Cysteine Dioxygenase, Type I (CDO1) ELISA Kits

Mouse (Murine) Cysteine Dioxygenase, Type I (CDO1) Interaktionspartner

1. Presented here are the results of O2-dependent 2-mercaptoaniline reaction using two different thiol dioxygenase enzymes mouse CDO and 3-mercaptopropionic acid dioxygenase isolated from Azotobacter vinelandii. Benzothiazoles are produced by the condensation of 2-mercaptoaniline with aldehydes formed by an off-pathway oxidation of primary alcohols added to aqueous reactions to solubilize the substrate.

2. Cdo is required for efficient cardiomyogenesis of pluripotent stem cells and an excellent target to improve the differentiation potential of stem cells for generation of transplantable cells to treat cardiomyopathies.

3. our findings indicate Cdo1 suppresses osteogenic differentiation of BMSCs, through a potential mechanism which involves in Wnt signaling reduction concomitantly

4. We investigated the ontogeny of Cdo1 mRNA expression in mouse fetal and placental tissues, which showed increasing levels from embryonic day 10.5 and was localised to the decidua and several fetal tissues including nasal cavities and brain.

5. Cdo1 is required for adipogenesis.Cdo1 interacts with Ppar-gamma during adipogenesis.

6. In light of these results, the minimal substrate requirements for CDO catalysis and O-activation are discussed.

7. the timing of chemical steps in the CDO kinetic mechanism is investigated by pH/pD-dependent steady-state kinetics and solvent isotope effects on kcat, kcat/KM, and (O2/CSA) coupling

8. Cdo1 knockout mice show increased cysteine concentrations and higher rates of metabolism of cysteine to hydrogen sulfide and thiosulfate.

9. A critical function of CDO appears to be to remove cysteine by a pathway in which the sulfur atom is oxidized in the first step.

10. Data from kinetic, spectroscopic, and computational studies suggest that in cysteine dioxygenase (CDO) a covalently cross-linked cysteine-tyrosine pair (C93-Y157) plays a vital role in CDO-mediated catalysis.

11. Cdo(-/-) mice displayed megaesophagus and achalasia, and their lower esophageal sphincter was resistant to nitric oxide-induced relaxation.

12. The hepatic CDO-knockout mice were able to maintain normal levels of glutathione, taurine, and sulfate.

13. The catalytic cycle of CDO is primed by one electron through chemical oxidation to produce CDO with ferric iron in the active site.

14. Control of cysteine levels by regulation of CDO may be necessary to maintain low H(2)S/sulfane sulfur levels and facilitate the use of H(2)S as a signaling molecule.

15. resting and substrate-bound forms of CDO in the Fe(II) and Fe(III) states, both of which are proposed to have important roles in this enzyme's catalytic mechanism, were characterized.

16. The CDO gene displays tissue-specific expression, with the highest mRNA level present in liver and with detectable levels found in kidney, lung, brain and small intestine.

17. The x-ray crystal structure of CDO from Mus musculus was solved to a nominal resolution of 1.75 Angstroms

18. Characterization of the nitrosyl adduct of substrate-bound mouse cysteine dioxygenase by electron paramagnetic resonance

Human Cysteine Dioxygenase, Type I (CDO1) Interaktionspartner

1. High CDO1 methylation is associated with colorectal cancer progression.

2. Promoter NA methylation of CDO1 was demonstrated for the first time to be a cancer-associated methylation in primary gallbladder cancer(GBC), and it has the potential to be a prognostic biomarker of GBC for high-risk patients with stage II GBC.

3. CDO1 methylation could be a potent prognostic predictor in primary esophageal squamous cell carcinoma and have great potential as a prognostic factor to guide the treatment of patients who need adjuvant chemotherapy.

4. High methylation of CDO1 gene is responsible of the development of the esophageal adenocarcinoma.

5. CDO1 promoter methylation is involved in gene regulation and is a potential prognostic biomarker for BCR-free survival in prostate cancer (PC) patients following radical prostatectomy. Further studies are needed to validate CDO1 methylation assays and to evaluate the clinical utility of CDO1 methylation for the management of PCa

6. methylation of the CDO1 gene promoter could be strong prognostic indicator in primary BC without preoperative treatment.

7. CDO1 promoter methylation may not substitute common prognostic makers to predict ccRCC survival, but offers additional, relevant prognostic information, indicating that it might be a novel molecular marker to determine ccRCC prognosis

8. Decreased expression of CDO1 is associated with esophageal squamous cell carcinoma.

9. A structural role of the Cys-Tyr cofactor coordinates the ferrous iron in the active site of CDO1.

10. A high negative correlation between promoter DNA methylation and gene expression was observed for CDO1, ZNF331 and ZSCAN18 in gastrointestinal tumors.

11. TGF-b1 suppressed Cdo1 gene transcription through the MEK/ERK pathway.

12. we define a three-gene panel, CDO1, HOXA9, and TAC1, which we subsequently validate in two independent cohorts of primary NSCLC samples

13. methylation status of serum CDO1 gene promoter may be helpful in the diagnosis of hepatocellular carcinoma (HCC) and the estimation of the HCC stages.

14. Our study shows the importance of CDO1 inactivation in breast cancer and its clinical potential as a biomarker and therapeutic target to overcome resistance to anthracyclines.

15. CDO1 as a novel tumor suppressor gene and a potentially valuable molecular marker for human cancer

16. We confirmed that the expression of CDO1 in squamous cell carcinoma is regulated by DNA methylation of its specific promoter region.

17. Cysteine dioxygenase contains a 3His ligand motif rather than 2His/1Asp. The former is essential for optimal dioxygenation activity. Mutants with a 2His/1Asp motif may give sulfoxides as byproduct due to incomplete dioxygenation.

18. DNA methylation of CDO1 predicted distant recurrence in lymph node-positive patients with estrogen receptor-positive tumors treated with adjuvant anthracycline containing therapy.

19. CDO is capable of altering intracellular cysteine levels as well as glutathione levels.

20. Upon comparison of PBMC and skin samples of Sezary syndrome versus mycosis fungoides, CDO1 and DNM3 were found upregulated only in Sezary syndrome.