1.1.1.284: S-(hydroxymethyl)glutathione dehydrogenase
This is an abbreviated version!
For detailed information about S-(hydroxymethyl)glutathione dehydrogenase, go to the full flat file.
Word Map on EC 1.1.1.284
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1.1.1.284
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prodrugs
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nitroaromatic
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s-nitrosothiols
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metronidazole
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typhimurium
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nitroreduction
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flavin
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genotoxic
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beta-glucuronidase
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azoreductase
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oxygen-insensitive
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fmn
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1-nitropyrene
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bystander
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nitrosative
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gene-directed
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nifurtimox
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beta-glucosidase
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microflora
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nitroimidazole
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gdept
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o-acetyltransferase
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tester
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nitrofuran
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2,4,6-trinitrotoluene
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denitrosylation
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nitrofurantoin
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s-nitrosation
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nitroarenes
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nitrobenzene
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cloacae
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benznidazole
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bioreductive
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enzyme-prodrug
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nitrofurazone
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prodrug-activating
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two-electron
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single-electron
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2-nitrofluorene
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phytoremediation
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metronidazole-resistant
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redox-based
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off-on
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explosives
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turn-on
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diagnostics
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medicine
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environmental protection
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degradation
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analysis
- 1.1.1.284
-
prodrugs
-
nitroaromatic
- s-nitrosothiols
- metronidazole
- typhimurium
-
nitroreduction
- flavin
-
genotoxic
- beta-glucuronidase
- azoreductase
-
oxygen-insensitive
- fmn
- 1-nitropyrene
-
bystander
-
nitrosative
-
gene-directed
- nifurtimox
- beta-glucosidase
-
microflora
-
nitroimidazole
-
gdept
- o-acetyltransferase
-
tester
-
nitrofuran
- 2,4,6-trinitrotoluene
-
denitrosylation
- nitrofurantoin
-
s-nitrosation
-
nitroarenes
- nitrobenzene
- cloacae
- benznidazole
-
bioreductive
-
enzyme-prodrug
- nitrofurazone
-
prodrug-activating
-
two-electron
-
single-electron
- 2-nitrofluorene
-
phytoremediation
-
metronidazole-resistant
-
redox-based
-
off-on
-
explosives
-
turn-on
- diagnostics
- medicine
- environmental protection
- degradation
- analysis
Reaction
Synonyms
ADH III, ADH3, ADH4, ADH5, AdhC, alcohol dehydrogenase 3, alcohol dehydrogenase 5, alcohol dehydrogenase class III, alcohol dehydrogenase class-3, Alcohol dehydrogenase SFA, AN7632.2, AtGSNOR, c-ADH, carbonyl reductase 1, CBR1, class III ADH, class III alcohol dehydrogenase, dehydrogenase, formaldehyde, EC 1.2.1.1, FALDH, FDH, FLD, FldA, formaldehyde dehydrogenase, formaldehyde dehydrogenase (glutathione), formic dehydrogenase, FrxA, GD-FAlDH, GFD, glutathione (GSH)-dependent formaldehyde dehydrogenase, glutathione-dependent alcohol dehydrogenase, Glutathione-dependent formaldehyde dehydrogenase, GS-FDH, GSH-FDH, GSNO reductase, GSNO-R, GSNOR, GSNOR1, HMGSH dehydrogenase, HOT5, MGG_06011, NAD- and glutathione-dependent formaldehyde dehydrogenase, NAD-dependent formaldehyde dehydrogenase, NAD-linked formaldehyde dehydrogenase, NADH-GSNO oxidoreductase, nitroreductase, NTRA, Os02g0815500, Os02G57040, OsGSNOR, PmFLD1, PmGSNOR, S-nitrosoglutathione reductase, SA0UHSC_00833, SFA1, SlGSNOR, SoGSNOR, Tc-GFD
ECTree
1.1.1.284 S-(hydroxymethyl)glutathione dehydrogenaseAdvanced search results
results (
results (Engineering
Engineering on EC 1.1.1.284 - S-(hydroxymethyl)glutathione dehydrogenase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
E283K
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activity compared with the wild type is 33.8% in hot5-1 plants. No significant change in GSNOR activity under heat stress conditions in the wild-type or mutant. Dark-grown seedlings of hot5-1 have a heat-stress phenotype in the dark, despite having apparently reasonable GSNOR activity at this stage
G288R
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activity compared with the wild type is 58.8% in hot5-3 plants. No significant change in GSNOR activity under heat stress conditions in the wild-type or mutant. Dark-grown seedlings of hot5-3 have a heat-stress phenotype in the dark, despite having apparently reasonable GSNOR activity at this stage
D57L/Y93F
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fall in ratio kcat/Km for hydroxymethylglutathione by a factor of 1250, alcohol dehydrogenase activity of the mutant has gained a characteristic class I property, complete inhibition by 4-methylpyrazole at concentrations only partially reducing the activity of the wild-type class III enzyme
K188A
site-directed mutagenesis, the mutation results in the loss of allosteric behavior of the enzyme
K323A
site-directed mutagenesis, the mutation results in the loss of allosteric behavior of the enzyme
T48A
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enzyme has essentially no alcohol dehydrogenase activity but has some glutathione-dependent formaldehyde dehydrogenase activity
Y93F
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decreased turnover number for substrates in general, inhibition of alcohol dehydrogenase activity by 4-methylpyrazole, which is not found in the wild-type enzyme
D267E/T269I
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Km-value for S-hydroxymethylglutathione is about 11fold lower than that of the wild-type enzyme, turnover-number for S-hydroxymethylglutathione is about 8fold lower than that of wild-type enzyme
D269I
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highly unstable enzyme, kinetic properties identical to that of wild-type enzyme
C47S
additional information
additional information
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thermotolerance-defective mutant hot5, which encodes GSNOR. Hot5 missense alleles cannot acclimate to heat as dark-grown seedlings but grow normally and can heat-acclimate in the light. The null alleles cannot heat-acclimate as light-grown plants and have other phenotypes, including failure to grow on nutrient plates, increased reproductive shoots, and reduced fertility. The fertility defect of hot5 is due to both reduced stamen elongation and male and female fertilization defects. The hot5 null alleles show increased nitrate and nitroso species levels, and the heat sensitivity of both missense and null alleles is associated with increased NO species. Heat sensitivity is enhanced in wild-type and mutant plants by NO donors, and the heat sensitivity of hot5 mutants can be rescued by an NO scavenger. An NO-overproducing mutant is also defective in thermotolerance
additional information
construction of GSNOR knockout plants that exhibit overall reductions in growth where root development, thought to be directly linked to redox activity. The GSNOR knockout mutant contains a pre-induced antioxidant protection system
additional information
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overexpression of the fdh in the central nervous system significantly increases GSNOR activity and induces visual pattern memory defects of Drosophila melanogaster, Overexpression of fdh results in NO imbalance, thereby affecting the NO-cGMPPKG pathway and protein S-nitrosation and, ultimately, learning and memory function, regulation of protein S-nitrosation by fdh in transgenic flies, overview. elav-Gal4 driven pan-neuronal GSNOR and PKG co-expression flies restore normal memory performance completely
additional information
chromosomal inactivation of either adhC or nmlRHI resulted in sensitivity to S-nitrosoglutathione and decreased S-nitrosoglutathione reductase activity, the NmlRHI-AdhC system in the genome sequences of nontypeable Haemophilus influenzae strains R2846, R2866, and 86-028NP shows variations, the adhC gene of strain 86-028NP is nonfunctional due to a premature stop codon, polymorphisms in the operator/promoter region of strain R2866 result in reduced enzyme activity, genotyping of clinical isolates, overview
additional information
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chromosomal inactivation of either adhC or nmlRHI resulted in sensitivity to S-nitrosoglutathione and decreased S-nitrosoglutathione reductase activity, the NmlRHI-AdhC system in the genome sequences of nontypeable Haemophilus influenzae strains R2846, R2866, and 86-028NP shows variations, the adhC gene of strain 86-028NP is nonfunctional due to a premature stop codon, polymorphisms in the operator/promoter region of strain R2866 result in reduced enzyme activity, genotyping of clinical isolates, overview
additional information
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chromosomal inactivation of either adhC or nmlRHI resulted in sensitivity to S-nitrosoglutathione and decreased S-nitrosoglutathione reductase activity, the NmlRHI-AdhC system in the genome sequences of nontypeable Haemophilus influenzae strains R2846, R2866, and 86-028NP shows variations, the adhC gene of strain 86-028NP is nonfunctional due to a premature stop codon, polymorphisms in the operator/promoter region of strain R2866 result in reduced enzyme activity, genotyping of clinical isolates, overview
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additional information
genetic deletion of GSNO-R. After 20 minutes of global ischemia and 60 minutes of reperfusion, contractile function is significantly impaired in male and female hearts, but post-ischemic functional recovery is significantly higher in female hearts and infarct size is reduced. Male GSNO-R-/- hearts show a significant reduction in infarct size compared to wild-type, while female GSNO-R-/- hearts show a significant increase in infarct size compared to wild-type
additional information
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genetic deletion of GSNO-R. After 20 minutes of global ischemia and 60 minutes of reperfusion, contractile function is significantly impaired in male and female hearts, but post-ischemic functional recovery is significantly higher in female hearts and infarct size is reduced. Male GSNO-R-/- hearts show a significant reduction in infarct size compared to wild-type, while female GSNO-R-/- hearts show a significant increase in infarct size compared to wild-type
additional information
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genetic deletion of GSNO-R. After 20 minutes of global ischemia and 60 minutes of reperfusion, contractile function is significantly impaired in male and female hearts, but post-ischemic functional recovery is significantly higher in female hearts and infarct size is reduced. Male GSNO-R-/- hearts show a significant reduction in infarct size compared to wild-type, while female GSNO-R-/- hearts show a significant increase in infarct size compared to wild-type
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additional information
RNAi-based gene silencing of the enzyme does not impair wounding- and simulated herbivory-induced MAPK activity but alter methyl jasmonate resposes, phenotypes, overview
additional information
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RNAi-based gene silencing of the enzyme does not impair wounding- and simulated herbivory-induced MAPK activity but alter methyl jasmonate resposes, phenotypes, overview
additional information
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construction of a bi-enzyme biosensor based on NAD+- and glutathione-dependent recombinant genetically-engineered methylotrophic yeast formaldehyde dehydrogenase activity and from Bacillus stearothermophilus diaphorase activity as bio-recognition elements for a formaldehyde assay, overview, the sensor architecture comprises a first layer containing diaphorase cross-linked with an osmium complex-modified redox polymer (poly(vinylpyridine)-[osmium-(N,N'-methylated-2,2'-biimidalzole)3]3+/2+ complex) and a second layer formed by additional cross-linking of FDH with poly(ethylene glycol)(400)diglycidyl ether on the top, optimization, overview
additional information
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construction of a formaldehyde-selective biosensor using NAD+- and glutathione-dependent recombinant formaldehyde dehydrogenase as a bio-recognition element immobilized on the surface of Si/SiO2/Si3N4 structure, evaluation by capacitance measurements, best sensitivity is observed in 2.5 mM borate buffer, pH 8.4
additional information
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construction of a formaldehyde-selective biosensor using NAD+- and glutathione-dependent recombinant formaldehyde dehydrogenase as a bio-recognition element immobilized on the surface of Si/SiO2/Si3N4 structure, evaluation by capacitance measurements, best sensitivity is observed in 2.5 mM borate buffer, pH 8.4
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additional information
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construction of a bi-enzyme biosensor based on NAD+- and glutathione-dependent recombinant genetically-engineered methylotrophic yeast formaldehyde dehydrogenase activity and from Bacillus stearothermophilus diaphorase activity as bio-recognition elements for a formaldehyde assay, overview, the sensor architecture comprises a first layer containing diaphorase cross-linked with an osmium complex-modified redox polymer (poly(vinylpyridine)-[osmium-(N,N'-methylated-2,2'-biimidalzole)3]3+/2+ complex) and a second layer formed by additional cross-linking of FDH with poly(ethylene glycol)(400)diglycidyl ether on the top, optimization, overview
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additional information
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construction of a formaldehyde-selective biosensor using NAD+- and glutathione-dependent recombinant formaldehyde dehydrogenase as a bio-recognition element immobilized on the surface of Si/SiO2/Si3N4 structure, evaluation by capacitance measurements, best sensitivity is observed in 2.5 mM borate buffer, pH 8.4
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additional information
knockout of OsGSNOR (Os02G57040), using the CRISPR/Cas9 system. The root growth in two OsGSNOR knockout lines (Osgsnor-1 and Osgsnor-2) is significantly more sensitive to NH4+ than in wild-type. Compared with the wild-type, the root K+ content in Osgsnor knockout lines is lower under NH4+
additional information
construction of GSNOR knockout plants that exhibit overall reductions in growth where root development, thought to be directly linked to redox activity. The GSNOR knockout mutant contains a pre-induced antioxidant protection system
additional information
enzyme SlGSNOR knockout by gene silencing with RNAi using Agrobacterium tumefaciens transfection method. The accumulation of SlGSNOR1 transcripts is tightly regulated in tomato MicroTom and a significant reduction in its expression leads to lethality, as SlGSNOR-RNAi lines with greater than about 60% reduction in SlGSNOR1 expression are not viable. Both SlGSNOR-RNAi and SlGSNOR-overexpressing(OE) lines convey significant effects on the overall development of tomato plants, ranging from seed germination to fruiting and net yield per plant. Reduced GSNOR expression in SlGSNOR-RNAi lines drastically affects seed development and reduces the number of seeds produced in the fruits of the resulting transgenic plants, phenotype, overview. SlGSNOR-RNAi plants also show faster germination as compared with wild-type and SlGSNOR-OE plants on either MS medium or soil, and show the appearance of fresh green tissues at least 1 d before the wild-type and overexpressing plants
additional information
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enzyme SlGSNOR knockout by gene silencing with RNAi using Agrobacterium tumefaciens transfection method. The accumulation of SlGSNOR1 transcripts is tightly regulated in tomato MicroTom and a significant reduction in its expression leads to lethality, as SlGSNOR-RNAi lines with greater than about 60% reduction in SlGSNOR1 expression are not viable. Both SlGSNOR-RNAi and SlGSNOR-overexpressing(OE) lines convey significant effects on the overall development of tomato plants, ranging from seed germination to fruiting and net yield per plant. Reduced GSNOR expression in SlGSNOR-RNAi lines drastically affects seed development and reduces the number of seeds produced in the fruits of the resulting transgenic plants, phenotype, overview. SlGSNOR-RNAi plants also show faster germination as compared with wild-type and SlGSNOR-OE plants on either MS medium or soil, and show the appearance of fresh green tissues at least 1 d before the wild-type and overexpressing plants
additional information
GSNOR knockdown tomato lines are established by RNA interference (RNAi) approach
additional information
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GSNOR knockdown tomato lines are established by RNA interference (RNAi) approach
additional information
there are no significant changes in the physiological or chlorophyll fluorescence parameters between tomato leaves of wild-type and transgenic GSNOR overexpressing lines under control conditions. In contrast, apparent chlorosis is observed in the wild-type lines after 20 d under Fe-deficiency conditions, while transgenic lines show significantly higher Fe-deficiency tolerance levels than wild-type lines as assessed by morphological characteristics, especially the color of the stem apices and new leaves
additional information
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there are no significant changes in the physiological or chlorophyll fluorescence parameters between tomato leaves of wild-type and transgenic GSNOR overexpressing lines under control conditions. In contrast, apparent chlorosis is observed in the wild-type lines after 20 d under Fe-deficiency conditions, while transgenic lines show significantly higher Fe-deficiency tolerance levels than wild-type lines as assessed by morphological characteristics, especially the color of the stem apices and new leaves
additional information
overexpression of SoGSNOR alleviates excess nitrate-induced oxidative stress in transgenic Nicotiana tabacum cv. NC89 seedlings, phenotype, overview. Overexpression SoGSNOR enhances the germination rate of transgenic tobacco seeds under nitrate stress, and overexpression of SoGSNOR results in lower NO and SNOs contents in the tobacco seedlings
additional information
GSNOR dsRNA is employed to knockdown the expression of GSNO. GSNOR knock-down induces oxidative stress-derived apoptosis and DNA damage, as well as inhibits autophagic process
additional information
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GSNOR dsRNA is employed to knockdown the expression of GSNO. GSNOR knock-down induces oxidative stress-derived apoptosis and DNA damage, as well as inhibits autophagic process
