EC Number   |
General Information |
Reference |
|---|
   1.13.11.71 | evolution |
the enzyme BCO2 is a member of the polyene oxygenase gene family. The major difference between human BCO2a enzyme and mouse BCO2 is the presence of 4 aa residues, GKAA, in human BCO2, suggesting the loss of an alternate splice site in the human gene. GKAA represents an extension of human BCO2 exon 3 caused by use of an alternate donor splice site. There has been considerable genetic drift since primate BCO2 first acquired the GKAA insertion and lost its xanthophyll cleavage function |
746290 |
| 1.13.11.71 | evolution |
the enzyme BCO2 is a member of the polyene oxygenase gene family. The major difference between human BCO2a enzyme and mouse BCO2 is the presence of 4 aa residues, GKAA, in human BCO2, suggesting the loss of an alternate splice site in the human gene. There has been considerable genetic drift since primate BCO2 first acquired the GKAA insertion and lost its xanthophyll cleavage function |
-, 746290 |
| 1.13.11.71 | malfunction |
BCO2 knockout mice, unlike wild-type mice, accumulate zeaxanthin in their retinas |
-, 746290 |
| 1.13.11.71 | malfunction |
enzyme loss induces mitochondrial hyperactivation, mitochondrial stress and changes of the mitochondrial proteome, leading to mitochondrial energy insufficiency |
765402 |
| 1.13.11.71 | malfunction |
epigenetic loss of BCO2 expression is associated with prostate cancer progression, molecular mechanisms of BCO2 actions in prostate cancer, overview |
745753 |
| 1.13.11.71 | malfunction |
knockdown of Bcdo2 by siRNA treatment in T47D cells enhances reactive oxygen species production upon carotenoid treatment. Bcdo2 siRNA-treated T47D cells show initiation of apoptosis evidenced by caspase 3 and PARP1 cleavage as established by immunoblot analyses |
727353 |
| 1.13.11.71 | malfunction |
systemic depletion of BCO2 causes increased food intake and impaired hepatic lipid metabolism in mice. Compared to wild-type, BCO2 knockout mice exhibit widespread disruptions in metabolism and metabolite homeostasis, an increase in fasting blood glucose, a decrease in circulating glucagon and leptin, an elevation of plasma interleukin 1 beta and tumor necrosis factor alpha, and impaired AMP activated protein kinase signaling. The global hypothalamic metabolomic results reveal that depletion of BCO2 results in striking metabolic changes, including suppression of long-chain fatty acids transport into mitochondria, inhibition of the metabolism of dipeptides and sulfur-containing amino acids, and stimulation of local oxidative stress and inflammation in the hypothalamus of BCO2 knockout mice. Complex interplay between the hormone signaling and impaired lipid and glucose metabolism seems to account for initiation of oxidative stress, inflammation and eventual metabolic disorders in BCO2 knockout mice. Phenotype, overview |
745596 |
| 1.13.11.71 | malfunction |
targeted knockdown of BCDO2 results in anemia at larval stages. Marker gene analysis and staining for hemoglobin revealed that erythropoiesis is not impaired but that erythrocytes undergo apoptosis in BCDO2- deficient larvae |
727353 |
| 1.13.11.71 | malfunction |
using BCO2 knock out mice it is shown that BCO2 catalyzes beta-apocarotenoid production in vivo. Bco2-/- mice show a significant hepatic accumulation of beta-cryptoxanthin as compared to Bco1-/- and wild-type mice |
727965 |
| 1.13.11.71 | malfunction |
using transgenic LjCCD7-silenced plants an overall characterization of its role in the regulation of plant architecture, reproductive development senescence, and root symbiosis is reported. The results also link CCD7 expression with the regulation of determinate nodulation, reproduction, and senescence in Lotus japonicus |
728057 |
