Disease relevance of SNORA63

• Production and characterization of improved adenovirus vectors with the E1, E2b, and E3 genes deleted [1].
• Mutations in the parkin gene, encoding an E3 ubiquitin-protein ligase, are a frequent cause of autosomal recessive parkinsonism and are also involved in sporadic Parkinson's disease [2].

High impact information on SNORA63

• Biochemical analysis of Parkinson's disease-causing variants of Parkin, an E3 ubiquitin-protein ligase with monoubiquitylation capacity [2].
• Activation of separase occurs at anaphase onset, when securin is targeted for destruction by the anaphase-promoting complex or cyclosome E3 ubiquitin protein ligase [3].
• The adenovirus E3/19K protein binds to major histocompatibility complex (MHC) class I antigens in the endoplasmic reticulum, thereby preventing their transport to the cell surface [4].
• The phenotype E 3-2 was much rarer (13% vs 16%, respectively) [5].
• Nitric oxide inhibits Parkin's E-3 ligase activity and its protective function by nitric oxide through S-nitrosylation both in vitro and in vivo [6].

Biological context of SNORA63

• Most Ad vectors are engineered such that a transgene replaces the Ad E1a, E1b, and E3 genes; subsequently the replication-defective vector can be propagated only in human 293 cells that supply the deleted E1 gene functions in trans [1].

Associations of SNORA63 with chemical compounds

• Parkin is E3-ubiquitin-protein ligase that ubiquitinates itself and promotes its own degradation [6].
• The APO E 3-2 phenotype showed reduced average levels of total cholesterol, apolipoprotein B (APO B) and low-density lipoprotein cholesterol (LDLc), and the APO E 4-3 phenotype showed increased levels (P less than or equal to .0497) [7].

Other interactions of SNORA63

• Three common phenotypes, APO E 3-2, APO E 3-3, and APO E 4-3, were used in analysis of variance on four quantitative lipid variables [7].

References