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dc.contributor.authorSmida, Michal
dc.contributor.authorCammann, Clemens
dc.contributor.authorGurbiel, Slavyana
dc.contributor.authorKerstin, Nadja
dc.contributor.authorLingel, Holger
dc.contributor.authorLindquist, Sabine
dc.contributor.authorSimeoni, Luca
dc.contributor.authorBrunner-Weinzierl, Monika C
dc.contributor.authorSuchanek, Miloslav
dc.contributor.authorSchraven, Burkhart
dc.contributor.authorLindquist, Jonathan A
dc.date.accessioned2013-06-20T09:16:48Z
dc.date.available2013-06-20T09:16:48Z
dc.date.issued2013
dc.identifier.citationPAG/Cbp suppression reveals a contribution of CTLA-4 to setting the activation threshold in T cells. 2013, 11 (1):28 Cell Commun. Signalen_GB
dc.identifier.issn1478-811X
dc.identifier.pmid23601194
dc.identifier.doi10.1186/1478-811X-11-28
dc.identifier.urihttp://hdl.handle.net/10033/294281
dc.description.abstractPAG/Cbp represents a ubiquitous mechanism for regulating Src family kinases by recruiting Csk to the plasma membrane, thereby controlling cellular activation. Since Src kinases are known oncogenes, we used RNA interference in primary human T cells to test whether the loss of PAG resulted in lymphocyte transformation.
dc.language.isoenen
dc.rightsArchived with thanks to Cell communication and signaling : CCSen_GB
dc.titlePAG/Cbp suppression reveals a contribution of CTLA-4 to setting the activation threshold in T cells.en
dc.typeArticleen
dc.contributor.departmentInstitute of Molecular and Clinical Immunology, Otto-von-Guericke University, Leipziger Strasse 44, Magdeburg, 39120, Germany. jon.lindquist@med.ovgu.de.en_GB
dc.identifier.journalCell communication and signaling : CCSen_GB
refterms.dateFOA2018-06-13T00:19:13Z
html.description.abstractPAG/Cbp represents a ubiquitous mechanism for regulating Src family kinases by recruiting Csk to the plasma membrane, thereby controlling cellular activation. Since Src kinases are known oncogenes, we used RNA interference in primary human T cells to test whether the loss of PAG resulted in lymphocyte transformation.


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