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- Publisher Website: 10.1083/jcb.201501094
- Scopus: eid_2-s2.0-84938371994
- PMID: 26101216
- WOS: WOS:000356998200006
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Article: GMFβ controls branched actin content and lamellipodial retraction in fibroblasts
Title | GMFβ controls branched actin content and lamellipodial retraction in fibroblasts |
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Authors | |
Issue Date | 2015 |
Citation | Journal of Cell Biology, 2015, v. 209, n. 6, p. 803-812 How to Cite? |
Abstract | The lamellipodium is an important structure for cell migration containing branched actin nucleated via the Arp2/3 complex. The formation of branched actin is relatively well studied, but less is known about its disassembly and how this influences migration. GMF is implicated in both Arp2/3 debranching and inhibition of Arp2/3 activation. Modulation of GMFβ, a ubiquitous GMF isoform, by depletion or overexpression resulted in changes in lamellipodial dynamics, branched actin content, and migration. Acute pharmacological inhibition of Arp2/3 by CK-666, coupled to quantitative live-cell imaging of the complex, showed that depletion of GMFβ decreased the rate of branched actin disassembly. These data, along with mutagenesis studies, suggest that debranching (not inhibition of Arp2/3 activation) is a primary activity of GMFβ in vivo. Furthermore, depletion or overexpression of GMFβ disrupted the ability of cells to directionally migrate to a gradient of fibronectin (haptotaxis). These data suggest that debranching by GMFβ plays an important role in branched actin regulation, lamellipodial dynamics, and directional migration. |
Persistent Identifier | http://hdl.handle.net/10722/311399 |
ISSN | 2023 Impact Factor: 7.4 2023 SCImago Journal Rankings: 3.717 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Haynes, Elizabeth M. | - |
dc.contributor.author | Asokan, Sreeja B. | - |
dc.contributor.author | King, Samantha J. | - |
dc.contributor.author | Johnson, Heath E. | - |
dc.contributor.author | Haugh, Jason M. | - |
dc.contributor.author | Bear, James E. | - |
dc.date.accessioned | 2022-03-22T11:53:51Z | - |
dc.date.available | 2022-03-22T11:53:51Z | - |
dc.date.issued | 2015 | - |
dc.identifier.citation | Journal of Cell Biology, 2015, v. 209, n. 6, p. 803-812 | - |
dc.identifier.issn | 0021-9525 | - |
dc.identifier.uri | http://hdl.handle.net/10722/311399 | - |
dc.description.abstract | The lamellipodium is an important structure for cell migration containing branched actin nucleated via the Arp2/3 complex. The formation of branched actin is relatively well studied, but less is known about its disassembly and how this influences migration. GMF is implicated in both Arp2/3 debranching and inhibition of Arp2/3 activation. Modulation of GMFβ, a ubiquitous GMF isoform, by depletion or overexpression resulted in changes in lamellipodial dynamics, branched actin content, and migration. Acute pharmacological inhibition of Arp2/3 by CK-666, coupled to quantitative live-cell imaging of the complex, showed that depletion of GMFβ decreased the rate of branched actin disassembly. These data, along with mutagenesis studies, suggest that debranching (not inhibition of Arp2/3 activation) is a primary activity of GMFβ in vivo. Furthermore, depletion or overexpression of GMFβ disrupted the ability of cells to directionally migrate to a gradient of fibronectin (haptotaxis). These data suggest that debranching by GMFβ plays an important role in branched actin regulation, lamellipodial dynamics, and directional migration. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Cell Biology | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.title | GMFβ controls branched actin content and lamellipodial retraction in fibroblasts | - |
dc.type | Article | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1083/jcb.201501094 | - |
dc.identifier.pmid | 26101216 | - |
dc.identifier.pmcid | PMC4477851 | - |
dc.identifier.scopus | eid_2-s2.0-84938371994 | - |
dc.identifier.volume | 209 | - |
dc.identifier.issue | 6 | - |
dc.identifier.spage | 803 | - |
dc.identifier.epage | 812 | - |
dc.identifier.eissn | 1540-8140 | - |
dc.identifier.isi | WOS:000356998200006 | - |