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   	<dc:title>The actin-disassembly protein glia maturation factor γ enhances actin remodeling and B cell antigen receptor signaling at the immune synapse</dc:title>
   	<dc:creator>Deretic, Nikola</dc:creator>
   	<dc:creator>Bolger-Munro, Madison ; https://orcid.org/0000-0002-8176-4824</dc:creator>
   	<dc:creator>Choi, Kate</dc:creator>
   	<dc:creator>Abraham, Libin</dc:creator>
   	<dc:creator>Gold, Michael R.</dc:creator>
   	<dc:subject>Cell Biology</dc:subject>
   	<dc:subject>Developmental Biology</dc:subject>
   	<dc:subject>ddc:570</dc:subject>
   	<dc:description>Signaling by the B cell antigen receptor (BCR) initiates actin remodeling. The assembly of branched actin networks that are nucleated by the Arp2/3 complex exert outward force on the plasma membrane, allowing B cells to form membrane protrusions that can scan the surface of antigen-presenting cells (APCs). The resulting Arp2/3 complex-dependent actin retrograde flow promotes the centripetal movement and progressive coalescence of BCR microclusters, which amplifies BCR signaling. Glia maturation factor γ (GMFγ) is an actin disassembly-protein that releases Arp2/3 complex-nucleated actin filaments from actin networks. By doing so, GMFγ could either oppose the actions of the Arp2/3 complex or support Arp2/3 complex-nucleated actin polymerization by contributing to the recycling of actin monomers and Arp2/3 complexes. We now show that reducing the levels of GMFγ in human B cell lines via transfection with a specific siRNA impairs the ability of B cells to spread on antigen-coated surfaces, decreases the velocity of actin retrograde flow, diminishes the coalescence of BCR microclusters into a central cluster at the B cell-APC contact site, and decreases APC-induced BCR signaling. These effects of depleting GMFγ are similar to what occurs when the Arp2/3 complex is inhibited. This suggests that GMFγ cooperates with the Arp2/3 complex to support BCR-induced actin remodeling and amplify BCR signaling at the immune synapse.</dc:description>
   	<dc:publisher>Frontiers Media</dc:publisher>
   	<dc:date>2021</dc:date>
   	<dc:type>info:eu-repo/semantics/article</dc:type>
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   	<dc:type>http://purl.org/coar/resource_type/c_2df8fbb1</dc:type>
   	<dc:identifier>https://research-explorer.ista.ac.at/record/15264</dc:identifier>
   	<dc:identifier>https://research-explorer.ista.ac.at/download/15264/15291</dc:identifier>
   	<dc:source>Deretic N, Bolger-Munro M, Choi K, Abraham L, Gold MR. The actin-disassembly protein glia maturation factor γ enhances actin remodeling and B cell antigen receptor signaling at the immune synapse. &lt;i&gt;Frontiers in Cell and Developmental Biology&lt;/i&gt;. 2021;9. doi:&lt;a href=&quot;https://doi.org/10.3389/fcell.2021.647063&quot;&gt;10.3389/fcell.2021.647063&lt;/a&gt;</dc:source>
   	<dc:language>eng</dc:language>
   	<dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.3389/fcell.2021.647063</dc:relation>
   	<dc:relation>info:eu-repo/semantics/altIdentifier/issn/2296-634X</dc:relation>
   	<dc:relation>info:eu-repo/semantics/altIdentifier/pmid/34336818</dc:relation>
   	<dc:rights>https://creativecommons.org/licenses/by/4.0/</dc:rights>
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