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5 sulfur + 2 O2 + 2 H2O + 4 H+
sulfite + thiosulfate + 2 sulfide
bacillithiol persulfide + O2
bacillithiol + sulfite
-
-
-
?
CoASSH + O2
CoA + sulfite
-
-
-
?
gamma-glutamyl-homocysteinyl-glycine + O2
gamma-glutamyl-homocysteinyl-SO2H + ?
mechanism-based inhibitor, accepted as an alternative substrate and converted to glutamyl-homocysteinyl-SO2H
-
-
?
glutathione + sulfite + 2 H+
S-sulfanylglutathione + O2 + H2O
S-sulfanyl-L-cysteine + O2
L-cysteine + sulfite
-
-
-
?
S-sulfanylglutathione + O2
glutathione + sulfite
-
-
-
?
S-sulfanylglutathione + O2
sulfite + glutathione + H+
-
-
-
-
?
S-sulfanylglutathione + O2 + H2O
glutathione + sulfite + 2 H+
sulfur + O2 + H2O
sulfite
sulfur + O2 + H2O
thiosulfate
-
-
in the presence of reduced glutathione and 2,2'-dipyridyl
-
?
additional information
?
-
5 sulfur + 2 O2 + 2 H2O + 4 H+
sulfite + thiosulfate + 2 sulfide
-
-
-
-
?
5 sulfur + 2 O2 + 2 H2O + 4 H+
sulfite + thiosulfate + 2 sulfide
-
incorporation of elemental sulfur, possible role in thiosulfate metabolism, reaction provides energy
-
-
?
5 sulfur + 2 O2 + 2 H2O + 4 H+
sulfite + thiosulfate + 2 sulfide
-
-
-
-
?
5 sulfur + 2 O2 + 2 H2O + 4 H+
sulfite + thiosulfate + 2 sulfide
-
incorporation of elemental sulfur, possible role in thiosulfate metabolism, reaction provides energy
-
-
?
glutathione + sulfite + 2 H+
S-sulfanylglutathione + O2 + H2O
-
-
-
r
glutathione + sulfite + 2 H+
S-sulfanylglutathione + O2 + H2O
-
-
-
-
r
S-sulfanylglutathione + O2 + H2O
glutathione + sulfite + 2 H+
-
-
-
r
S-sulfanylglutathione + O2 + H2O
glutathione + sulfite + 2 H+
-
-
-
?
sulfur + O2 + H2O
sulfite
-
-
low amount of thiosulfate observed may result from a chemical reaction between sulfite and elemental sulfur
ir
sulfur + O2 + H2O
sulfite
-
-
further reacts non-enzymically to form sulfate, thiosulfate or in the presence of glutathione glutathione S-sulfonate
-
?
sulfur + O2 + H2O
sulfite
-
incorporation of elemental sulfur
further reacts non-enzymically to form sulfate, thiosulfate or in the presence of glutathione glutathione S-sulfonate
-
?
sulfur + O2 + H2O
sulfite
-
-
further reacts non-enzymically to form sulfate, thiosulfate or in the presence of glutathione glutathione S-sulfonate
-
?
sulfur + O2 + H2O
sulfite
-
incorporation of elemental sulfur
further reacts non-enzymically to form sulfate, thiosulfate or in the presence of glutathione glutathione S-sulfonate
-
?
sulfur + O2 + H2O
sulfite
-
-
further reacts non-enzymically to form sulfate, thiosulfate or in the presence of glutathione glutathione S-sulfonate
-
?
sulfur + O2 + H2O
sulfite
-
incorporation of elemental sulfur
further reacts non-enzymically to form sulfate, thiosulfate or in the presence of glutathione glutathione S-sulfonate
-
?
sulfur + O2 + H2O
sulfite
-
-
-
?
sulfur + O2 + H2O
sulfite
-
-
S2O32- may be formed through a secondary, non-enzymatic reaction
ir
sulfur + O2 + H2O
sulfite
-
-
further reacts non-enzymically to form sulfate, thiosulfate or in the presence of glutathione glutathione S-sulfonate
-
?
sulfur + O2 + H2O
sulfite
-
incorporation of elemental sulfur
further reacts non-enzymically to form sulfate, thiosulfate or in the presence of glutathione glutathione S-sulfonate
-
?
sulfur + O2 + H2O
sulfite
-
-
-
?
sulfur + O2 + H2O
sulfite
-
-
-
ir
sulfur + O2 + H2O
sulfite
-
-
-
-
?
sulfur + O2 + H2O
sulfite
-
incorporation of elemental sulfur
-
-
?
sulfur + O2 + H2O
sulfite
-
-
-
ir
sulfur + O2 + H2O
sulfite
-
-
S2O32- may be formed through a secondary, non-enzymatic reaction
ir
additional information
?
-
Arabidopsis ETHE1 catalyzes the glutathione persulfide-dependent consumption of oxygen
-
-
?
additional information
?
-
-
BpPRF is a bifunctional enzyme that uses the rhodanese domain to preferentially catalyze sulfur transfer from thiosulfate to GSH to form sulfite and GSSH and uses the PDO domain to oxidize GSSH to sulfite
-
-
?
additional information
?
-
-
cysteine persulfide and thiosulfate are no substrates
-
-
?
additional information
?
-
coupled persulfide dioxygenase-persulfide transferase (cPDO-PT) activity assay producing thiosulfate as product preferentially from CoASSH and bacillithiol persulfide. CstB does not catalyze the formation of thiosulfate from reduced low molecular weight thiol, oxidized low molecular weight disulfide or Na2S. Cysteine persulfide (CSSH) and glutathione persulfide (GSSH) also serve as persulfide substrates for wild-type CstB but are poorer substrates
-
-
?
additional information
?
-
-
coupled persulfide dioxygenase-persulfide transferase (cPDO-PT) activity assay producing thiosulfate as product preferentially from CoASSH and bacillithiol persulfide. CstB does not catalyze the formation of thiosulfate from reduced low molecular weight thiol, oxidized low molecular weight disulfide or Na2S. Cysteine persulfide (CSSH) and glutathione persulfide (GSSH) also serve as persulfide substrates for wild-type CstB but are poorer substrates
-
-
?
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Acquired Immunodeficiency Syndrome
Intergroup contact, social dominance, and environmental concern: A test of the cognitive-liberalization hypothesis.
Adenomatous Polyposis Coli
ETHE1 overexpression promotes SIRT1 and PGC1? mediated aerobic glycolysis, oxidative phosphorylation, mitochondrial biogenesis and colorectal cancer.
Anemia, Hypochromic
The mitochondrial sulfur dioxygenase ETHE1 is required for amino acid catabolism during carbohydrate starvation and embryo development in Arabidopsis thaliana.
Brain Diseases
Acute and Chronic Management in an Atypical Case of Ethylmalonic Encephalopathy.
Brain Diseases
Acute Strokelike Presentation and Long-term Evolution of Diffusion Restriction Pattern in Ethylmalonic Encephalopathy.
Brain Diseases
Arabidopsis ETHE1 Encodes a Sulfur Dioxygenase That Is Essential for Embryo and Endosperm Development.
Brain Diseases
Characterization of patient mutations in human persulfide dioxygenase (ETHE1) involved in H2S catabolism.
Brain Diseases
Chronic Exposure to Sulfide causes Accelerated Degradation of Cytochrome c oxidase in Ethylmalonic Encephalopathy.
Brain Diseases
Combined treatment with oral metronidazole and N-acetylcysteine is effective in ethylmalonic encephalopathy.
Brain Diseases
Compromised therapeutic value of pediatric liver transplantation in ethylmalonic encephalopathy: A case report.
Brain Diseases
Crystal structure of human persulfide dioxygenase: structural basis of ethylmalonic encephalopathy.
Brain Diseases
Deficiency of the mitochondrial sulfide regulator ETHE1 disturbs cell growth, glutathione level and causes proteome alterations outside mitochondria.
Brain Diseases
Distribution, diversity, and activities of sulfur dioxygenases in heterotrophic bacteria.
Brain Diseases
ETHE1 mutations are specific to ethylmalonic encephalopathy.
Brain Diseases
ETHE1 overexpression promotes SIRT1 and PGC1? mediated aerobic glycolysis, oxidative phosphorylation, mitochondrial biogenesis and colorectal cancer.
Brain Diseases
Ethylmalonic encephalopathy associated with crescentic glomerulonephritis.
Brain Diseases
Ethylmalonic encephalopathy ETHE1 p. D165H mutation alters the mitochondrial function in human skeletal muscle proteome.
Brain Diseases
Ethylmalonic encephalopathy ETHE1 R163W/R163Q mutations alter protein stability and redox properties of the iron centre.
Brain Diseases
Ethylmalonic encephalopathy is caused by mutations in ETHE1, a gene encoding a mitochondrial matrix protein.
Brain Diseases
Ethylmalonic encephalopathy: Clinical course and therapy response in an uncommon mild case with a severe ETHE1 mutation.
Brain Diseases
Expression of abiotic stress inducible ETHE1-like protein from rice is higher in roots and is regulated by calcium.
Brain Diseases
Expression of abiotic stress inducible ETHE1?like protein from rice is higher in roots and is regulated by calcium
Brain Diseases
Identification of a novel homozygous nonsense variant in a Chinese patient with ethylmalonic encephalopathy and a genotype-phenotype spectrum review.
Brain Diseases
Identification of new mutations in the ETHE1 gene in a cohort of 14 patients presenting with ethylmalonic encephalopathy.
Brain Diseases
Improved clinical outcome following liver transplant in patients with ethylmalonic encephalopathy.
Brain Diseases
Loss of ETHE1, a mitochondrial dioxygenase, causes fatal sulfide toxicity in ethylmalonic encephalopathy.
Brain Diseases
Mitochondrial diseases caused by toxic compound accumulation: from etiopathology to therapeutic approaches.
Brain Diseases
Mitochondrial Dysfunction and Redox Homeostasis Impairment as Pathomechanisms of Brain Damage in Ethylmalonic Encephalopathy: Insights from Animal and Human Studies.
Brain Diseases
Multiple sources of metabolic disturbance in ETHE1-related ethylmalonic encephalopathy.
Brain Diseases
Novel Compound Heterozygous Variants of ETHE1 Causing Ethylmalonic Encephalopathy in a Chinese Patient: A Case Report.
Brain Diseases
Novel ETHE1 mutation in a carrier couple having prior offspring affected with ethylmalonic encephalopathy: Genetic analysis, clinical management and reproductive outcome.
Brain Diseases
Protein polysulfidation-dependent persulfide dioxygenase activity of ethylmalonic encephalopathy protein 1.
Brain Diseases
Proteomics Reveals that Redox Regulation Is Disrupted in Patients with Ethylmalonic Encephalopathy.
Brain Diseases
Quantitative proteomics suggests metabolic reprogramming during ETHE1 deficiency.
Brain Diseases
Response to medical and a novel dietary treatment in newborn screen identified patients with ethylmalonic encephalopathy.
Brain Diseases
Severe early onset ethylmalonic encephalopathy with West syndrome.
Brain Diseases
Spectroscopic studies on Arabidopsis ETHE1, a glyoxalase II-like protein.
Brain Diseases
Staphylococcus aureus CstB Is a Novel Multidomain Persulfide Dioxygenase-Sulfurtransferase Involved in Hydrogen Sulfide Detoxification.
Brain Diseases
Stress response of OsETHE1 is altered in response to light and dark conditions.
Brain Diseases
Structure of an ETHE1-like protein from Arabidopsis thaliana.
Brain Diseases
Sulfide detoxification in plant mitochondria.
Brain Diseases
Untargeted Metabolomics Analysis Reveals a Link between ETHE1-Mediated Disruptive Redox State and Altered Metabolic Regulation.
Brain Diseases
[Clinical and genetic analysis of a case with atypical ethyl malonate encephalopathy].
Carcinogenesis
ETHE1 overexpression promotes SIRT1 and PGC1? mediated aerobic glycolysis, oxidative phosphorylation, mitochondrial biogenesis and colorectal cancer.
Colorectal Neoplasms
ETHE1 overexpression promotes SIRT1 and PGC1? mediated aerobic glycolysis, oxidative phosphorylation, mitochondrial biogenesis and colorectal cancer.
Colorectal Neoplasms
Systems Biomedicine of Primary and Metastatic Colorectal Cancer Reveals Potential Therapeutic Targets.
Congenital Abnormalities
Total hip arthroplasty requiring subtrochanteric osteotomy for developmental hip dysplasia 5- to 14-year results.
COVID-19
U.S. public support for COVID-19 vaccine donation to low- and middle-income countries during the COVID-19 pandemic.
Craniocerebral Trauma
Increased Risks of Suicide Attempt and Suicidal Drug Overdose Following Admission for Head Injury in Patients with Depression.
Craniocerebral Trauma
Increasing Risks of Suicide Attempt and Suicidal Drug Overdose After Head Trauma in Patients With Sleep-Disordered Breathing: A Population-Based Study.
Craniosynostoses
Piezosurgical Suturectomy and Sutural Distraction Osteogenesis for the Treatment of Unilateral Coronal Synostosis.
Cytochrome-c Oxidase Deficiency
Chronic Exposure to Sulfide causes Accelerated Degradation of Cytochrome c oxidase in Ethylmalonic Encephalopathy.
Diabetic Nephropathies
Evaluating Pharmacological Effects of Two Major Components of Shuangdan Oral Liquid: Role of Danshensu and Paeonol in Diabetic Nephropathy Rat.
Enteritis
[Epidemiological impact of RV gastroenteritis in the Abruzzo Region: SDO analysis]
Epilepsy
Differences in Incidence and Risks of Suicide Attempt and Suicidal Drug Overdose between Patients with Epilepsy with and without Comorbid Depression.
Gastroenteritis
[Epidemiological impact of RV gastroenteritis in the Abruzzo Region: SDO analysis]
Hyperlipidemias
Metabolomics analysis of the therapeutic mechanism of Semen Descurainiae Oil on hyperlipidemia rats using 1 H-NMR and LC-MS.
Hypospadias
Hypospadias prevalence in the Emilia Romagna Region registry: Increasing or methodology?
Infections
The role of short-chain dehydrogenase/oxidoreductase, induced by salt stress, on host interaction of B. pseudomallei.
Melanoma
Second Diagnostic Opinion by Experienced Dermatopathologists in the Setting of a Referral Regional Melanoma Unit Significantly Improves the Clinical Management of Patients With Cutaneous Melanoma.
Melioidosis
Altered proteome of a Burkholderia pseudomallei mutant defective in short-chain dehydrogenase affects cell adhesion, biofilm formation and heat stress tolerance.
Metabolic Syndrome
Lipogenesis is decreased by grape seed proanthocyanidins according to liver proteomics of rats fed a high fat diet.
Mitochondrial Diseases
Acute Strokelike Presentation and Long-term Evolution of Diffusion Restriction Pattern in Ethylmalonic Encephalopathy.
Mitochondrial Diseases
Improved clinical outcome following liver transplant in patients with ethylmalonic encephalopathy.
Mitochondrial Diseases
Mitochondrial diseases caused by toxic compound accumulation: from etiopathology to therapeutic approaches.
Neoplasms
[Extending traceability of malignant testicular tumours using hospital discharge records: an experience in Veneto Region (Northern Italy)].
Neurodegenerative Diseases
Identification of a novel homozygous nonsense variant in a Chinese patient with ethylmalonic encephalopathy and a genotype-phenotype spectrum review.
Neurodegenerative Diseases
Response to medical and a novel dietary treatment in newborn screen identified patients with ethylmalonic encephalopathy.
Obesity
Obesity discrimination: the role of physical appearance, personal ideology, and anti-fat prejudice.
Ovarian Neoplasms
Salpingectomy for the Risk Reduction of Ovarian Cancer: Is It Time for a Salpingectomy-alone Approach?
Overweight
Feminist identification, social dominance orientation, and weight bias in men.
Paraparesis, Spastic
Ethylmalonic encephalopathy: Clinical course and therapy response in an uncommon mild case with a severe ETHE1 mutation.
Parkinson Disease
Spatiotemporal characteristics of postsaccadic dynamic overshoot in young and elderly subjects.
persulfide dioxygenase deficiency
Deficiency of the mitochondrial sulfide regulator ETHE1 disturbs cell growth, glutathione level and causes proteome alterations outside mitochondria.
persulfide dioxygenase deficiency
ETHE1 and MOCS1 deficiencies: Disruption of mitochondrial bioenergetics, dynamics, redox homeostasis and endoplasmic reticulum-mitochondria crosstalk in patient fibroblasts.
persulfide dioxygenase deficiency
Evidence that thiol group modification and reactive oxygen species are involved in hydrogen sulfide-induced mitochondrial permeability transition pore opening in rat cerebellum.
persulfide dioxygenase deficiency
Evidence that Thiosulfate Inhibits Creatine Kinase Activity in Rat Striatum via Thiol Group Oxidation.
persulfide dioxygenase deficiency
Morphologic evidence of diffuse vascular damage in human and in the experimental model of ethylmalonic encephalopathy.
persulfide dioxygenase deficiency
Quantitative proteomics suggests metabolic reprogramming during ETHE1 deficiency.
persulfide dioxygenase deficiency
The Role of Persulfide Metabolism During Arabidopsis Seed Development Under Light and Dark Conditions.
persulfide dioxygenase deficiency
Untargeted Metabolomics Analysis Reveals a Link between ETHE1-Mediated Disruptive Redox State and Altered Metabolic Regulation.
Pulmonary Disease, Chronic Obstructive
Suicide Attempt and Suicidal Drug Overdose in Chronic Obstructive Pulmonary Disease Patients With or Without Depression.
Purpura
Ethylmalonic encephalopathy associated with crescentic glomerulonephritis.
Starvation
Stress response of OsETHE1 is altered in response to light and dark conditions.
Starvation
The mitochondrial sulfur dioxygenase ETHE1 is required for amino acid catabolism during carbohydrate starvation and embryo development in Arabidopsis thaliana.
Starvation
The Role of Persulfide Metabolism During Arabidopsis Seed Development Under Light and Dark Conditions.
Stroke
Suicidal drug overdose following stroke in elderly patients: a retrospective population-based cohort study.
Synostosis
Piezosurgical Suturectomy and Sutural Distraction Osteogenesis for the Treatment of Unilateral Coronal Synostosis.
Synovitis
Identification of pathways and genes associated with synovitis in osteoarthritis using bioinformatics analyses.
Testicular Neoplasms
[Extending traceability of malignant testicular tumours using hospital discharge records: an experience in Veneto Region (Northern Italy)].
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additional information
-
residue Cys314, located in the rhodanese-active site, is captured in its persulfidated Cys-SSH form. The PDO-active site is located at the bottom of a large pocket framed on one side by a positively charged ridge comprising residues Arg193-Lys216 and by Tyr176 on the other
evolution
CstB is a multifunctional Fe(II)-containing persulfide dioxygenase (PDO), analogous to the vertebrate protein ETHE1, ethylmalonic encephalopathy protein 1
evolution
-
enzyme persulfide dioygenase, PDO, is a member of the 2His-1Asp mononuclear iron-containing enzyme superfamily
malfunction
-
ethylmalonic encephalopathy is caused by mutations in the mitochondrial matrix sulfur dioxygenase ETHE1 leading to failure to detoxify sulfide, a product of intestinal anaerobes and, in trace amounts, tissues
malfunction
-
ethylmalonic encephalopathy is caused by mutations in the mitochondrial matrix sulfur dioxygenase ETHE1 leading to failure to detoxify sulfide, a product of intestinal anaerobes and, in trace amounts, tissues
malfunction
seeds homozygous for a DNA insertion in ETHE1 exhibit alterations in endosperm development that are accompanied by a delay in embryo development followed by embryo arrest by early heart stage
malfunction
by overexpressing sdo in strain ATCC 23270, a 91fold increased sdo transcriptional level and a 2.5fold increase in SDO activity are observed when sulfur S0 is used as sole energy source. The sdo knockout mutant displays a slightly reduced growth capacity in S0-medium compared with the wild type but still maintains high S0-oxidizing activity, suggesting that there is at least one other S0-oxidizing enzyme besides SDO in Acidithiobacillus ferrooxidans ATCC 23270 cells
malfunction
stB C201S and C408S mutants are unable to rescue a NaHS-induced DELTAcstB
physiological function
ETHE1 appears to play an essential role in regulating sulfide levels in seeds, it is essential for early seed development
physiological function
-
natural fusions between the non-heme iron containing PDO and rhodanese, a thiol sulfurtransferase, exist in some bacteria, e.g. in Burkholderia phytofirmans. The two active sites in PRF are distant and do not show evidence of direct communication. The Burkholderia phytofirmans PRF exhibits robust PDO activity and preferentially catalyzes sulfur transfer in the direction of thiosulfate to sulfite and glutathione persulfide, while sulfur transfer in the reverse direction is detectable only under limited turnover conditions. Burkholderia phytofirmans PRF is poised to metabolize thiosulfate to sulfite in a sulfur assimilation pathway rather than in sulfide stress response
physiological function
the enzyme is a multidomain persulfide dioxygenase-sulfurtransferase, a multifunctional Fe(II)-containing persulfide dioxygenase. Enzyme CstB oxidizes major cellular low molecular weight persulfide substrates from Staphylococcus aureus, coenzyme A persulfide (CoASSH) and bacillithiol persulfide (BSSH), directly to generate thiosulfate and reduced thiols, thereby avoiding the cellular toxicity of sulfite. Both residue Cys201 in the N-terminal PDO domain (CstBPDO) and residue Cys408 in the C-terminal rhodanese domain (CstBRhod) strongly enhance the thiosulfate generating activity of CstB. CstB also possesses persulfide transferase (reverse rhodanese) activity which generates thiosulfate when provided with LMW persulfides and sulfite, as well as conventional thiosulfate transferase (TST, rhodanese) activity. Both activities require residue Cys408. CstB protects Staphylococcus aureus against H2S toxicity
physiological function
-
the worm living in coastal burrows is periodically exposed to the sulfide, a mixture of H2S, HS- and S2+, during low tide. Mitochondrial sulfide oxidation is an important strategy that allows organisms to avoid injury from sulfide exposure, and sulfur dioxygenase (SDO) plays an essential role. The hindgut of the worm plays more important role than the midgut in sulfide tolerance
physiological function
shading of the siliques has no morphological effect on embryogenesis in wild-type plants. In a knock-down line ethe1-1 with about 1% residual sulfur dioxygenase activity, the developmental delay is already visible in seeds under control conditions and is further enhanced in the darkness. Dark conditions strongly affect seed uality parameters of both wild-ype and mutant plants. Sulfur dioxygenase deficiency leads to defects in endosperm development
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D130A
mutation in putative iron ligand, 0.5-2% residual activity
D130E
mutation in putative iron ligand, 0.5-2% residual activity
D130H
mutation in putative iron ligand, 0.5-2% residual activity
D141A
inactive concomitant to a decrease of melting point by 3-8 K
H113A
mutation in putative iron ligand, inactive
H113G
mutation in putative iron ligand, inactive
H171A
inactive concomitant to a decrease of melting point by 3-8 K
H57A
mutation in putative iron ligand, 6% residual activity
H57G
mutation in putative iron ligand, inactive
R139A
inactive concomitant to a decrease of melting point by 3-8 K
C161Y
mutation reported in ethylmalonic encephalopathy patients, drastic reduction in iron content
R163W
mutation reported in ethylmalonic encephalopathy patients
T136A
mutation reported in ethylmalonic encephalopathy patients
C314S
-
site-directed mutagenesis, structure comparison with wild-type enzyme. C314S BpPRF exhibits a 29fold lower kcat and an 5fold higher Km for GSSH than the wild-type
C201S
site-directed mutagenesis, the mutant protein structure is similar to the wild-type, but it shows reduced activity
C201S/C408S
site-directed mutagenesis
C2S
site-directed mutagenesis, the mutant is larger than the wild-type and is a hexamer
C408S
site-directed mutagenesis, the mutant is larger than the wild-type and is a hexamer. Substitution of the presumed Rhod active-site C408 also appears to destabilize the native protein fold. Catalytically inactive mutant
L55P
-
the mutation is associated with ethylmalonic encephalopathy
L55P
mutation reported in ethylmalonic encephalopathy patients, drastic reduction in iron content
additional information
residues located in the predicted GSH/GSSH binding site and in the central hydrogen bond networks including the iron ligands are essential for activity
additional information
-
residues located in the predicted GSH/GSSH binding site and in the central hydrogen bond networks including the iron ligands are essential for activity
additional information
construction of an sdo knockout mutant and an sdo overexpression strain from Acidithiobacillus ferrooxidans strain ATCC 23270. By overexpressing sdo in strain ATCC 23270, a 91fold increased sdo transcriptional level and a 2.5fold increase in SDO activity are observed when sulfur S0 is used as sole energy source. The sdo knockout mutant of displays a slightly reduced growth capacity in S0-medium compared with the wild type but still maintains high S0-oxidizing activity, suggesting that there is at least one other S0-oxidizing enzyme besides SDO in Acidithiobacillus ferrooxidans ATCC 23270 cells
additional information
-
construction of an sdo knockout mutant and an sdo overexpression strain from Acidithiobacillus ferrooxidans strain ATCC 23270. By overexpressing sdo in strain ATCC 23270, a 91fold increased sdo transcriptional level and a 2.5fold increase in SDO activity are observed when sulfur S0 is used as sole energy source. The sdo knockout mutant of displays a slightly reduced growth capacity in S0-medium compared with the wild type but still maintains high S0-oxidizing activity, suggesting that there is at least one other S0-oxidizing enzyme besides SDO in Acidithiobacillus ferrooxidans ATCC 23270 cells
additional information
generation of a ETHE1 loss-of-function mutation by DNA insertion, phenotpe overview
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Oh, J.K.; Suzuki, I.
Resolution of a membrane-associated thiosulfate-oxidizing complex of Thiobacillus novellus
J. Gen. Microbiol.
99
413-423
1977
Starkeya novella
-
brenda
Emmel, T.; Sand, W.; Knig, W.; Bock, E.
Evidence for the existence of a sulfur oxygenase in Sulfolobus brierleyi
J. Gen. Microbiol.
132
3415-3420
1986
Acidianus brierleyi
-
brenda
Justin, P.; Kelly, D.P.
Metabolic changes in Thiobacillus denitrificans accompanying the transition from aerobic to anaerobic growth in continuous chemostat culture
J. Gen. Microbiol.
107
131-137
1978
Thiobacillus denitrificans
-
brenda
Suzuki, I.; Silver, M.
The initial product and properties of the sulfur-oxidizing enzyme of thiobacilli
Biochim. Biophys. Acta
122
22-33
1966
Acidithiobacillus thiooxidans, Thiobacillus thioparus
brenda
Nogami, Y.; Maeda, T.; Negishi, A.; Sugio, T.
Inhibition of sulfur oxidizing activity by nickel ion in Thiobacillus thiooxidans NB1-3 isolated from the corroded concrete
Biosci. Biotechnol. Biochem.
61
1373-1375
1997
Acidithiobacillus thiooxidans, Acidithiobacillus thiooxidans NB1-3
-
brenda
Krasil'nikova, E.N.; Bogdanova, T.I.; Zakharchuk, L.M.; Tsaplina, I.A.
Sulfur-metabolizing enzymes in thermoacidophilic bacteria Sulfobacillus sibiricus
Appl. Biochem. Microbiol.
40
53-56
2004
Sulfobacillus sibiricus
-
brenda
Sun, C.W.; Chen, Z.W.; He, Z.G.; Zhou, P.J.; Liu, S.J.
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Rohwerder, T.; Sand, W.
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Holdorf, M.M.; Owen, H.A.; Lieber, S.R.; Yuan, L.; Adams, N.; Dabney-Smith, C.; Makaroff, C.A.
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Shen, J.; Keithly, M.E.; Armstrong, R.N.; Higgins, K.A.; Edmonds, K.A.; Giedroc, D.P.
Staphylococcus aureus CstB is a novel multidomain persulfide dioxygenase-sulfurtransferase involved in hydrogen sulfide detoxification
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Staphylococcus aureus (G5ELA4), Staphylococcus aureus
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Zhang, L.; Liu, X.; Qin, Z.; Liu, J.; Zhang, Z.
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Motl, N.; Skiba, M.A.; Kabil, O.; Smith, J.L.; Banerjee, R.
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Lorenz, C.; Brandt, S.; Borisjuk, L.; Rolletschek, H.; Heinzel, N.; Tohge, T.; Fernie, A.R.; Braun, H.P.; Hildebrandt, T.M.
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Arabidopsis thaliana (Q9C8L4), Arabidopsis thaliana
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Kabil, O.; Motl, N.; Strack, M.; Seravalli, J.; Metzler-Nolte, N.; Banerjee, R.
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Homo sapiens (O95571), Homo sapiens
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