File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: TLR ligand-induced podosome disassembly in dendritic cells is ADAM17 dependent

TitleTLR ligand-induced podosome disassembly in dendritic cells is ADAM17 dependent
Authors
Issue Date2008
PublisherRockefeller University Press. The Journal's web site is located at http://www.jcb.org
Citation
Journal Of Cell Biology, 2008, v. 182 n. 5, p. 993-1005 How to Cite?
AbstractToll-like receptor (TLR) signaling induces a rapid reorganization of the actin cytoskeleton in cultured mouse dendritic cells (DC), leading to enhanced antigen endocytosis and a concomitant loss of filamentous actin-rich podosomes. We show that as podosomes are lost, TLR signaling induces prominent focal contacts and a transient reduction in DC migratory capacity in vitro. We further show that podosomes in mouse DC are foci of pronounced gelatinase activity, dependent on the enzyme membrane type I matrix metalloprotease (MT1-MMP), and that DC transiently lose the ability to degrade the extracellular matrix after TLR signaling. Surprisingly, MMP inhibitors block TLR signaling-induced podosome disassembly, although stimulated endocytosis is unaffected, which demonstrates that the two phenomena are not obligatorily coupled. Podosome disassembly caused by TLR signaling occurs normally in DC lacking MT1-MMP, and instead requires the tumor necrosis factor α-converting enzyme ADAM17 (a disintegrin and metalloprotease 17), which demonstrates a novel role for this sheddase in regulating an actin-based structure. © 2008 West et al.
Persistent Identifierhttp://hdl.handle.net/10722/58262
ISSN
2015 Impact Factor: 8.717
2015 SCImago Journal Rankings: 7.923
ISI Accession Number ID
Funding AgencyGrant Number
Medical Research CouncilGO200536
Hong Kong Research Grant CouncilCERG 751303
Funding Information:

We are grateful to the Medical Research Council for program grant GO200536 (to C. Watts and A. R. Prescott) and the Hong Kong Research Grant Council (grant CERG 751303 to Z. Zhou) for funding.

References

 

DC FieldValueLanguage
dc.contributor.authorWest, MAen_HK
dc.contributor.authorPrescott, ARen_HK
dc.contributor.authorKui, MCen_HK
dc.contributor.authorZhou, Zen_HK
dc.contributor.authorRoseJohn, Sen_HK
dc.contributor.authorScheller, Jen_HK
dc.contributor.authorWatts, Cen_HK
dc.date.accessioned2010-05-31T03:27:00Z-
dc.date.available2010-05-31T03:27:00Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Cell Biology, 2008, v. 182 n. 5, p. 993-1005en_HK
dc.identifier.issn0021-9525en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58262-
dc.description.abstractToll-like receptor (TLR) signaling induces a rapid reorganization of the actin cytoskeleton in cultured mouse dendritic cells (DC), leading to enhanced antigen endocytosis and a concomitant loss of filamentous actin-rich podosomes. We show that as podosomes are lost, TLR signaling induces prominent focal contacts and a transient reduction in DC migratory capacity in vitro. We further show that podosomes in mouse DC are foci of pronounced gelatinase activity, dependent on the enzyme membrane type I matrix metalloprotease (MT1-MMP), and that DC transiently lose the ability to degrade the extracellular matrix after TLR signaling. Surprisingly, MMP inhibitors block TLR signaling-induced podosome disassembly, although stimulated endocytosis is unaffected, which demonstrates that the two phenomena are not obligatorily coupled. Podosome disassembly caused by TLR signaling occurs normally in DC lacking MT1-MMP, and instead requires the tumor necrosis factor α-converting enzyme ADAM17 (a disintegrin and metalloprotease 17), which demonstrates a novel role for this sheddase in regulating an actin-based structure. © 2008 West et al.en_HK
dc.languageengen_HK
dc.publisherRockefeller University Press. The Journal's web site is located at http://www.jcb.orgen_HK
dc.relation.ispartofJournal of Cell Biologyen_HK
dc.rightsJournal of Cellular Biochemistry. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshADAM Proteins - metabolism - physiologyen_HK
dc.subject.meshActin Cytoskeleton - metabolism - ultrastructureen_HK
dc.subject.meshActins - metabolismen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Movementen_HK
dc.subject.meshDendritic Cells - enzymology - metabolism - ultrastructureen_HK
dc.subject.meshExtracellular Matrix - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGelatinases - metabolismen_HK
dc.subject.meshLigandsen_HK
dc.subject.meshMatrix Metalloproteinases - antagonists & inhibitors - metabolismen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred Strainsen_HK
dc.subject.meshPinocytosis - drug effectsen_HK
dc.subject.meshProtease Inhibitors - pharmacologyen_HK
dc.subject.meshSignal Transduction - drug effectsen_HK
dc.subject.meshToll-Like Receptors - metabolismen_HK
dc.titleTLR ligand-induced podosome disassembly in dendritic cells is ADAM17 dependenten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0730-2312&volume=182&spage=993&epage=1005&date=2008&atitle=Tlr+Ligand-induced+Podosome+Disassembly+In+Dendritic+Cells+Is+Adam17+Dependenten_HK
dc.identifier.emailZhou, Z:zhongjun@hkucc.hku.hken_HK
dc.identifier.authorityZhou, Z=rp00503en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1083/jcb.200801022en_HK
dc.identifier.pmid18762577en_HK
dc.identifier.scopuseid_2-s2.0-51649088232en_HK
dc.identifier.hkuros153649en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-51649088232&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume182en_HK
dc.identifier.issue5en_HK
dc.identifier.spage993en_HK
dc.identifier.epage1005en_HK
dc.identifier.isiWOS:000259050700017-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWest, MA=35605973600en_HK
dc.identifier.scopusauthoridPrescott, AR=7005983965en_HK
dc.identifier.scopusauthoridKui, MC=24780760100en_HK
dc.identifier.scopusauthoridZhou, Z=8631856300en_HK
dc.identifier.scopusauthoridRoseJohn, S=7005838522en_HK
dc.identifier.scopusauthoridScheller, J=7004433319en_HK
dc.identifier.scopusauthoridWatts, C=7202527327en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats