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enzyme crucial for the metabolism of cysteine [RGD, Feb 2006].. Additionally we are shipping CDO1 Antibodies (31) and CDO1 Proteins (12) and many more products for this protein.
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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.
Cdo1 is required for adipogenesis.Cdo1 interacts with Ppar-gamma (show PPARG ELISA Kits) during adipogenesis.
In light of these results, the minimal substrate requirements for CDO catalysis and O-activation are discussed.
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
Cdo1 knockout mice show increased cysteine concentrations and higher rates of metabolism of cysteine to hydrogen sulfide and thiosulfate.
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.
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.
Cdo(-/-) mice displayed megaesophagus and achalasia, and their lower esophageal sphincter was resistant to nitric oxide-induced relaxation.
The hepatic CDO-knockout mice were able to maintain normal levels of glutathione, taurine, and sulfate.
The catalytic cycle of CDO is primed by one electron through chemical oxidation to produce CDO with ferric iron in the active site.
methylation of the CDO1 gene promoter could be strong prognostic indicator in primary BC without preoperative treatment.
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
Decreased expression of CDO1 is associated with esophageal squamous cell carcinoma.
A structural role of the Cys (show DNAJC5 ELISA Kits)-Tyr (show TYR ELISA Kits) cofactor coordinates the ferrous iron in the active site of CDO1.
A high negative correlation between promoter DNA methylation and gene expression was observed for CDO1, ZNF331 and ZSCAN18 in gastrointestinal tumors.
TGF-b1 suppressed Cdo1 gene transcription through the MEK (show MAP2K1 ELISA Kits)/ERK (show EPHB2 ELISA Kits) pathway.
we define a three-gene panel, CDO1, HOXA9 (show HOXA9 ELISA Kits), and TAC1 (show TAC1 ELISA Kits), which we subsequently validate in two independent cohorts of primary NSCLC samples
methylation status of serum CDO1 gene promoter may be helpful in the diagnosis of hepatocellular carcinoma (HCC (show FAM126A ELISA Kits)) and the estimation of the HCC (show FAM126A ELISA Kits) stages.
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.
CDO1 as a novel tumor suppressor gene and a potentially valuable molecular marker for human cancer
enzyme crucial for the metabolism of cysteine
cysteine dioxygenase, type I
, cysteine dioxygenase type 1
, cysteine dioxygenase type I
, cytosolic cysteine dioxygenase 1
, cysteine dioxygenase 1, cytosolic