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Article: CD28 regulates the translation of Bcl-xL via the phosphatidylinositol 3-kinase/mammalian target of rapamycin pathway

TitleCD28 regulates the translation of Bcl-x<inf>L</inf> via the phosphatidylinositol 3-kinase/mammalian target of rapamycin pathway
Authors
Issue Date2005
Citation
Journal of Immunology, 2005, v. 174, n. 1, p. 180-194 How to Cite?
AbstractIn concert with the TCR, CD28 promotes T cell survival by regulating the expression of the antiapoptotic protein Bd-xL. The mechanism by which CD28 mediates the induction of Bcl-xL remains unknown. We show that although signaling through the TCR is sufficient to stimulate transcription of Bcl-xL mRNA, CD28, by activating PI3K and mammalian target of rapamycin, provides a critical signal that regulates the translation of Bcl-xL transcripts. We observe that CD28 induced 4E-binding protein-1 phosphorylation, an inhibitor of the translational machinery, and that CD28 costimulation directly augmented the translation of a Bcl-xL 5′-untranslated region reporter construct. Lastly, costimulation by CD28 shifted the distribution of Bcl-xL mRNA transcripts from the pretranslation complex to the translationally active polyribosomes. These results demonstrate that CD28 relieves the translational inhibition of Bcl-xL in a PI3K/mammalian target of rapamycin-dependent manner.
Persistent Identifierhttp://hdl.handle.net/10722/291679
ISSN
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 1.558
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWu, Linda X.-
dc.contributor.authorLa Rose, Jose-
dc.contributor.authorChen, Liane-
dc.contributor.authorNeale, Chris-
dc.contributor.authorMak, Tak-
dc.contributor.authorOkkenhaug, Klaus-
dc.contributor.authorWange, Ronald-
dc.contributor.authorRottapel, Robert-
dc.date.accessioned2020-11-17T14:54:53Z-
dc.date.available2020-11-17T14:54:53Z-
dc.date.issued2005-
dc.identifier.citationJournal of Immunology, 2005, v. 174, n. 1, p. 180-194-
dc.identifier.issn0022-1767-
dc.identifier.urihttp://hdl.handle.net/10722/291679-
dc.description.abstractIn concert with the TCR, CD28 promotes T cell survival by regulating the expression of the antiapoptotic protein Bd-xL. The mechanism by which CD28 mediates the induction of Bcl-xL remains unknown. We show that although signaling through the TCR is sufficient to stimulate transcription of Bcl-xL mRNA, CD28, by activating PI3K and mammalian target of rapamycin, provides a critical signal that regulates the translation of Bcl-xL transcripts. We observe that CD28 induced 4E-binding protein-1 phosphorylation, an inhibitor of the translational machinery, and that CD28 costimulation directly augmented the translation of a Bcl-xL 5′-untranslated region reporter construct. Lastly, costimulation by CD28 shifted the distribution of Bcl-xL mRNA transcripts from the pretranslation complex to the translationally active polyribosomes. These results demonstrate that CD28 relieves the translational inhibition of Bcl-xL in a PI3K/mammalian target of rapamycin-dependent manner.-
dc.languageeng-
dc.relation.ispartofJournal of Immunology-
dc.titleCD28 regulates the translation of Bcl-x<inf>L</inf> via the phosphatidylinositol 3-kinase/mammalian target of rapamycin pathway-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.4049/jimmunol.174.1.180-
dc.identifier.pmid15611240-
dc.identifier.scopuseid_2-s2.0-10844280747-
dc.identifier.volume174-
dc.identifier.issue1-
dc.identifier.spage180-
dc.identifier.epage194-
dc.identifier.isiWOS:000225852900022-
dc.identifier.issnl0022-1767-

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