Abstract
Two recent publications have explored the mechanisms by which a mutant of the host protein Sam68 blocks HIV-1 structural protein synthesis and expands its activity to encompass Nef. Although the two studies propose different mechanisms for the responses observed, it is possible that a common activity is responsible. Understanding how this Sam68 mutant discriminates among the multiple viral mRNAs promises to reveal unique properties of HIV-1 RNA metabolism.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adaptor Proteins, Signal Transducing / genetics
-
Adaptor Proteins, Signal Transducing / metabolism*
-
DNA-Binding Proteins / genetics
-
DNA-Binding Proteins / metabolism*
-
Gene Expression Regulation, Viral*
-
HIV Infections / genetics
-
HIV Infections / metabolism*
-
HIV Infections / virology
-
HIV-1 / genetics*
-
HIV-1 / metabolism
-
Humans
-
RNA, Viral / genetics
-
RNA, Viral / metabolism
-
RNA-Binding Proteins / genetics
-
RNA-Binding Proteins / metabolism*
Substances
-
Adaptor Proteins, Signal Transducing
-
DNA-Binding Proteins
-
KHDRBS1 protein, human
-
RNA, Viral
-
RNA-Binding Proteins