 524C/T polymorphisms of methionine synthase reductase (MSR) gene with essential hypertension (EH) in ethnic Uygurs and Hans from Xinjiang.	Homocysteine	61-64	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	141-144
25979628-0	2015	Dysfunction of methionine sulfoxide reductases to repair damaged proteins by nickel nanoparticles.	Nickel	77-83	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	15-46
25979628-11	2015	CONCLUSIONS: MSR was made aberrant by NiNP, which could lead to the dysfunction of autophagy and ERK phosphorylation.	ninp	38-42	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	13-16
25544674-3	2015	We conducted a case-control study to explore polymorphisms of the major folate pathway genes, including methylenetetrahydrofolate reductase (MTHFR) 677C&gt;T, MTHFR 1298A&gt;C, methionine synthase (MTR) 2756A&gt;G, methionine synthase reductase (MTRR) 66A&gt;G and reduced folate carrier 1 (RFC-1) 80A&gt;G, and their associations with URPL.	Folic Acid	72-78	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	215-244
25648260-5	2015	Gene-gene interactions within one-carbon metabolic pathway were observed in CAD (GCPII 1561 C>T, SHMT 1420 C>T and MTHFR 677 C>T) and PD (cSHMT 1420 C>T, MTRR 66 A>G and RFC1 80 G>A).	Carbon	34-40	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	154-158
25544674-3	2015	We conducted a case-control study to explore polymorphisms of the major folate pathway genes, including methylenetetrahydrofolate reductase (MTHFR) 677C&gt;T, MTHFR 1298A&gt;C, methionine synthase (MTR) 2756A&gt;G, methionine synthase reductase (MTRR) 66A&gt;G and reduced folate carrier 1 (RFC-1) 80A&gt;G, and their associations with URPL.	Folic Acid	72-78	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	246-250
25809864-10	2015	Maternal prepregnancy folic acid supplementation showed a stronger negative association with CBT risk where the child, mother, or father had the MTRR 66GG genotype (Pinteraction = 0.07, 0.10, and 0.18, respectively).	Folic Acid	22-32	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	145-149
25809864-12	2015	There was possible protection by the MTRR 66GG genotype, particularly when combined with maternal prepregnancy folic acid supplementation; these results are novel and require replication.	Folic Acid	111-121	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-41
25809864-13	2015	IMPACT: The possible interaction between folic acid supplementation and MTRR 66A&gt;G, if confirmed, would strengthen evidence for prepregnancy folate protection against CBT.	Folic Acid	41-51	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	72-76
25809864-13	2015	IMPACT: The possible interaction between folic acid supplementation and MTRR 66A&gt;G, if confirmed, would strengthen evidence for prepregnancy folate protection against CBT.	Folic Acid	144-150	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	72-76
25809864-13	2015	IMPACT: The possible interaction between folic acid supplementation and MTRR 66A&gt;G, if confirmed, would strengthen evidence for prepregnancy folate protection against CBT.	N,N-BIS(4-CHLOROBENZYL)-1H-1,2,3,4-TETRAAZOL-5-AMINE	170-173	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	72-76
25815774-6	2015	Four SNPs are located in the MTRR gene, and another four SNPs showed significant association with 5-fluoro-uracil cytotoxicity in a recent in-vitro genome-wide association study.	Fluorouracil	98-113	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	29-33
25815774-8	2015	RESULTS: In patients receiving capecitabine monotherapy, rs4702484, located in ADCY2 and close to MTRR, was associated with slightly reduced PFS for homozygous wild-type patients (CC 6.2 vs. CT 8.0 months; P=0.018).	Capecitabine	31-43	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	98-102
25878036-0	2015	Splice-shifting oligonucleotide (SSO) mediated blocking of an exonic splicing enhancer (ESE) created by the prevalent c.903+469T&gt;C MTRR mutation corrects splicing and restores enzyme activity in patient cells.	Oligonucleotides	16-31	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	134-138
25840420-6	2015	MTRR 66 GA + GG genotypes decreased the risk of death (HR = 0.793, 95% CI = 0.651-0.967) in general, and in subgroups with more pronounced diffuse type, greater depth of invasion (T2/T3/T4), higher level lymph node metastasis (N1/N2/N3), advanced TNM stages (II/III level) and 5-Fu treatment.	Fluorouracil	277-281	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-4
25754229-1	2015	INTRODUCTION: Our objective was to investigate the association between gene polymorphisms of folate cycle (MTHFR 677 C&gt;T, MTHFR 1298 A&gt;C, MTR 2756 A&gt;G, and MTRR 66 A&gt;G) and the risk of pulmonary embolism (PE) in a case-control study.	Folic Acid	93-99	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	165-169
25801727-2	2015	The studies suggest that both polymorphisms and changes of expression in genes encoding enzymes involved in the methionine and homocysteine metabolism (MHM), such as methylenetetrahydrofolate, reductase (MTHFR), methionine synthase (MTR), methionine synthase reductase (MTRR) and cystathionine gamma-lyase (CSE), could play a role in the development of hypertension during pregnancy.	Methionine	112-122	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	239-268
25801727-2	2015	The studies suggest that both polymorphisms and changes of expression in genes encoding enzymes involved in the methionine and homocysteine metabolism (MHM), such as methylenetetrahydrofolate, reductase (MTHFR), methionine synthase (MTR), methionine synthase reductase (MTRR) and cystathionine gamma-lyase (CSE), could play a role in the development of hypertension during pregnancy.	Methionine	112-122	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	270-274
25634728-0	2015	Individualized supplementation of folic acid according to polymorphisms of methylenetetrahydrofolate reductase (MTHFR), methionine synthase reductase (MTRR) reduced pregnant complications.	Folic Acid	34-44	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	120-149
26673393-9	2015	Natural 5-methyltetrahydrofolate intake is interesting: Wildtype A1298C-MTHFR, heterozygote C677T-MTHFR, wildtype A2756G-MS and recessive A66G-MSR individuals all show a significant reciprocal association with homocysteine.	5-methyltetrahydrofolate	8-32	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	143-146
25634728-0	2015	Individualized supplementation of folic acid according to polymorphisms of methylenetetrahydrofolate reductase (MTHFR), methionine synthase reductase (MTRR) reduced pregnant complications.	Folic Acid	34-44	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	151-155
25456744-4	2014	In animal models, elevated Hcy concentrations are induced either by diet (high methionine, low B-vitamins, or both), gene knockouts (Mthfr, Cbs, Mtrr or Mtr) or combination of both to investigate their effects on DNA methylation or its markers.	Homocysteine	27-30	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	145-149
25322900-0	2014	Riboflavin status modifies the effects of methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) polymorphisms on homocysteine.	Riboflavin	0-10	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	90-119
25429430-2	2014	Methylenetetrahydrofolate reductase (MTHFR) C677T and methionine synthase reductase (MTRR) A66G polymorphisms are common genetic determinants of homocysteine levels.	Homocysteine	145-157	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	54-83
25429430-2	2014	Methylenetetrahydrofolate reductase (MTHFR) C677T and methionine synthase reductase (MTRR) A66G polymorphisms are common genetic determinants of homocysteine levels.	Homocysteine	145-157	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	85-89
25429430-7	2014	Furthermore, the MTRR 66GG genotype was associated with high fasting blood glucose and triglycerides.	Glucose	75-82	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	17-21
25429430-7	2014	Furthermore, the MTRR 66GG genotype was associated with high fasting blood glucose and triglycerides.	Triglycerides	87-100	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	17-21
25322900-0	2014	Riboflavin status modifies the effects of methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) polymorphisms on homocysteine.	Riboflavin	0-10	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	121-125
25130546-10	2014	In conclusion, we have identified four diflavin reductases (POR, MTRR, NOS2A and NDOR1) capable of reducing both SN30000 and EF5, further supporting use of 2-nitroimidazole probes to predict the ability of hypoxic cells to activate SN30000.	azomycin	156-172	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	65-69
25337902-8	2014	In addition, we detected potential heterogeneity across alcohol drinking status for ORs relating MTRR rs1801394 to esophageal (posterior homogeneity P = 0.005) and stomach cancer (posterior homogeneity P = 0.004), and ORs relating MTR rs1805087 to liver cancer (posterior homogeneity P = 0.021).	Alcohols	56-63	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	97-101
25337902-11	2014	Heterogeneity across alcohol consumption status of the associations between MTR/MTRR polymorphisms and these cancers indicates potential interactions between alcohol drinking and one-carbon metabolic pathway.	Alcohols	21-28	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	80-84
25337902-11	2014	Heterogeneity across alcohol consumption status of the associations between MTR/MTRR polymorphisms and these cancers indicates potential interactions between alcohol drinking and one-carbon metabolic pathway.	Alcohols	158-165	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	80-84
25337902-11	2014	Heterogeneity across alcohol consumption status of the associations between MTR/MTRR polymorphisms and these cancers indicates potential interactions between alcohol drinking and one-carbon metabolic pathway.	Carbon	183-189	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	80-84
25322900-6	2014	In the lowest cobalamin quartile (&lt;=273 pmol/L), riboflavin status modifies the relationship between the MTRR 66 A&gt;G polymorphism and tHcy (p for interaction: 0.034).	Vitamin B 12	14-23	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	108-112
25322900-6	2014	In the lowest cobalamin quartile (&lt;=273 pmol/L), riboflavin status modifies the relationship between the MTRR 66 A&gt;G polymorphism and tHcy (p for interaction: 0.034).	Riboflavin	52-62	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	108-112
25322900-6	2014	In the lowest cobalamin quartile (&lt;=273 pmol/L), riboflavin status modifies the relationship between the MTRR 66 A&gt;G polymorphism and tHcy (p for interaction: 0.034).	thcy	140-144	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	108-112
25322900-7	2014	tHcy was 6.6 % higher in MTRR 66G allele carriers compared to the 66AA genotype with marginally deficient or optimal riboflavin status, but there was no difference when riboflavin status was deficient (p for interaction: 0.059).	thcy	0-4	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	25-29
25322900-8	2014	tHcy was 13.7 % higher in MTRR 524T allele carriers compared to the 524CC genotype when cobalamin status was low (p &lt; 0.01), but no difference was observed when we stratified by riboflavin status.	thcy	0-4	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	26-30
25322900-9	2014	The effect of the MTHFR 677C&gt;T polymorphism on tHcy depends on riboflavin status, that of the MTRR 66A&gt;G polymorphism on cobalamin and riboflavin status and that of the MTRR 524C&gt;T polymorphism on cobalamin status.	thcy	50-54	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	175-179
26835343-0	2014	Association of folate metabolism genes MTHFR and MTRR with multiple complex congenital malformation risk in Chinese population of Shanxi.	Folic Acid	15-21	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	49-53
25140779-0	2014	[Association of folate metabolism genes MTRR and MTHFR with complex congenital abnormalities among Chinese population in Shanxi Province, China].	Folic Acid	16-22	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	40-44
26461361-4	2014	Indeed methionine sulfoxide is catalytically reduced back to methionine by the methionine sulfoxide reductase (Msr) system.	methionine sulfoxide	7-27	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	79-109
26461361-4	2014	Indeed methionine sulfoxide is catalytically reduced back to methionine by the methionine sulfoxide reductase (Msr) system.	methionine sulfoxide	7-27	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	111-114
26461361-4	2014	Indeed methionine sulfoxide is catalytically reduced back to methionine by the methionine sulfoxide reductase (Msr) system.	Methionine	7-17	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	79-109
26461361-4	2014	Indeed methionine sulfoxide is catalytically reduced back to methionine by the methionine sulfoxide reductase (Msr) system.	Methionine	7-17	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	111-114
24261678-1	2014	Methionine synthase reductase (MTRR) is required for the reductive methylation of cobalamin, which is the functional cofactorial form of methionine synthase (MS) in the remethylation of homocysteine to methionine.	Homocysteine	186-198	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
24261678-1	2014	Methionine synthase reductase (MTRR) is required for the reductive methylation of cobalamin, which is the functional cofactorial form of methionine synthase (MS) in the remethylation of homocysteine to methionine.	Homocysteine	186-198	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
24261678-1	2014	Methionine synthase reductase (MTRR) is required for the reductive methylation of cobalamin, which is the functional cofactorial form of methionine synthase (MS) in the remethylation of homocysteine to methionine.	Methionine	137-147	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
24261678-1	2014	Methionine synthase reductase (MTRR) is required for the reductive methylation of cobalamin, which is the functional cofactorial form of methionine synthase (MS) in the remethylation of homocysteine to methionine.	Methionine	137-147	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
26835343-3	2014	In the present study 250 Chinese birth defects cases who suffered 1-8 types of birth defect disease phenotypes were subjected and two genetic variants in two folate metabolism key enzymes, rs1801394 of methionine synthase reductase (MTRR) and rs1801133 of methylenetetrahydrofolate reductase (MTHFR) were genotyped by using SNaPshot method.	Folic Acid	158-164	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	202-231
26835343-3	2014	In the present study 250 Chinese birth defects cases who suffered 1-8 types of birth defect disease phenotypes were subjected and two genetic variants in two folate metabolism key enzymes, rs1801394 of methionine synthase reductase (MTRR) and rs1801133 of methylenetetrahydrofolate reductase (MTHFR) were genotyped by using SNaPshot method.	Folic Acid	158-164	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	233-237
24589657-0	2014	Proximal FAD histidine residue influences interflavin electron transfer in cytochrome P450 reductase and methionine synthase reductase.	Histidine	13-22	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	105-134
24686188-6	2014	Homocysteine levels showed positive correlation with male gender (r=0.39, p<0.0001) and MTRR 66 A>G (r=0.31, p<0.0001) whereas an inverse correlation was observed with cSHMT 1420 C>T polymorphism.	Homocysteine	0-12	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	88-92
24589657-7	2014	For MSR, swapping Ala(312) for a histidine residue resulted in the kinetic coupling of hydride and interflavin electron transfer, and eliminated the formation of the FAD hydroquinone intermediate.	fad hydroquinone	166-182	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-7
24589657-0	2014	Proximal FAD histidine residue influences interflavin electron transfer in cytochrome P450 reductase and methionine synthase reductase.	interflavin	42-53	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	105-134
24589657-1	2014	Cytochrome P450 reductase (CPR) and methionine synthase reductase (MSR) transfer reducing equivalents from NADPH to FAD to FMN.	NADP	107-112	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-65
24589657-1	2014	Cytochrome P450 reductase (CPR) and methionine synthase reductase (MSR) transfer reducing equivalents from NADPH to FAD to FMN.	NADP	107-112	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	67-70
24589657-1	2014	Cytochrome P450 reductase (CPR) and methionine synthase reductase (MSR) transfer reducing equivalents from NADPH to FAD to FMN.	Flavin-Adenine Dinucleotide	116-119	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-65
24589657-1	2014	Cytochrome P450 reductase (CPR) and methionine synthase reductase (MSR) transfer reducing equivalents from NADPH to FAD to FMN.	Flavin-Adenine Dinucleotide	116-119	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	67-70
24589657-1	2014	Cytochrome P450 reductase (CPR) and methionine synthase reductase (MSR) transfer reducing equivalents from NADPH to FAD to FMN.	Flavin Mononucleotide	123-126	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-65
24589657-1	2014	Cytochrome P450 reductase (CPR) and methionine synthase reductase (MSR) transfer reducing equivalents from NADPH to FAD to FMN.	Flavin Mononucleotide	123-126	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	67-70
24589657-2	2014	In CPR, hydride transfer and interflavin electron transfer are kinetically coupled steps, but in MSR the two catalytic steps are represented by two distinct kinetic phases leading to transient formation of the FAD hydroquinone.	fad hydroquinone	210-226	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	97-100
24585533-9	2014	By analyzing a dataset from the National Birth Defects Prevention Study (NBDPS), we identified seven genes (GSTA1, SOD2, MTRR, AHCYL2, GCLC, GSTM3, and RFC1) associated with the development of CTDs.	beta-cyclodextrin tetradecasulfate	193-197	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	121-125
24559276-3	2014	The serine hydroxymethyhransferase (SHMT), methionine synthase (MS), methionine synthase reductase (MTRR) and cystathionine beta synthase (CBS) regulate key reactions in the folate and Hcy metabolism.	Folic Acid	174-180	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	69-98
24595101-2	2014	Both Methionine synthase reductase (MTRR) and Methionine synthase (MTR) are key enzymes involved in the metabolic pathway of homocysteine, which are significant in the earlier period embryogenesis, particularly in the cardiac development.	Homocysteine	125-137	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	5-34
24595101-2	2014	Both Methionine synthase reductase (MTRR) and Methionine synthase (MTR) are key enzymes involved in the metabolic pathway of homocysteine, which are significant in the earlier period embryogenesis, particularly in the cardiac development.	Homocysteine	125-137	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-40
24559276-3	2014	The serine hydroxymethyhransferase (SHMT), methionine synthase (MS), methionine synthase reductase (MTRR) and cystathionine beta synthase (CBS) regulate key reactions in the folate and Hcy metabolism.	Folic Acid	174-180	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	100-104
24559276-3	2014	The serine hydroxymethyhransferase (SHMT), methionine synthase (MS), methionine synthase reductase (MTRR) and cystathionine beta synthase (CBS) regulate key reactions in the folate and Hcy metabolism.	Homocysteine	185-188	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	69-98
24559276-3	2014	The serine hydroxymethyhransferase (SHMT), methionine synthase (MS), methionine synthase reductase (MTRR) and cystathionine beta synthase (CBS) regulate key reactions in the folate and Hcy metabolism.	Homocysteine	185-188	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	100-104
25406481-8	2014	It is suggested that the loss of MSR in mixed systems is the consequence of the very different properties of the binary systems, so that either one of the components (Zn) or a product formed gradually without ignition (e.g. SnSe) can act as an inert component relative to the rest of the system.	Zinc	167-169	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	33-36
24416422-5	2014	Evidence for the possible physiological relevance of this reaction is provided by the formation of ferrous-nitrosyl (Fe(II)-NO) CBS in the presence of NADPH, the human diflavin methionine synthase reductase (MSR) and nitrite.	ferrous-nitrosyl	99-115	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	208-211
24416422-5	2014	Evidence for the possible physiological relevance of this reaction is provided by the formation of ferrous-nitrosyl (Fe(II)-NO) CBS in the presence of NADPH, the human diflavin methionine synthase reductase (MSR) and nitrite.	fe(ii)-no	117-126	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	208-211
24416422-5	2014	Evidence for the possible physiological relevance of this reaction is provided by the formation of ferrous-nitrosyl (Fe(II)-NO) CBS in the presence of NADPH, the human diflavin methionine synthase reductase (MSR) and nitrite.	NADP	151-156	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	208-211
24416422-5	2014	Evidence for the possible physiological relevance of this reaction is provided by the formation of ferrous-nitrosyl (Fe(II)-NO) CBS in the presence of NADPH, the human diflavin methionine synthase reductase (MSR) and nitrite.	Nitrites	217-224	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	208-211
24342607-0	2014	Effect of methionine sulfoxide reductase B1 (SelR) gene silencing on peroxynitrite-induced F-actin disruption in human lens epithelial cells.	Peroxynitrous Acid	69-82	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	10-40
24342607-2	2014	Methionine sulfoxide reductase (Msr) B1 is a selenium-dependent enzyme (selenoprotein R) that may act as a reactive oxygen species (ROS) scavenger.	Selenium	45-53	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-30
24342607-2	2014	Methionine sulfoxide reductase (Msr) B1 is a selenium-dependent enzyme (selenoprotein R) that may act as a reactive oxygen species (ROS) scavenger.	Selenium	45-53	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	32-35
24342607-2	2014	Methionine sulfoxide reductase (Msr) B1 is a selenium-dependent enzyme (selenoprotein R) that may act as a reactive oxygen species (ROS) scavenger.	Reactive Oxygen Species	107-130	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-30
24342607-2	2014	Methionine sulfoxide reductase (Msr) B1 is a selenium-dependent enzyme (selenoprotein R) that may act as a reactive oxygen species (ROS) scavenger.	Reactive Oxygen Species	107-130	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	32-35
24342607-2	2014	Methionine sulfoxide reductase (Msr) B1 is a selenium-dependent enzyme (selenoprotein R) that may act as a reactive oxygen species (ROS) scavenger.	Reactive Oxygen Species	132-135	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-30
24342607-2	2014	Methionine sulfoxide reductase (Msr) B1 is a selenium-dependent enzyme (selenoprotein R) that may act as a reactive oxygen species (ROS) scavenger.	Reactive Oxygen Species	132-135	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	32-35
25531578-1	2014	The methionine sulfoxide reductase (Msr) family of proteins is a class of repair enzymes that reduce methionine-S (MsrA) or methionine-R (MsrB) sulfoxide to methionine.	Methionine	101-113	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	4-34
25531578-1	2014	The methionine sulfoxide reductase (Msr) family of proteins is a class of repair enzymes that reduce methionine-S (MsrA) or methionine-R (MsrB) sulfoxide to methionine.	Methionine	101-113	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-39
25531578-1	2014	The methionine sulfoxide reductase (Msr) family of proteins is a class of repair enzymes that reduce methionine-S (MsrA) or methionine-R (MsrB) sulfoxide to methionine.	Methionine	4-14	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-39
23459165-2	2013	The single nucleotide polymorphisms, MTHFR C677T, A1298C, MTR A2756G and MTRR A66G, cause alteration in the homocysteine levels and reduced enzymatic activity that generates deficiency in the assimilation of folates associated with DNA damage; that is, why it is important to know if the single nucleotide polymorphisms are associated with the pathological characteristics and development of prostate cancer, through a case-control retrospective study.	Homocysteine	108-120	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	73-77
23459165-2	2013	The single nucleotide polymorphisms, MTHFR C677T, A1298C, MTR A2756G and MTRR A66G, cause alteration in the homocysteine levels and reduced enzymatic activity that generates deficiency in the assimilation of folates associated with DNA damage; that is, why it is important to know if the single nucleotide polymorphisms are associated with the pathological characteristics and development of prostate cancer, through a case-control retrospective study.	Folic Acid	208-215	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	73-77
23988788-1	2013	Methionine sulfoxide reductases (Msr"s) are key enzymes proficient in catalyzing the reduction of oxidized methionines.	Methionine	107-118	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	33-36
24019620-1	2013	BACKGROUND AND OBJECTIVES: Methionine synthase reductase (MTRR) is a vital enzyme of homocysteine/methionine metabolic pathway and is required for the conversion of inactive form of methionine synthase (MTR) to its active form.	Homocysteine	85-97	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	27-56
22147344-7	2013	GCPII C1561T, MTHFR C677T and MTRR A66G polymorphisms were observed to influence the homocysteine levels (P &lt; 0.05).	Homocysteine	85-97	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	30-34
25702417-1	2013	Methionine sulfoxide reductase plays a regulatory role in plant growth and development, especially in scavenging reactive oxygen species by restoration of the oxidation of methionine in protein.	Reactive Oxygen Species	113-136	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-30
25702417-1	2013	Methionine sulfoxide reductase plays a regulatory role in plant growth and development, especially in scavenging reactive oxygen species by restoration of the oxidation of methionine in protein.	Methionine	172-182	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-30
23628113-5	2013	Of eight genes responsible for the defects of the Cbl metabolic pathway (cblA-G and mut), MMAA, MMACHC, MTRR and MUT harboured polymorphisms that showed evidence of association with Cbl levels.	Vitamin B 12	50-53	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	104-108
23959833-3	2013	It is still controversial and ambiguous between the functional polymorphisms of folate metabolism genes 5,10-methylenetetrahydrofolate reductase (MTHFR), methionine synthase (MTRR), and methionine synthase reductase (MTR) and risk of adult meningioma.	Folic Acid	80-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	175-179
23959833-3	2013	It is still controversial and ambiguous between the functional polymorphisms of folate metabolism genes 5,10-methylenetetrahydrofolate reductase (MTHFR), methionine synthase (MTRR), and methionine synthase reductase (MTR) and risk of adult meningioma.	Folic Acid	80-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	186-215
23959833-3	2013	It is still controversial and ambiguous between the functional polymorphisms of folate metabolism genes 5,10-methylenetetrahydrofolate reductase (MTHFR), methionine synthase (MTRR), and methionine synthase reductase (MTR) and risk of adult meningioma.	Folic Acid	80-86	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	175-178
23858048-5	2013	Expression of SLC19A1, GGH, FPGS, ABCC1, and MTRR was significantly higher in patients receiving MTX compared to those not receiving MTX (p &lt; 0.05).	Methotrexate	97-100	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	45-49
23790103-7	2013	The reaction of Fe(III)-CBS with the reduced form of the flavoprotein methionine synthase reductase in the presence of CO and NADPH resulted in its reduction and carbonylation to form Fe(II)CO-CBS.	ferric sulfate	16-23	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	70-99
23790103-7	2013	The reaction of Fe(III)-CBS with the reduced form of the flavoprotein methionine synthase reductase in the presence of CO and NADPH resulted in its reduction and carbonylation to form Fe(II)CO-CBS.	Carbon Monoxide	119-121	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	70-99
23790103-7	2013	The reaction of Fe(III)-CBS with the reduced form of the flavoprotein methionine synthase reductase in the presence of CO and NADPH resulted in its reduction and carbonylation to form Fe(II)CO-CBS.	NADP	126-131	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	70-99
23790103-7	2013	The reaction of Fe(III)-CBS with the reduced form of the flavoprotein methionine synthase reductase in the presence of CO and NADPH resulted in its reduction and carbonylation to form Fe(II)CO-CBS.	ammonium ferrous sulfate	184-190	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	70-99
23503767-0	2013	Atypical glomerulopathy associated with the cblE inborn error of vitamin B12 metabolism.	Vitamin B 12	65-76	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	44-48
23503767-1	2013	BACKGROUND: The cblE disorder is an inherited disorder of vitamin B12 metabolism that results in elevated levels of homocysteine and decreased methionine in body fluids.	Vitamin B 12	58-69	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	16-20
23503767-1	2013	BACKGROUND: The cblE disorder is an inherited disorder of vitamin B12 metabolism that results in elevated levels of homocysteine and decreased methionine in body fluids.	Homocysteine	116-128	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	16-20
23503767-1	2013	BACKGROUND: The cblE disorder is an inherited disorder of vitamin B12 metabolism that results in elevated levels of homocysteine and decreased methionine in body fluids.	Methionine	143-153	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	16-20
24019620-1	2013	BACKGROUND AND OBJECTIVES: Methionine synthase reductase (MTRR) is a vital enzyme of homocysteine/methionine metabolic pathway and is required for the conversion of inactive form of methionine synthase (MTR) to its active form.	Homocysteine	85-97	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	58-62
24019620-1	2013	BACKGROUND AND OBJECTIVES: Methionine synthase reductase (MTRR) is a vital enzyme of homocysteine/methionine metabolic pathway and is required for the conversion of inactive form of methionine synthase (MTR) to its active form.	Methionine	98-108	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	27-56
24019620-1	2013	BACKGROUND AND OBJECTIVES: Methionine synthase reductase (MTRR) is a vital enzyme of homocysteine/methionine metabolic pathway and is required for the conversion of inactive form of methionine synthase (MTR) to its active form.	Methionine	98-108	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	58-62
23332101-0	2013	Aromatic substitution of the FAD-shielding tryptophan reveals its differential role in regulating electron flux in methionine synthase reductase and cytochrome P450 reductase.	Flavin-Adenine Dinucleotide	29-32	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	115-144
22527288-6	2013	On its own, vitamin C also correlates with red cell folate (p = 0.0150) and is strongly influenced by genetic variation in TS, MTHFR and MSR, genes critical for DNA and methionine biosynthesis that underpin erythropoiesis.	Ascorbic Acid	12-21	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	137-140
22527288-6	2013	On its own, vitamin C also correlates with red cell folate (p = 0.0150) and is strongly influenced by genetic variation in TS, MTHFR and MSR, genes critical for DNA and methionine biosynthesis that underpin erythropoiesis.	Methionine	169-179	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	137-140
22961839-5	2013	However, statistically significant interactions modifying CC risk were observed for DNMT1 I311V with dietary folate, methionine, vitamin B2 , and vitamin B12 intake and for MTRR I22M with dietary folate, a predefined one-carbon dietary pattern, and vitamin B6 intake.	Folic Acid	196-202	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	173-177
23332101-6	2013	MSR W697Y, but not MSR W697F, showed detectable formation of the disemiquinone intermediate, indicating that the polarity of the aromatic side chain influences the rate of interflavin electron transfer.	disemiquinone	65-78	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
23332101-8	2013	We conclude for MSR that hydride transfer is "gated" by the free energy required to disrupt dispersion forces between the FAD isoalloxazine ring and W697.	fad isoalloxazine	122-139	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	16-19
23332101-0	2013	Aromatic substitution of the FAD-shielding tryptophan reveals its differential role in regulating electron flux in methionine synthase reductase and cytochrome P450 reductase.	Tryptophan	43-53	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	115-144
23332101-1	2013	Methionine synthase reductase (MSR) and cytochrome P450 reductase (CPR) transfer reducing equivalents from NADPH via an FAD and FMN cofactor to a redox partner protein.	NADP	107-112	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
23332101-1	2013	Methionine synthase reductase (MSR) and cytochrome P450 reductase (CPR) transfer reducing equivalents from NADPH via an FAD and FMN cofactor to a redox partner protein.	NADP	107-112	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-34
23332101-1	2013	Methionine synthase reductase (MSR) and cytochrome P450 reductase (CPR) transfer reducing equivalents from NADPH via an FAD and FMN cofactor to a redox partner protein.	Flavin-Adenine Dinucleotide	120-123	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
23332101-1	2013	Methionine synthase reductase (MSR) and cytochrome P450 reductase (CPR) transfer reducing equivalents from NADPH via an FAD and FMN cofactor to a redox partner protein.	Flavin-Adenine Dinucleotide	120-123	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-34
23332101-3	2013	Swapping the tryptophan for a smaller aromatic side chain revealed a distinct role for the residue in regulating MSR and CPR catalysis.	Tryptophan	13-23	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	113-116
23332101-4	2013	MSR W697F and W697Y showed enhanced catalysis, noted by increases in kcat and k(cat)/K(m)(NADPH) for steady-state cytochrome c(3+) reduction and a 10-fold increase in the rate constant (k(obs1)) associated with hydride transfer.	NADP	90-95	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
22925068-2	2013	Methionine synthase reductase (MTRR) is one of the key regulatory enzymes involved in the metabolic pathway of homocysteine.	Homocysteine	111-123	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
23398174-7	2013	When not bound to membrane, oxidized Met1 and Met5 of alphaS are excellent substrates for methionine sulfoxide reductase (Msr), thereby providing an efficient vehicle for water-soluble Msr enzymes to protect the membrane against oxidative damage.	Water	171-176	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	90-120
23398174-7	2013	When not bound to membrane, oxidized Met1 and Met5 of alphaS are excellent substrates for methionine sulfoxide reductase (Msr), thereby providing an efficient vehicle for water-soluble Msr enzymes to protect the membrane against oxidative damage.	Water	171-176	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	122-125
23398174-7	2013	When not bound to membrane, oxidized Met1 and Met5 of alphaS are excellent substrates for methionine sulfoxide reductase (Msr), thereby providing an efficient vehicle for water-soluble Msr enzymes to protect the membrane against oxidative damage.	Water	171-176	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	185-188
22925068-2	2013	Methionine synthase reductase (MTRR) is one of the key regulatory enzymes involved in the metabolic pathway of homocysteine.	Homocysteine	111-123	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
23178192-1	2013	The reduction of methionine sulfoxide in proteins is facilitated by the methionine sulfoxide reductase (Msr) system.	methionine sulfoxide	17-37	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	104-107
23358257-3	2013	Methionine synthase reductase (MTRR) and methylenetetrahydrofolate reductase (MTHFR) are two of the key regulatory enzymes involved in the metabolic pathway of homocysteine.	Homocysteine	160-172	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
23358257-3	2013	Methionine synthase reductase (MTRR) and methylenetetrahydrofolate reductase (MTHFR) are two of the key regulatory enzymes involved in the metabolic pathway of homocysteine.	Homocysteine	160-172	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
23178192-4	2013	Thus, in search of other similar Msr-inducing molecules, we examined the effects of pergolide, pergolide sulfoxide, and S-adenosyl-methionine on Msr activity in neuronal cells.	S-Adenosylmethionine	120-141	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	145-148
23178192-3	2013	Indeed, we have recently shown that treatment of cells with N-acetyl-methionine sulfoxide can increase Msr activity and protect neuronal cells from amyloid beta toxicity.	N-acetylmethionine sulfoxide	60-89	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	103-106
23178192-5	2013	Treatment of neuronal cells with a physiological range of pergolide and pergolide sulfoxide (0.5-1.0 muM) caused an increase of about 40% in total Msr activity compared with non-treated control cells.	Pergolide	58-67	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	147-150
23178192-5	2013	Treatment of neuronal cells with a physiological range of pergolide and pergolide sulfoxide (0.5-1.0 muM) caused an increase of about 40% in total Msr activity compared with non-treated control cells.	pergolide sulfoxide	72-91	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	147-150
23225059-0	2012	[Polymorphisms of homocysteine metabolism enzyme-related genes MS and MSR in Buyi, Dong and Miao ethnics from Guizhou].	Homocysteine	18-30	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	70-73
23178192-7	2013	Similarly, treatment of cells with S-adenosyl methionine also increased cellular Msr activity, which was milder compared to increases induced by pergolide and pergolide sulfoxide.	S-Adenosylmethionine	35-56	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	81-84
23472119-1	2013	BACKGROUND: Methylenetetrahydrofolate reductase (MTHFR) C677T, A1298C and methionine synthase reductase (MTRR) A66G polymorphisms are important genetic determinants for homocysteine (Hcy) levels, and are associated with several disorders.	Homocysteine	169-181	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	74-103
23472119-1	2013	BACKGROUND: Methylenetetrahydrofolate reductase (MTHFR) C677T, A1298C and methionine synthase reductase (MTRR) A66G polymorphisms are important genetic determinants for homocysteine (Hcy) levels, and are associated with several disorders.	Homocysteine	169-181	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	105-109
23472119-1	2013	BACKGROUND: Methylenetetrahydrofolate reductase (MTHFR) C677T, A1298C and methionine synthase reductase (MTRR) A66G polymorphisms are important genetic determinants for homocysteine (Hcy) levels, and are associated with several disorders.	Homocysteine	183-186	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	74-103
23472119-1	2013	BACKGROUND: Methylenetetrahydrofolate reductase (MTHFR) C677T, A1298C and methionine synthase reductase (MTRR) A66G polymorphisms are important genetic determinants for homocysteine (Hcy) levels, and are associated with several disorders.	Homocysteine	183-186	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	105-109
23094987-3	2013	Methionine synthase reductase (5-methyltetrahydrofolate-homocysteine methyltransferase reductase MTRR) plays an important role in folic acid pathway and a common polymorphism (c.66A&gt;G) has been associated with DS but results were controversial.	Folic Acid	130-140	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
23094987-3	2013	Methionine synthase reductase (5-methyltetrahydrofolate-homocysteine methyltransferase reductase MTRR) plays an important role in folic acid pathway and a common polymorphism (c.66A&gt;G) has been associated with DS but results were controversial.	Folic Acid	130-140	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	97-101
22887477-7	2013	ROS content and apoptosis rate increased in control fibroblasts and in a glioblastoma cell line by shRNA-mediated silencing of MTRR gene expression.	Reactive Oxygen Species	0-3	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	127-131
22887477-8	2013	In contrast, wild-type MTRR gene corrected mutant cell lines showed a decrease in ROS and apoptosis levels.	Reactive Oxygen Species	82-85	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	23-27
23225059-1	2012	OBJECTIVE: To investigate polymorphisms of homocysteine metabolism enzyme-related genes methionine synthase (MS) and methionine synthase reductase (MSR) in Buyi, Dong, Miao ethnics from Guizhou.	Homocysteine	43-55	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	117-146
23225059-1	2012	OBJECTIVE: To investigate polymorphisms of homocysteine metabolism enzyme-related genes methionine synthase (MS) and methionine synthase reductase (MSR) in Buyi, Dong, Miao ethnics from Guizhou.	Homocysteine	43-55	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	148-151
23166529-7	2012	To identify the genetic association with gastric cancer, we selected 17 SNPs sites in folate pathway-associated genes of MTHFR, MTR, and MTRR and tested in 1,261 gastric cancer patients and 375 healthy controls.	Folic Acid	86-92	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	137-141
22926161-7	2012	Similarly, the A allele carriers of the MTRR A66G variants showed a higher level of reduction in homocysteine levels (P&lt;0.001), severity of pain in migraine (P=0.002) and percentage of high migraine disability (P=0.006) compared with those with the GG genotypes.	Homocysteine	97-109	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	40-44
23166529-3	2012	In the folate pathway, several genes are involved, including methylenetetrahydrofolate reductase (MTHFR), methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR), and methyltetrahydrofolate-homocysteine methyltransferase (MTR).	Folic Acid	7-13	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	171-175
22864933-6	2012	This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells.	Methionine	175-185	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-101
22864933-6	2012	This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells.	Folic Acid	54-60	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	151-155
22864933-6	2012	This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells.	Folic Acid	54-60	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	151-155
22864933-6	2012	This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells.	Fluorouracil	261-265	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	36-101
22864933-6	2012	This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells.	Methionine	175-185	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	103-107
22864933-6	2012	This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells.	Fluorouracil	261-265	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	103-107
22864933-6	2012	This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells.	Fluorouracil	261-265	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	151-155
22864933-6	2012	This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells.	Methionine	175-185	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	151-155
22864933-6	2012	This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells.	Fluorouracil	261-265	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	151-155
22864933-6	2012	This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells.	Methionine	175-185	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	151-155
22864933-6	2012	This SNP is located upstream of the 5 methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) gene, and it is known that the enzyme for MTRR is involved in the methionine-folate biosynthesis and metabolism pathway, which is the primary target of 5-FU-related compounds, although the authors were unable to identify a direct relation between rs4702484 and MTRR expression in a tested subset of cells.	Folic Acid	54-60	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	103-107
22706675-2	2012	This study tested the hypothesis that maternal folic acid supplementation before or during pregnancy reduces AL risk, accounting for the SNPs rs1801133 (C677T) and rs1801131 (A1298C) in MTHFR and rs1801394 (A66G) and rs1532268 (C524T) in MTRR, assumed to modify folate metabolism.	Folic Acid	47-57	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	238-242
22665368-8	2012	These studies suggest that SNPs in CBS and MTRR have sex-specific associations with aberrant methylation in the lung epithelium of smokers that could be mediated by the affected one-carbon metabolism and transsulfuration in the cells.	Carbon	182-188	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	43-47
22706675-9	2012	However, AL was positively associated with homozygosity for any of the MTHFR polymorphisms and carriership of both MTRR variant alleles (OR = 1.6 [0.9-3.1]).	Aluminum	9-11	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	115-119
22706675-12	2012	The findings also suggest that the genotype homozygous for any of the MTHFR variants and carrying both MTRR variants could be a risk factor for AL.	Aluminum	144-146	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	103-107
22813657-3	2012	The studied polymorphisms included the MTHFR C677T and A1298C, and MTRR A66G, all of which result into amino acid changes, and were previously shown to yield decreased enzymatic activity and alter plasma homocysteine concentration.	Homocysteine	204-216	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	67-71
22236648-0	2012	Polymorphisms in the folate-metabolizing genes MTR, MTRR, and CBS and breast cancer risk.	Folic Acid	21-27	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	52-56
22339686-4	2012	OBJECTIVE: To investigate the association between 3 major polymorphisms in genes encoding enzymes involved in remethylation of homocysteine to methionine--methionine synthase (MTR) A2756G, methionine synthase reductase (MTRR) A66G, and betaine homocysteine methyltransferase (BHMT) G742A--and CAD, with assessment of small-study bias and differences between studies.	Homocysteine	127-139	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	220-224
22236648-2	2012	The aim of our study was to investigate the association of three single-nucleotide polymorphisms (SNPs) in the folate-metabolizing genes - A2756G MTR, A66G MTRR, and 844ins68 CBS - which have putative functional significance in breast cancer risk.	Folic Acid	111-117	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	156-160
22179537-2	2012	Methionine synthase reductase (MTRR) is essential for the adequate remethylation of homocysteine, which is the dominant pathway for homocysteine removal during early embryonic development.	Homocysteine	84-96	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
22334041-10	2012	In single-SNP adjusted analysis, nine SNPs in the XPC, CYP2C9, PAX4, MTRR, and GAN genes were associated with cyclosporine nephrotoxicity.	Cyclosporine	110-122	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	69-73
22468886-0	2012	Planning for Mars returned sample science: final report of the MSR End-to-End International Science Analysis Group (E2E-iSAG).	e2e-isag	116-124	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	63-66
22179537-2	2012	Methionine synthase reductase (MTRR) is essential for the adequate remethylation of homocysteine, which is the dominant pathway for homocysteine removal during early embryonic development.	Homocysteine	84-96	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
22377700-5	2012	The polymorphisms MTHFR c.677C&gt;T and solute carrier family 19 (folate transporter), member 1 (SLC19A1) c.80 A&gt;G modulate folate concentrations, whereas the 5-methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) c.66A&gt;G polymorphism affects the MMA concentration.	Folic Acid	66-72	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	162-227
22377700-5	2012	The polymorphisms MTHFR c.677C&gt;T and solute carrier family 19 (folate transporter), member 1 (SLC19A1) c.80 A&gt;G modulate folate concentrations, whereas the 5-methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) c.66A&gt;G polymorphism affects the MMA concentration.	Folic Acid	66-72	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	229-233
22097960-0	2011	Tryptophan 697 modulates hydride and interflavin electron transfer in human methionine synthase reductase.	Tryptophan	0-10	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	76-105
22097960-1	2011	Human methionine synthase reductase (MSR), a diflavin oxidoreductase, plays a vital role in methionine and folate metabolism by sustaining methionine synthase (MS) activity.	Methionine	6-16	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-40
22097960-1	2011	Human methionine synthase reductase (MSR), a diflavin oxidoreductase, plays a vital role in methionine and folate metabolism by sustaining methionine synthase (MS) activity.	Folic Acid	107-113	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	6-35
22097960-1	2011	Human methionine synthase reductase (MSR), a diflavin oxidoreductase, plays a vital role in methionine and folate metabolism by sustaining methionine synthase (MS) activity.	Folic Acid	107-113	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	37-40
22097960-2	2011	MSR catalyzes the oxidation of NADPH and shuttles electrons via its FAD and FMN cofactors to inactive MS-cob(II)alamin.	NADP	31-36	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
22097960-2	2011	MSR catalyzes the oxidation of NADPH and shuttles electrons via its FAD and FMN cofactors to inactive MS-cob(II)alamin.	Flavin-Adenine Dinucleotide	68-71	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
22097960-2	2011	MSR catalyzes the oxidation of NADPH and shuttles electrons via its FAD and FMN cofactors to inactive MS-cob(II)alamin.	Flavin Mononucleotide	76-79	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
22097960-2	2011	MSR catalyzes the oxidation of NADPH and shuttles electrons via its FAD and FMN cofactors to inactive MS-cob(II)alamin.	cob(II)alamin	105-118	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-3
22097960-8	2011	Binding of NADP(+), but not 2",5"-ADP, is tighter for all mutants than for native MSR.	NADP	11-18	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	82-85
21383205-6	2011	Previous results had indicated that the reduction of (S)-sulindac to sulindac sulfide, the active NSAID, was catalyzed by methionine sulfoxide reductase (Msr) A.	S-sulindac	53-65	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	122-152
21748308-7	2011	Levels of maternal folate intake modified associations with SNPs in CBS, MTRR, and TYMS.	Folic Acid	19-25	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	73-77
21784712-14	2011	Methionine sulfoxide reductase (Msr), a repair enzyme that reduces methionine sulfoxide residues in proteins damaged by oxidation, was also significantly upregulated (2.02-fold increase).	methionine sulfoxide	67-87	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-30
21784712-14	2011	Methionine sulfoxide reductase (Msr), a repair enzyme that reduces methionine sulfoxide residues in proteins damaged by oxidation, was also significantly upregulated (2.02-fold increase).	methionine sulfoxide	67-87	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	32-35
22057956-2	2011	Methionine synthase reductase (MTRR) is one of  the key regulatory enzymes involved in the metabolic pathway of homocysteine.	Homocysteine	112-124	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	0-29
22057956-2	2011	Methionine synthase reductase (MTRR) is one of  the key regulatory enzymes involved in the metabolic pathway of homocysteine.	Homocysteine	112-124	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	31-35
21383205-6	2011	Previous results had indicated that the reduction of (S)-sulindac to sulindac sulfide, the active NSAID, was catalyzed by methionine sulfoxide reductase (Msr) A.	S-sulindac	53-65	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	154-157
21383205-6	2011	Previous results had indicated that the reduction of (S)-sulindac to sulindac sulfide, the active NSAID, was catalyzed by methionine sulfoxide reductase (Msr) A.	sulindac sulfide	69-85	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	122-152
21383205-6	2011	Previous results had indicated that the reduction of (S)-sulindac to sulindac sulfide, the active NSAID, was catalyzed by methionine sulfoxide reductase (Msr) A.	sulindac sulfide	69-85	5-methyltetrahydrofolate-homocysteine methyltransferase reductase	Homo sapiens	154-157