FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2238654066> ?p ?o ?g. }

• W2238654066 endingPage "4246" @default.
• W2238654066 startingPage "4236" @default.
• W2238654066 abstract "Tetherin, also known as bone marrow stromal antigen 2 (BST-2), inhibits the release of a wide range of enveloped viruses, including human immunodeficiency virus, type 1 (HIV-1) by directly tethering nascent virions to the surface of infected cells. The HIV-1 accessary protein Vpu counteracts tetherin restriction via sequestration, down-regulation, and/or displacement mechanisms to remove tetherin from sites of virus budding. However, the exact mechanism of Vpu-mediated antagonism of tetherin restriction remains to be fully understood. Here we report a novel role for the actin cross-linking regulator filamin A (FLNa) in Vpu anti-tetherin activities. We demonstrate that FLNa associates with tetherin and that FLNa modulates tetherin turnover. FLNa deficiency was found to enhance cell surface and steady-state levels of tetherin expression. In contrast, we observed that overexpression of FLNa reduced tetherin expression levels both on the plasma membrane and in intracellular compartments. Although FLNb shows high amino acid sequence similarity with FLNa, we reveal that only FLNa, but not FLNb, plays an essential role in tetherin turnover. We further showed that FLNa deficiency inhibited Vpu-mediated enhancement of virus release through interfering with the activity of Vpu to down-regulate cellular tetherin. Taken together, our studies suggest that Vpu hijacks the FLNa function in the modulation of tetherin to neutralize the antiviral factor tetherin. These findings may provide novel strategies for the treatment of HIV-1 infection. Tetherin, also known as bone marrow stromal antigen 2 (BST-2), inhibits the release of a wide range of enveloped viruses, including human immunodeficiency virus, type 1 (HIV-1) by directly tethering nascent virions to the surface of infected cells. The HIV-1 accessary protein Vpu counteracts tetherin restriction via sequestration, down-regulation, and/or displacement mechanisms to remove tetherin from sites of virus budding. However, the exact mechanism of Vpu-mediated antagonism of tetherin restriction remains to be fully understood. Here we report a novel role for the actin cross-linking regulator filamin A (FLNa) in Vpu anti-tetherin activities. We demonstrate that FLNa associates with tetherin and that FLNa modulates tetherin turnover. FLNa deficiency was found to enhance cell surface and steady-state levels of tetherin expression. In contrast, we observed that overexpression of FLNa reduced tetherin expression levels both on the plasma membrane and in intracellular compartments. Although FLNb shows high amino acid sequence similarity with FLNa, we reveal that only FLNa, but not FLNb, plays an essential role in tetherin turnover. We further showed that FLNa deficiency inhibited Vpu-mediated enhancement of virus release through interfering with the activity of Vpu to down-regulate cellular tetherin. Taken together, our studies suggest that Vpu hijacks the FLNa function in the modulation of tetherin to neutralize the antiviral factor tetherin. These findings may provide novel strategies for the treatment of HIV-1 infection." @default.
• W2238654066 created "2016-06-24" @default.
• W2238654066 creator A5014905602 @default.
• W2238654066 creator A5015573817 @default.
• W2238654066 creator A5039821059 @default.
• W2238654066 creator A5071864923 @default.
• W2238654066 date "2016-02-01" @default.
• W2238654066 modified "2023-10-14" @default.
• W2238654066 title "Filamin A Is Involved in HIV-1 Vpu-mediated Evasion of Host Restriction by Modulating Tetherin Expression" @default.
• W2238654066 cites W1571744798 @default.
• W2238654066 cites W1659719610 @default.
• W2238654066 cites W1898326375 @default.
• W2238654066 cites W1963508527 @default.
• W2238654066 cites W1964422613 @default.
• W2238654066 cites W1966824637 @default.
• W2238654066 cites W1972516366 @default.
• W2238654066 cites W1973079961 @default.
• W2238654066 cites W1976867329 @default.
• W2238654066 cites W1979078796 @default.
• W2238654066 cites W1985756888 @default.
• W2238654066 cites W1994324680 @default.
• W2238654066 cites W1994683562 @default.
• W2238654066 cites W2001430278 @default.
• W2238654066 cites W2002472695 @default.
• W2238654066 cites W2010458160 @default.
• W2238654066 cites W2016913504 @default.
• W2238654066 cites W2017980922 @default.
• W2238654066 cites W2021067210 @default.
• W2238654066 cites W2021701271 @default.
• W2238654066 cites W2025830466 @default.
• W2238654066 cites W2026237846 @default.
• W2238654066 cites W2027859676 @default.
• W2238654066 cites W2034568446 @default.
• W2238654066 cites W2036161664 @default.
• W2238654066 cites W2037024435 @default.
• W2238654066 cites W2041025244 @default.
• W2238654066 cites W2042781130 @default.
• W2238654066 cites W2043090465 @default.
• W2238654066 cites W2046390241 @default.
• W2238654066 cites W2047452261 @default.
• W2238654066 cites W2047649641 @default.
• W2238654066 cites W2050297098 @default.
• W2238654066 cites W2050646165 @default.
• W2238654066 cites W2058828092 @default.
• W2238654066 cites W2061391296 @default.
• W2238654066 cites W2062611394 @default.
• W2238654066 cites W2064818197 @default.
• W2238654066 cites W2068635948 @default.
• W2238654066 cites W2070311973 @default.
• W2238654066 cites W2072416882 @default.
• W2238654066 cites W2075562524 @default.
• W2238654066 cites W2077237370 @default.
• W2238654066 cites W2084602076 @default.
• W2238654066 cites W2085283692 @default.
• W2238654066 cites W2095640275 @default.
• W2238654066 cites W2097244362 @default.
• W2238654066 cites W2100978222 @default.
• W2238654066 cites W2101352435 @default.
• W2238654066 cites W2112949694 @default.
• W2238654066 cites W2113413125 @default.
• W2238654066 cites W2114651598 @default.
• W2238654066 cites W2115395564 @default.
• W2238654066 cites W2115662151 @default.
• W2238654066 cites W2116713053 @default.
• W2238654066 cites W2120231116 @default.
• W2238654066 cites W2123913956 @default.
• W2238654066 cites W2124660271 @default.
• W2238654066 cites W2125200507 @default.
• W2238654066 cites W2125420106 @default.
• W2238654066 cites W2126346789 @default.
• W2238654066 cites W2132869487 @default.
• W2238654066 cites W2140456056 @default.
• W2238654066 cites W2147579012 @default.
• W2238654066 cites W2151558536 @default.
• W2238654066 cites W2152113918 @default.
• W2238654066 cites W2152327707 @default.
• W2238654066 cites W2160718001 @default.
• W2238654066 cites W2160923835 @default.
• W2238654066 cites W2162589243 @default.
• W2238654066 cites W2164439474 @default.
• W2238654066 cites W2165070219 @default.
• W2238654066 cites W2168606329 @default.
• W2238654066 cites W2171338663 @default.
• W2238654066 cites W2329321343 @default.
• W2238654066 doi "https://doi.org/10.1074/jbc.m115.708123" @default.
• W2238654066 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4759197" @default.
• W2238654066 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26742839" @default.
• W2238654066 hasPublicationYear "2016" @default.
• W2238654066 type Work @default.
• W2238654066 sameAs 2238654066 @default.
• W2238654066 citedByCount "10" @default.
• W2238654066 countsByYear W22386540662017 @default.
• W2238654066 countsByYear W22386540662018 @default.
• W2238654066 countsByYear W22386540662019 @default.
• W2238654066 countsByYear W22386540662021 @default.
• W2238654066 countsByYear W22386540662023 @default.
• W2238654066 crossrefType "journal-article" @default.
• W2238654066 hasAuthorship W2238654066A5014905602 @default.

• next