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Gene Review

SNORA73A  -  small nucleolar RNA, H/ACA box 73A

Homo sapiens

Synonyms: E1, E1-7, E1b, RNE1, RNU17A, ...
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Disease relevance of SNORA73A

  • Replication of all these plasmids was absolutely dependent on the presence of the HPV-18 E1 and E2 proteins [1].
  • Soluble extracts from uninfected murine cells supplemented with purified viral E1 and E2 proteins support the replication of exogenously added papilloma virus DNA [2].
  • Previous studies defining the viral genes affecting HPV-16 transformation functions have used the "prototype" viral genome, which was cloned from a human cervical carcinoma and later discovered to harbor a mutation in the E1 gene [3].
  • The HPV-11 E2 protein appears not to be essential for elongation, but it must be present in the preinitiation complex for the E1 protein to recruit host DNA replication machinery to the ori [4].
  • The replication of the human papillomavirus type 11 (HPV-11) origin was achieved by using human 293 cell extracts supplemented with the HPV-11 E1 and E2 proteins purified from insect cells infected with recombinant baculoviruses [5].

High impact information on SNORA73A

  • Second generation E1 deleted viruses further crippled by a temperature sensitive mutation in the E2a gene were associated with substantially longer recombinant gene expression and less inflammation [6].
  • We have also revised the nucleotide sequence of the E1b region of Ad5 [7].
  • The E2 transactivator stimulates the binding of the E1 replication protein to the minimal origin of replication and activates DNA replication [2].
  • The structure and associated mutational analyses reveal molecular details of Ubc12 recruitment by NEDD8's E1 [8].
  • Structural basis for recruitment of Ubc12 by an E2 binding domain in NEDD8's E1 [8].

Chemical compound and disease context of SNORA73A

  • The maturation of rubella virus (RV) glycoproteins E2 and E1 was examined by using brefeldin A (BFA) and monensin [9].
  • A murine monoclonal antibody directed against the E1 membrane glycoprotein of rubella virus was immobilized on an N-hydroxysuccinimide-activated chromatographic support [10].
  • Adeno-P450, a replication-defective, E1/E3 region-deleted adenovirus engineered to express CYP2B6-IRES-P450R, induced intracellular CPA 4-hydroxylation, and CPA cytotoxicity, in a broad range of human cancer cell lines [11].
  • These signals include transactivation by: adenovirus E1a/E1b proteins; activated p21ras; and in CHO cells, treatment with the DNA damaging agent MNNG [12].
  • To address this problem, we developed an E1b 55 kDa attenuated, replication-competent adenovirus (Ad.TKRC) which expresses the herpes simplex-1 thymidine kinase (HSVtk) gene to sensitize tumors to ganciclovir (GCV) [13].

Biological context of SNORA73A

  • Binding of E1 to the origin was increased by E2 proteins and required the presence of E2 binding sites [14].
  • To examine the interplay of these replication proteins, we have analyzed the binding of human papillomavirus (HPV) type 31b E1 and E2 proteins to the origin of replication [14].
  • These observations suggest a model whereby modulation of the relative levels of E1 and E2 during the viral life cycle may alter the pattern of origin binding and possibly episomal copy number [14].
  • mRNA splicing regulates human papillomavirus type 11 E1 protein production and DNA replication [15].
  • The origins of DNA replication in bovine and human papillomavirus genomes have been localized to a specific part of the upstream regulatory region (URR) which includes recognition sites for E1 and E2 proteins [16].

Anatomical context of SNORA73A

  • The present article describes specific psoralen photocross-linking in whole HeLa cells of E1, E2, and E3 RNAs to nucleolar pre-rRNA [17].
  • To address the mechanisms by which the viral DNA is stably propagated in the transformed cells, we have constructed a cell line CH04.15 expressing constitutively the viral proteins E1 and E2, that are required for initiation of viral DNA replication [18].
  • In this study, we have corrected this mutation and have evaluated the effect of mutations of either the E1 or the E2 gene on the efficiency of HPV-16 immortalization of human keratinocytes [3].
  • Injection of the human E1, E2, and E3 genes into Xenopus oocytes generated sequence-specific transcripts of the approximate sizes of the respective snoRNAs [19].
  • The human E1 alpha and the previously isolated human E2 cDNAs were used as probes in Northern blot analysis with cultured fibroblasts and lymphoblasts from seven unrelated MSUD patients [20].

Associations of SNORA73A with chemical compounds

  • Sequence components adjacent to the E1 and E2 binding sites, comprising AT-rich and purine-rich elements and the consensus TATA box sequence, probably contribute to the overall efficiency of replication, though they are nonessential [16].
  • An E1 gene mutant at threonine 102 encodes for a protein which is no longer a substrate for the p34cdc2 kinase [21].
  • This additional guanine shifted the reading frame and erased an interruption in the E1 gene described by Seedorf et al [22].
  • The monovalent ionophore monensin, which inhibits intracellular transport of proteins through the ER-Golgi complex, was used to block the transport of E1 and E2 glycoproteins through the Golgi complex [9].
  • The E1 protein of HPV-33 purified by affinity chromatography using glutathione S-transferase as tag displayed specific DNA-binding activity in footprint analyses protecting HPV-33 nucleotides 7896 to 7909/1 to 18 from DNasel digestion [23].

Physical interactions of SNORA73A

  • The mechanism by which these proteins are recruited to the origin and the role of the E1/E2 complex in replication remain undefined [14].
  • E1 also bound in vitro to H1 isolated under native conditions in association with intact nucleosomes [24].
  • The transcription factor YY1 has been shown to regulate RNA transcription by binding to a sequence overlapping the putative E1 protein binding site in the HPV-18 ori [25].

Regulatory relationships of SNORA73A

  • Binding of the human papillomavirus E1 origin-recognition protein is regulated through complex formation with the E2 enhancer-binding protein [14].
  • We also found that E2 but not E1 protein expressed in mammalian cells is bound tightly to GRP78 [26].

Other interactions of SNORA73A

  • Therefore, changes in the relative amounts of E1 and E2 proteins can dramatically alter the pattern of binding of viral replication factors to the origin [14].
  • The E1 gene is located within the first intron of the gene for RCC1, a protein that regulates onset of mitosis [19].
  • Production and characterization of improved adenovirus vectors with the E1, E2b, and E3 genes deleted [27].
  • Bound H1 was displaced from HPV-11 DNA by the addition of E1, suggesting that E1 can promote replication initiation and elongation by alteration of viral chromatin structure and disruption of nucleosomes at the replication fork [24].

Analytical, diagnostic and therapeutic context of SNORA73A


  1. Two E2 binding sites alone are sufficient to function as the minimal origin of replication of human papillomavirus type 18 DNA. Sverdrup, F., Khan, S.A. J. Virol. (1995) [Pubmed]
  2. Activation of BPV-1 replication in vitro by the transcription factor E2. Yang, L., Li, R., Mohr, I.J., Clark, R., Botchan, M.R. Nature (1991) [Pubmed]
  3. Disruption of either the E1 or the E2 regulatory gene of human papillomavirus type 16 increases viral immortalization capacity. Romanczuk, H., Howley, P.M. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  4. The functions of human papillomavirus type 11 E1, E2, and E2C proteins in cell-free DNA replication. Liu, J.S., Kuo, S.R., Broker, T.R., Chow, L.T. J. Biol. Chem. (1995) [Pubmed]
  5. Cell-free replication of the human papillomavirus DNA with homologous viral E1 and E2 proteins and human cell extracts. Kuo, S.R., Liu, J.S., Broker, T.R., Chow, L.T. J. Biol. Chem. (1994) [Pubmed]
  6. Inactivation of E2a in recombinant adenoviruses improves the prospect for gene therapy in cystic fibrosis. Yang, Y., Nunes, F.A., Berencsi, K., Gönczöl, E., Engelhardt, J.F., Wilson, J.M. Nat. Genet. (1994) [Pubmed]
  7. The 2.2 kb E1b mRNA of human Ad12 and Ad5 codes for two tumor antigens starting at different AUG triplets. Bos, J.L., Polder, L.J., Bernards, R., Schrier, P.I., van den Elsen, P.J., van der Eb, A.J., van Ormondt, H. Cell (1981) [Pubmed]
  8. Structural basis for recruitment of Ubc12 by an E2 binding domain in NEDD8's E1. Huang, D.T., Paydar, A., Zhuang, M., Waddell, M.B., Holton, J.M., Schulman, B.A. Mol. Cell (2005) [Pubmed]
  9. Brefeldin A and monensin arrest cell surface expression of membrane glycoproteins and release of rubella virus. Qiu, Z., Tufaro, F., Gillam, S. J. Gen. Virol. (1995) [Pubmed]
  10. Purification of rubella virus E1-E2 protein complexes by immunoaffinity chromatography. van Sommeren, A.P., Machielsen, P.A., Schielen, W.J., Bloemers, H.P., Gribnau, T.C. J. Virol. Methods (1997) [Pubmed]
  11. Use of replication-conditional adenovirus as a helper system to enhance delivery of P450 prodrug-activation genes for cancer therapy. Jounaidi, Y., Waxman, D.J. Cancer Res. (2004) [Pubmed]
  12. DNA damage response of cloned DNA beta-polymerase promoter is blocked in mutant cell lines deficient in protein kinase A. Englander, E.W., Wilson, S.H. Nucleic Acids Res. (1992) [Pubmed]
  13. Adenoviral vectors capable of replication improve the efficacy of HSVtk/GCV suicide gene therapy of cancer. Wildner, O., Morris, J.C., Vahanian, N.N., Ford, H., Ramsey, W.J., Blaese, R.M. Gene Ther. (1999) [Pubmed]
  14. Binding of the human papillomavirus E1 origin-recognition protein is regulated through complex formation with the E2 enhancer-binding protein. Frattini, M.G., Laimins, L.A. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  15. mRNA splicing regulates human papillomavirus type 11 E1 protein production and DNA replication. Deng, W., Jin, G., Lin, B.Y., Van Tine, B.A., Broker, T.R., Chow, L.T. J. Virol. (2003) [Pubmed]
  16. cis-Acting components of human papillomavirus (HPV) DNA replication: linker substitution analysis of the HPV type 11 origin. Russell, J., Botchan, M.R. J. Virol. (1995) [Pubmed]
  17. Three new small nucleolar RNAs that are psoralen cross-linked in vivo to unique regions of pre-rRNA. Rimoldi, O.J., Raghu, B., Nag, M.K., Eliceiri, G.L. Mol. Cell. Biol. (1993) [Pubmed]
  18. Cis and trans requirements for stable episomal maintenance of the BPV-1 replicator. Piirsoo, M., Ustav, E., Mandel, T., Stenlund, A., Ustav, M. EMBO J. (1996) [Pubmed]
  19. Genes for E1, E2, and E3 small nucleolar RNAs. Nag, M.K., Thai, T.T., Ruff, E.A., Selvamurugan, N., Kunnimalaiyaan, M., Eliceiri, G.L. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  20. Molecular phenotypes in cultured maple syrup urine disease cells. Complete E1 alpha cDNA sequence and mRNA and subunit contents of the human branched chain alpha-keto acid dehydrogenase complex. Fisher, C.W., Chuang, J.L., Griffin, T.A., Lau, K.S., Cox, R.P., Chuang, D.T. J. Biol. Chem. (1989) [Pubmed]
  21. The E1 replication protein of bovine papillomavirus type 1 contains an extended nuclear localization signal that includes a p34cdc2 phosphorylation site. Lentz, M.R., Pak, D., Mohr, I., Botchan, M.R. J. Virol. (1993) [Pubmed]
  22. Cloning of monomeric human papillomavirus type 16 DNA integrated within cell DNA from a cervical carcinoma. Matsukura, T., Kanda, T., Furuno, A., Yoshikawa, H., Kawana, T., Yoshiike, K. J. Virol. (1986) [Pubmed]
  23. Characterization of the DNA-binding activity of the E1 and E2 proteins and the E1/E2 complex of human papillomavirus type 33. Müller, F., Giroglou, T., Sapp, M. J. Gen. Virol. (1997) [Pubmed]
  24. Association of the human papillomavirus type 11 E1 protein with histone H1. Swindle, C.S., Engler, J.A. J. Virol. (1998) [Pubmed]
  25. Transcription factor YY1 represses cell-free replication from human papillomavirus origins. Lee, K.Y., Broker, T.R., Chow, L.T. J. Virol. (1998) [Pubmed]
  26. Activation of the grp78 and grp94 promoters by hepatitis C virus E2 envelope protein. Liberman, E., Fong, Y.L., Selby, M.J., Choo, Q.L., Cousens, L., Houghton, M., Yen, T.S. J. Virol. (1999) [Pubmed]
  27. 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]
  28. Selective tolerance to the E1 protein of rubella virus in congenital rubella syndrome. Mauracher, C.A., Mitchell, L.A., Tingle, A.J. J. Immunol. (1993) [Pubmed]
  29. Inhibition of human papillomavirus DNA replication by small molecule antagonists of the E1-E2 protein interaction. White, P.W., Titolo, S., Brault, K., Thauvette, L., Pelletier, A., Welchner, E., Bourgon, L., Doyon, L., Ogilvie, W.W., Yoakim, C., Cordingley, M.G., Archambault, J. J. Biol. Chem. (2003) [Pubmed]
  30. A C-terminal helicase domain of the human papillomavirus E1 protein binds E2 and the DNA polymerase alpha-primase p68 subunit. Masterson, P.J., Stanley, M.A., Lewis, A.P., Romanos, M.A. J. Virol. (1998) [Pubmed]
  31. Genome amplification of human papillomavirus types 16 and 18 in cervical carcinomas is related to the retention of E1/E2 genes. Berumen, J., Casas, L., Segura, E., Amezcua, J.L., Garcia-Carranca, A. Int. J. Cancer (1994) [Pubmed]
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