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Glucose를 비타민 C로 변형시키는 과정의 최적화에 대한 연구
정종경(Jong Kyeong Chung),구양모(Yang Mo Goo),김공환(Kong Hwan Kim) 대한약학회 1988 약학회지 Vol.32 No.6
Chemical transformation of D-glucose to 2-keto-L-gulonic acid and L-ascorbic acid has been examined. D-Sorbitol obtained from D-glucose was microbiologically oxidized to L-sorbose by G. suboxydans in 90% yield. On treatment of L-sorbose with acetone in the presence of sulfuric acid, its diacetonide is obtained in 95% yield. This diacetonide is oxidized to the corresponding acid with nickel chloride-hypochlorite, and the acid is directly transformed to L-ascorbic acid. The over all yield of Vitamin C from D-glucose achieved is 54%.
PINK1 as a Molecular Checkpoint in the Maintenance of Mitochondrial Function and Integrity
고형종,정종경 한국분자세포생물학회 2012 Molecules and cells Vol.34 No.1
Parkinson’s disease (PD), the most prevalent neurodegenerative movement disorder, is characterized by an age-dependent selective loss of dopaminergic (DA) neurons. Although most PD cases are sporadic, more than 20 responsible genes in familial cases were identified recently. Genetic studies using Drosophila models demonstrate that PINK1, a mitochondrial kinase encoded by a PD-linked gene PINK1, is critical for maintaining mitochondrial function and integrity. This suggests that mitochondrial dysfunction is the main cause of PD pathogenesis. Further genetic and cell biological studies revealed that PINK1 recruits Parkin, an E3 ubiquitin ligase encoded by another PD-linked gene parkin, to mitochondria and regulates the mitochondrial remodeling process via the Parkin-mediated ubiquitination of various mitochondrial proteins. PINK1 also directly phosphorylates the mitochondrial proteins Miro and TRAP1, subsequently inhibiting mitochondrial transport and mitochondrial oxidative damage, respectively. Moreover, recent Drosophila genetic analyses demonstrate that the neuroprotective molecules Sir2 and FOXO specifically complement mito-chondrial dysfunction and DA neuron loss in PINK1 null mutants, suggesting that Sir2 and FOXO protect mitochondria and DA neurons downstream of PINK1. Collectively, these recent results suggest that PINK1 plays multiple roles in mitochondrial quality control by regulating its mitochondrial, cytosolic, and nuclear targets.