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Internal ribosomal entry site function

Holcik, M., and Korneluk, R. G. (2000). Functional characterization of the X-linked inhibitor of apoptosis (XIAP) internal ribosome entry site element Role of La autoantigen in XIAP translation. Mol. Cell Biol. 20, 4648-4657. [Pg.328]

Kruger, M., Beger, C., Li, Q.X., Welch, P.J., Tritz, R., Leavitt, M., Barber, J.R. and Wong-Staal, F. (2000) Identification of eIF2Bgamma and eIF2gamma as cofactors of hepatitis C virus internal ribosome entry site-mediated translation using a functional genomics approach. Proc. Natl. Acad. Sci. USA, 97, 8566-8571. [Pg.63]

Anwar, A., Ali, N., Tanveer, R. and Siddiqui, A. (2000) Demonstration of functional requirement of polypyrimidine tract-binding protein by SELEX RNA during hepatitis C virus internal ribosome entry site-mediated translation initiation. J. Biol. Chem., 275, 34231-34235. [Pg.101]

A second viral strategy to disrupt PKR function involves antagonistic viral nucleic adds. For example, the internal ribosome entry site (IRES) of Hepatitis C virus (HCV) has been shown to be able to bind to PKR in competition with dsRNA and prevent autophosphor tion and activation of PKR in vitro. EBV nucleic acid can also antagonise PKR, since fflV-encoded RNA1 (EBER-1) and EBER-2can bind PKR in vitro and EBER-1 can reverse the inhibitory eflfects of dsRNA on protein synthesis. AdV-encoded VAI RNA binds to PKR in competition with dsRNA but fails to lead to PKR autophosphorylation or activation. [Pg.52]


See other pages where Internal ribosomal entry site function is mentioned: [Pg.371]    [Pg.82]    [Pg.167]    [Pg.89]    [Pg.132]    [Pg.228]    [Pg.254]    [Pg.496]    [Pg.98]    [Pg.112]    [Pg.30]    [Pg.167]    [Pg.122]   
See also in sourсe #XX -- [ Pg.273 ]




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