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Article: Spatial regulation of Raf kinase signaling by RKTG

TitleSpatial regulation of Raf kinase signaling by RKTG
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2007
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings of the National Academy of Sciences of the United States of America, 2007, v. 104 n. 36, p. 14348-14353 How to Cite?
AbstractSubcellular compartmentalization has become an important theme in cell signaling such as spatial regulation of Ras by RasGRP1 and MEK/ERK by Sef. Here, we report spatial regulation of Raf kinase by RKTG (Raf kinase trapping to Golgi). RKTG is a seven-transmembrane protein localized at the Golgi apparatus. RKTG expression inhibits EGF-stimulated ERK and RSK phosphorylation, blocks NGF-mediated PC12 cell differentiation, and antagonizes Ras- and Raf-1-stimulated Elk-1 transactivation. Through interaction with Raf-1, RKTG changes the localization of Raf-1 from cytoplasm to the Golgi apparatus, blocks EGF-stimulated Raf-1 membrane translocation, and reduces the interaction of Raf-1 with Ras and MEK1. In RKTG-null mice, the basal ERK phosphorylation level is increased in the brain and liver. In RKTG-deleted mouse embryonic fibroblasts, EGF-induced ERK phosphorylation is enhanced. Collectively, our results reveal a paradigm of spatial regulation of Raf kinase by RKTG via sequestrating Raf-1 to the Golgi apparatus and thereby inhibiting the ERK signaling pathway. © 2007 by The National Academy of Sciences of the USA.
Persistent Identifierhttp://hdl.handle.net/10722/92386
ISSN
2015 Impact Factor: 9.423
2015 SCImago Journal Rankings: 6.883
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFeng, Len_HK
dc.contributor.authorXie, Xen_HK
dc.contributor.authorDing, Qen_HK
dc.contributor.authorLuo, Xen_HK
dc.contributor.authorHe, Jen_HK
dc.contributor.authorFan, Fen_HK
dc.contributor.authorLiu, Wen_HK
dc.contributor.authorWang, Zen_HK
dc.contributor.authorChen, Yen_HK
dc.date.accessioned2010-09-17T10:44:32Z-
dc.date.available2010-09-17T10:44:32Z-
dc.date.issued2007en_HK
dc.identifier.citationProceedings of the National Academy of Sciences of the United States of America, 2007, v. 104 n. 36, p. 14348-14353en_HK
dc.identifier.issn0027-8424en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92386-
dc.description.abstractSubcellular compartmentalization has become an important theme in cell signaling such as spatial regulation of Ras by RasGRP1 and MEK/ERK by Sef. Here, we report spatial regulation of Raf kinase by RKTG (Raf kinase trapping to Golgi). RKTG is a seven-transmembrane protein localized at the Golgi apparatus. RKTG expression inhibits EGF-stimulated ERK and RSK phosphorylation, blocks NGF-mediated PC12 cell differentiation, and antagonizes Ras- and Raf-1-stimulated Elk-1 transactivation. Through interaction with Raf-1, RKTG changes the localization of Raf-1 from cytoplasm to the Golgi apparatus, blocks EGF-stimulated Raf-1 membrane translocation, and reduces the interaction of Raf-1 with Ras and MEK1. In RKTG-null mice, the basal ERK phosphorylation level is increased in the brain and liver. In RKTG-deleted mouse embryonic fibroblasts, EGF-induced ERK phosphorylation is enhanced. Collectively, our results reveal a paradigm of spatial regulation of Raf kinase by RKTG via sequestrating Raf-1 to the Golgi apparatus and thereby inhibiting the ERK signaling pathway. © 2007 by The National Academy of Sciences of the USA.en_HK
dc.languageengen_HK
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.orgen_HK
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of Americaen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.titleSpatial regulation of Raf kinase signaling by RKTGen_HK
dc.typeArticleen_HK
dc.identifier.emailChen, Y:ychenc@hkucc.hku.hken_HK
dc.identifier.authorityChen, Y=rp1318en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1073/pnas.0701298104en_HK
dc.identifier.pmid17724343-
dc.identifier.pmcidPMC1964828-
dc.identifier.scopuseid_2-s2.0-35448964335en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-35448964335&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume104en_HK
dc.identifier.issue36en_HK
dc.identifier.spage14348en_HK
dc.identifier.epage14353en_HK
dc.identifier.isiWOS:000249333600032-
dc.identifier.f10001093890-
dc.identifier.citeulike2819510-

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