FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1966734154> ?p ?o ?g. }

• W1966734154 endingPage "1985" @default.
• W1966734154 startingPage "1975" @default.
• W1966734154 abstract "ABSTRACT The influenza virus hemagglutinin (HA) envelope protein mediates virus entry by first binding to cell surface receptors and then fusing viral and endosomal membranes during endocytosis. Cleavage of the HA precursor (HA0) into a surface receptor-binding subunit (HA1) and a fusion-inducing transmembrane subunit (HA2) by host cell enzymes primes HA for fusion competence by repositioning the fusion peptide to the newly created N terminus of HA2. We previously reported that the influenza virus M2 protein enhances pandemic 2009 influenza A virus [(H1N1)pdm09] HA-pseudovirus infectivity, but the mechanism was unclear. In this study, using cell-cell fusion and HA-pseudovirus infectivity assays, we found that the ion channel function of M2 was required for enhancement of HA fusion and HA-pseudovirus infectivity. The M2 activity was needed only during HA biosynthesis, and proteolysis experiments indicated that M2 proton channel activity helped to protect (H1N1)pdm09 HA from premature conformational changes as it traversed low-pH compartments during transport to the cell surface. While M2 has previously been shown to protect avian influenza virus HA proteins of the H5 and H7 subtypes that have polybasic cleavage motifs, this study demonstrates that M2 can protect HA proteins from human H1N1 strains that lack a polybasic cleavage motif. This finding suggests that M2 proton channel activity may play a wider role in preserving HA fusion competence among a variety of HA subtypes, including HA proteins from emerging strains that may have reduced HA stability. IMPORTANCE Influenza virus infects cells when the hemagglutinin (HA) surface protein undergoes irreversible pH-induced conformational changes after the virus is taken into the cell by endocytosis. HA fusion competence is primed when host cell enzymes cleave the HA precursor. The proton channel function of influenza virus M2 protein has previously been shown to protect avian influenza virus HA proteins that contain a polybasic cleavage site from pH-induced conformational changes during biosynthesis, but this effect is less well understood for human influenza virus HA proteins that lack polybasic cleavage sites. Using assays that focus on HA entry and fusion, we found that the M2 protein also protects (H1N1)pdm09 influenza A virus HA from premature conformational changes as it transits low-pH compartments during biosynthesis. This work suggests that M2 may play a wider role in preserving HA function in a variety of influenza virus subtypes that infect humans and may be especially important for HA proteins that are less stable." @default.
• W1966734154 created "2016-06-24" @default.
• W1966734154 creator A5037390063 @default.
• W1966734154 creator A5047905566 @default.
• W1966734154 creator A5082080465 @default.
• W1966734154 creator A5085933304 @default.
• W1966734154 creator A5086459849 @default.
• W1966734154 creator A5091553173 @default.
• W1966734154 date "2015-02-15" @default.
• W1966734154 modified "2023-10-17" @default.
• W1966734154 title "Influenza Virus M2 Protein Ion Channel Activity Helps To Maintain Pandemic 2009 H1N1 Virus Hemagglutinin Fusion Competence during Transport to the Cell Surface" @default.
• W1966734154 cites W113442559 @default.
• W1966734154 cites W1553486320 @default.
• W1966734154 cites W1585610099 @default.
• W1966734154 cites W1589869891 @default.
• W1966734154 cites W1925381193 @default.
• W1966734154 cites W1970960203 @default.
• W1966734154 cites W1974428710 @default.
• W1966734154 cites W1976694080 @default.
• W1966734154 cites W1980318325 @default.
• W1966734154 cites W1986152551 @default.
• W1966734154 cites W1989764838 @default.
• W1966734154 cites W1989788129 @default.
• W1966734154 cites W1993829010 @default.
• W1966734154 cites W1994451477 @default.
• W1966734154 cites W1997176483 @default.
• W1966734154 cites W2004313038 @default.
• W1966734154 cites W2006519535 @default.
• W1966734154 cites W2009761723 @default.
• W1966734154 cites W2013911193 @default.
• W1966734154 cites W2014683141 @default.
• W1966734154 cites W2015121618 @default.
• W1966734154 cites W2016665377 @default.
• W1966734154 cites W2016677998 @default.
• W1966734154 cites W2021827364 @default.
• W1966734154 cites W2022180444 @default.
• W1966734154 cites W2023459687 @default.
• W1966734154 cites W2026756569 @default.
• W1966734154 cites W2027707550 @default.
• W1966734154 cites W2035088373 @default.
• W1966734154 cites W2037115572 @default.
• W1966734154 cites W2037831301 @default.
• W1966734154 cites W2046182783 @default.
• W1966734154 cites W2046470284 @default.
• W1966734154 cites W2048010092 @default.
• W1966734154 cites W2051781399 @default.
• W1966734154 cites W2062135212 @default.
• W1966734154 cites W2064805716 @default.
• W1966734154 cites W2065959626 @default.
• W1966734154 cites W2067036816 @default.
• W1966734154 cites W2071219890 @default.
• W1966734154 cites W2071376586 @default.
• W1966734154 cites W2073521270 @default.
• W1966734154 cites W2074499311 @default.
• W1966734154 cites W2075472820 @default.
• W1966734154 cites W2082814008 @default.
• W1966734154 cites W2102335249 @default.
• W1966734154 cites W2104589227 @default.
• W1966734154 cites W2106773656 @default.
• W1966734154 cites W2108107193 @default.
• W1966734154 cites W2112170460 @default.
• W1966734154 cites W2112679913 @default.
• W1966734154 cites W2125500604 @default.
• W1966734154 cites W2133017128 @default.
• W1966734154 cites W2135386122 @default.
• W1966734154 cites W2138198678 @default.
• W1966734154 cites W2138204737 @default.
• W1966734154 cites W2138602400 @default.
• W1966734154 cites W2143784163 @default.
• W1966734154 cites W2150768033 @default.
• W1966734154 cites W2153074293 @default.
• W1966734154 cites W2156171429 @default.
• W1966734154 cites W2158112812 @default.
• W1966734154 cites W2161496722 @default.
• W1966734154 cites W2162244167 @default.
• W1966734154 cites W2163638699 @default.
• W1966734154 cites W2164695068 @default.
• W1966734154 cites W2165264740 @default.
• W1966734154 cites W2168973617 @default.
• W1966734154 cites W2320132905 @default.
• W1966734154 cites W41359786 @default.
• W1966734154 doi "https://doi.org/10.1128/jvi.03253-14" @default.
• W1966734154 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4338904" @default.
• W1966734154 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25473053" @default.
• W1966734154 hasPublicationYear "2015" @default.
• W1966734154 type Work @default.
• W1966734154 sameAs 1966734154 @default.
• W1966734154 citedByCount "39" @default.
• W1966734154 countsByYear W19667341542015 @default.
• W1966734154 countsByYear W19667341542016 @default.
• W1966734154 countsByYear W19667341542017 @default.
• W1966734154 countsByYear W19667341542018 @default.
• W1966734154 countsByYear W19667341542019 @default.
• W1966734154 countsByYear W19667341542020 @default.
• W1966734154 countsByYear W19667341542021 @default.
• W1966734154 countsByYear W19667341542022 @default.
• W1966734154 countsByYear W19667341542023 @default.
• W1966734154 crossrefType "journal-article" @default.

• next