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Example sentences for: inactivates
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Cellulose acetate phthalate (CAP) is a promising microbicide candidate for prevention of infection by sexually transmitted disease (STD) pathogens, including HIV-1 [ 1 2 3 4 5 6 7 ] . CAP inactivates HIV-1 and blocks the coreceptor binding site on the virus envelope glycoprotein gp120, while leaving the site for the primary cellular receptor CD4 accessible [ 8 9 ] Soluble CD4 (sCD4) was shown to inhibit HIV-1 infection by two mechanisms: reversible blockage of virus binding to receptors, and irreversible inactivation of virus infectivity [ 10 ] . Since CAP and sCD4 bind to distinct domains on the HIV-1 envelope, it was of interest to determine whether or not these two ligands affect virus infectivity synergistically as do other combinations of anti-HIV-1 drugs and sCD4 [ 11 12 ] Binding of sCD4 leads to conformational changes in gp120 [ 13 14 15 16 17 ] . Binding of gp120 to coreceptors CXCR4 and CCR5, respectively, triggers additional conformational changes in HIV-1 envelope glycoproteins [ 18 19 ] For these reasons it was of interest to determine whether a) pretreatment of HIV-1 with sCD4 would affect subsequent binding of CAP to virus particles, and b) CAP binding to virus particles in the presence or absence of sCD4 would elicit conformational changes which could affect HIV-1 infectivity.
However, the introduction of a mutation into one subunit of a single-chain heterodimer causes a defect in only one half-site and therefore inactivates only one of the two RNA-binding sites.
Results presented here explain how micronized CAP inactivates HIV-1.
This has lead to the hypothesis that small GTP binding proteins act sequentially, in the GTPase cascade Cdc42→Rac→Rho [ 35 ] . Facilitating the study of Rho in regulation of cell activity has been the use of C3 exoenzyme, a toxin from Clostridium botulinum that ADP-ribosylates [ 15 16 ] and inactivates Rho proteins.
Earlier studies identified tab2 and TAB6 as mutations in NET1 and CDC14, respectively [ 15 18 ] . Net1 detains Cdc14 in the nucleolus and inactivates it until a Tem1-dependent signal sets Cdc14 free to promote exit from mitosis [ 15 16 17 ] . The fact that both Net1 and Cdc14 are directly involved in exit from mitosis prompted us to further analyze tab mutants.
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