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Gene Review

SNORA63  -  small nucleolar RNA, H/ACA box 63

Homo sapiens

Synonyms: E3, E3-2, RNE3, RNU107
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Disease relevance of SNORA63


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


  1. Production and characterization of improved adenovirus vectors with the E1, E2b, and E3 genes deleted. Amalfitano, A., Hauser, M.A., Hu, H., Serra, D., Begy, C.R., Chamberlain, J.S. J. Virol. (1998) [Pubmed]
  2. Biochemical analysis of Parkinson's disease-causing variants of Parkin, an E3 ubiquitin-protein ligase with monoubiquitylation capacity. Hampe, C., Ardila-Osorio, H., Fournier, M., Brice, A., Corti, O. Hum. Mol. Genet. (2006) [Pubmed]
  3. Protein phosphatase 2A stabilizes human securin, whose phosphorylated forms are degraded via the SCF ubiquitin ligase. Gil-Bernabé, A.M., Romero, F., Limón-Mortés, M.C., Tortolero, M. Mol. Cell. Biol. (2006) [Pubmed]
  4. The amyloid precursor-like protein 2 associates with the major histocompatibility complex class I molecule K(d). Sester, M., Feuerbach, D., Frank, R., Preckel, T., Gutermann, A., Burgert, H.G. J. Biol. Chem. (2000) [Pubmed]
  5. Apolipoprotein E phenotype frequency and cerebrospinal fluid concentration are not associated with Creutzfeldt-Jakob disease. Zerr, I., Helmhold, M., Poser, S., Armstrong, V.W., Weber, T. Arch. Neurol. (1996) [Pubmed]
  6. Parkin and defective ubiquitination in Parkinson's disease. Dawson, T.M. J. Neural Transm. Suppl. (2006) [Pubmed]
  7. Phenotypic effects of apolipoprotein structural variation on lipid profiles. IV. Apolipoprotein polymorphisms in a small group of black women from the healthy women study. Eichner, J.E., Kuller, L.H., Ferrell, R.E., Kamboh, M.I. Genet. Epidemiol. (1989) [Pubmed]
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