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HIV-1 mRNA 3' end processing is distinctively regulated by elF3f, CDK11, and splice factor 9G8

Academic Article
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Overview

authors

  • Valente, Susana Tereno
  • Gilmartin, G. M.
  • Venkatarama, K.
  • Arriagada, G.
  • Goff, S. P.

publication date

  • October 2009

journal

  • Molecular Cell  Journal

abstract

  • A genetic screen previously identified the N-terminal 91 amino acids of the eukaryotic initiation factor 3 subunit f (N91-eIF3f) as a potent inhibitor of HIV-1 replication. Overexpression of N91-eIF3f or full-length eIF3f reduced the level of HIV-1 mRNAs in the infected cell. Here we show that N91-eIF3f and eIF3f act by specifically blocking the 3' end processing of the HIV-1 pre-mRNA both in vivo and in vitro. Furthermore, the results suggest that eIF3f mediates this restriction of HIV-1 expression through the previously unsuspected involvement of a set of factors that includes eIF3f, the SR protein 9G8, and the cyclin-dependent kinase 11 (CDK11). eIF3f affects HIV-1 3' end processing by modulating the sequence-specific recognition of the HIV-1 pre-mRNA by 9G8.

subject areas

  • Base Sequence
  • Binding Sites
  • Cell Extracts
  • Cell Nucleus
  • Cyclin-Dependent Kinases
  • Eukaryotic Initiation Factor-3
  • HIV Long Terminal Repeat
  • HIV-1
  • HeLa Cells
  • Humans
  • Models, Biological
  • Molecular Sequence Data
  • Nuclear Proteins
  • Nucleocytoplasmic Transport Proteins
  • Poly A
  • Protein Binding
  • RNA 3' End Processing
  • RNA, Messenger
  • RNA, Viral
  • RNA-Binding Proteins
  • Serine-Arginine Splicing Factors
  • Virus Replication
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Identity

PubMed Central ID

  • PMC3068534

International Standard Serial Number (ISSN)

  • 1097-2765

Digital Object Identifier (DOI)

  • 10.1016/j.molcel.2009.10.004

PubMed ID

  • 19854136
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Additional Document Info

start page

  • 279

end page

  • 289

volume

  • 36

issue

  • 2

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