Literature DB >> 1849798

Adenovirus inhibition of cellular protein synthesis involves inactivation of cap-binding protein.

J T Huang1, R J Schneider.   

Abstract

Adenovirus (Ad) infection results in a marked inhibition of cellular protein synthesis that initiates during the late phase of the viral infectious cycle. We show that the mechanism used for suppression of cellular protein synthesis during cell cycle progression is exploited by Ad to repress host and enhance late viral mRNA translation. Discrimination between cellular and late Ad mRNAs and inhibition of host protein synthesis are shown to involve viral-mediated underphosphorylation of cap-binding protein (CBP) and subsequent inactivation of CBP complex, a large enzymatic complex required for cap-dependent mRNA translation. Late Ad mRNAs, like those of poliovirus, possess the unique ability to translate independent of a normal cap recognition process and do not require the activity of CBP complex. Inhibition of cellular translation by these two viruses is quite similar, except that whereas CBP complex is proteolytically degraded by poliovirus, it is functionally inactivated by Ad.

Entities:  

Mesh:

Substances:

Year:  1991        PMID: 1849798     DOI: 10.1016/0092-8674(91)90161-q

Source DB:  PubMed          Journal:  Cell        ISSN: 0092-8674            Impact factor:   41.582


  54 in total

1.  p53-Independent and -dependent requirements for E1B-55K in adenovirus type 5 replication.

Authors:  J N Harada; A J Berk
Journal:  J Virol       Date:  1999-07       Impact factor: 5.103

2.  Picornavirus internal ribosome entry site elements target RNA cleavage events induced by the herpes simplex virus virion host shutoff protein.

Authors:  M M Elgadi; J R Smiley
Journal:  J Virol       Date:  1999-11       Impact factor: 5.103

Review 3.  Translational control of viral gene expression in eukaryotes.

Authors:  M Gale; S L Tan; M G Katze
Journal:  Microbiol Mol Biol Rev       Date:  2000-06       Impact factor: 11.056

4.  Adenovirus-specific translation by displacement of kinase Mnk1 from cap-initiation complex eIF4F.

Authors:  R Cuesta; Q Xi; R J Schneider
Journal:  EMBO J       Date:  2000-07-03       Impact factor: 11.598

5.  Inhibition of host translation by virus infection in vivo.

Authors:  René Toribio; Iván Ventoso
Journal:  Proc Natl Acad Sci U S A       Date:  2010-05-10       Impact factor: 11.205

6.  Adenovirus E4orf4 protein reduces phosphorylation of c-Fos and E1A proteins while simultaneously reducing the level of AP-1.

Authors:  U Müller; T Kleinberger; T Shenk
Journal:  J Virol       Date:  1992-10       Impact factor: 5.103

7.  The 11,600-MW protein encoded by region E3 of adenovirus is expressed early but is greatly amplified at late stages of infection.

Authors:  A E Tollefson; A Scaria; S K Saha; W S Wold
Journal:  J Virol       Date:  1992-06       Impact factor: 5.103

8.  Transient expression of the vaccinia virus DNA polymerase is an intrinsic feature of the early phase of infection and is unlinked to DNA replication and late gene expression.

Authors:  W F McDonald; V Crozel-Goudot; P Traktman
Journal:  J Virol       Date:  1992-01       Impact factor: 5.103

9.  RNA-binding properties of a translational activator, the adenovirus L4 100-kilodalton protein.

Authors:  D Riley; S J Flint
Journal:  J Virol       Date:  1993-06       Impact factor: 5.103

10.  Cap-binding protein (eukaryotic initiation factor 4E) and 4E-inactivating protein BP-1 independently regulate cap-dependent translation.

Authors:  D Feigenblum; R J Schneider
Journal:  Mol Cell Biol       Date:  1996-10       Impact factor: 4.272

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.