Transcription adenovirus

Adenovirus transcription factor (ATF) is a protein activated by the adenovirus protein E2a and has turned out to be CREB (cAMP-responsive, element-binding protein) Jun is named for avian sarcoma virus 17 (I am told that junana is 17 in Japanese). 

Synthesis and processing of adenovirus transcripts. The adenovirus genome contains six promoters which give rise to multiple transcripts. The major late promoter is especially active and generates several classes of transcripts which terminate at any one of five polyadenylation signals. Through an elaborate alternative splicing pathway, each class of major late transcript is processed to include the same aminoterminal protein sequences linked to various carboxy terminal residues. 

Akusjarvi, G., and Persson, H., 1981, Controls of RNA splicing and termination in the major late adenovirus transcription unit. Nature London) 292 420. 

Lu W, Peterson R, Dasgupta A, Scovell WM (2000) Influence of HMG-1 and adenovirus oncoprotein ElA on early stages of transcriptional preinitiation complex assembly. J Biol Chem 275 35006-35012 Luger K, Mader AW, Richmond RK, Sargent DF, Richmond TJ (1997) Crystal structure of the nucle-osome core particle at 2.8 A resolution. Nature 389 251—260 Lusser A, Kadonaga JT (2004) Strategies for the reconstitution of chromatin. Nat Methods 1 19-26 Maeshima K, Laemmli UK (2003) A two-step scaffolding model for mitotic chromosome assembly. Dev Cell 4 467-480... 

Zhang Q, Yao H, Vo N, Goodman RH (2000) Acetylation of adenovirus EIA regulates binding of the transcriptional corepressor CtBP. PNAS 97(26) 14323-14328... 

TRRAP transformation/transcription domain-associated protein. Subunit of the Tip60/NuA4 HAT complex. Required for cell transformation and transcriptional activation by c-Myc, E2F1 and adenovirus ElA. 

Watt, F. and Molloy, P.L. (1988) Cytosine methylation prevents binding to DNA of a HeLa cell transcription factor required for optimal expression of the adenovirus major late promoter. Genes and Development, 2, 1136-1143. 

DNA viruses that can trigger tumors are found in the classes of the polyomaviruses, the adenoviruses and the papUloma viruses. The polyoma viruses with the SV40 virus as a well studied representative, adenoma virus and human papUloma virus (HPV) are associated with formation of tumors in humans and have genes coding for proteins with the properties of oncoproteins. The oncoproteins of aU three viruses interfere with the pRb function by Ufting its inhibition of transcription factor E2F. It is assumed that the tumor-promoting activity of the proteins is due, in particular, to this property. 

A replication-deficient adenovirus has been used to deliver a gene construct, which contains within its promoter region a radiation-responsive element. Upon irradiation with conventional doses of X rays, this construct initiates transcription of the gene coding for the toxic cytokine, tumor necrosis factor-a (35). The above is an exquisite example of how emerging delivery and gene therapies are fast blurring the distinction between an active and an excipient (Fig. 3D). 

Figure 28-13 (A) Stereoscopic ribbon drawing of the phyloge-netically conserved 180-residue C-terminal portion of the TATA-binding protein (TBP) from Arabidopsis thaliana. The sequence consists of two direct repeats, giving the protein an approximate twofold symmetry. From Nikolov et al.337 (B) Structure of the corresponding C-terminal core (residues 155-335) of the human TATA-binding protein (TBP) bound to the TATA sequence of a promoter in adenovirus DNA. From Nikolov et al.327 (C) Structure of human transcription factor IIB bound to a TBP from Arabidopsis thaliana, which, in turn, is bound to an adenovirus TATA sequence. Hypothetical B DNA extensions have been modeled at both ends of the DNA segment. The +1 at the left end is the transcription start site and the —43 upstream end is to the right. From Nikolov et al.338 Courtesy of Stephen K. Burley.

Phil Sharp and Leonard Guarente showed that at least four transcription factors are required in addition to polymerase II for initiation from the major late promoter of adenovirus. In vitro studies indicate that these factors assemble in an orderly fashion (see fig. 28.12b). First the TFIID complex binds to the TATA box. Sequential binding of TFIIA, TFIIB, RNA polymerase II, and TFIIE follow. It is believed that this multifactor complex functions for a large number of eukaryotic promoters that contain TATA boxes. 

Sawadogo, M. Roeder, R.G. (1985). Interaction of a gene-specific transcription factor with the adenovirus major late promoter upstream of the TATA box region. Cell 43, 165-75. 

Steinwaerder, D.S. and Lieber, A. (2000) Insulation from viral transcriptional regulatory elements improves inducible transgene expression from adenovirus vectors in vitro and in vivo. Gene Then, 7, 556-567. 

Yu DC, Sakamoto GT, Henderson DR. Identification of the transcriptional regulatory sequences of human kallikrein 2 and their use in the construction of calydon virus 764, an attenuated replication competent adenovirus for prostate cancer therapy. Cancer Res 1999 59 1498-1504. 

Shi, Y., Seto, E., Chang, L. S. and Shenk, T. (1991). Transcriptional repression by YY1, a human GLI-Kruppel-related protein, and relief of repression by adenovirus E1A protein. Cell 67, 377-388. 

Fig. 14.1 The life cycle of coxsackievirus B3. CVB3 starts its life cycle by attaching to its receptor CAR and coreceptor DAF. Internalized virus releases its viral RNA, which can be used as the template for translation of polyprotein or transcription by RNA-dependent RNA polymerase 3D to replicate its genome. The polyprotein is self-cleaved by virus-encoded proteases to release structural proteins and nonstructural proteins. Later, structural proteins and viral RNA will assemble into progeny virions to be released from infected cell. Abbreviations CVB3, coxsackievirus B3 DAF, decay accelerating factor CAR, coxsackievirus and adenovirus receptor 3Dpo1, RNA-dependent RNA polymerase.

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