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dc.contributor.authorJanes, Mandy Elaine
dc.date.accessioned2011-02-09T10:28:09Z
dc.date.available2011-02-09T10:28:09Z
dc.date.issued2008
dc.identifier.urihttps://qmro.qmul.ac.uk/xmlui/handle/123456789/580
dc.descriptionPhDen_US
dc.description.abstractThe role of ACTH in stimulating or inhibiting growth of adrenal cells has been a subject of some controversy. Reports that ACTH may stimulate Erk/MAP kinase in Y1 cells have suggested a role for cAMP in this process. In attempting to extend this work the ACTH responses in the human H295R cell line have been studied. This cell line makes only a very modest cAMP response to ACTH, yet the Erk1/2 response is highly reproducible and immediate, but not prolonged. It is minimally reduced by the protein kinase A inhibitor, H89, but unaffected by PKC and calcium inhibitors. Inhibition of EGF receptor or other tyrosine kinase receptor transactivation was without effect, as was inhibition of c-Src activity or c-Src phosphorylation. The most effective inhibitor of this pathway was dansylcadaverine, an inhibitor of receptor internalisation. These findings imply that ACTH-induced Erk1/2 activation in H295R cells is dependent on a mechanism distinct from that by which most G protein-coupled receptors activate Erk1/2, but which nevertheless seems to depend on receptor internalisation.en_US
dc.language.isoenen_US
dc.subjectMedicineen_US
dc.titleMechanisms of adrenocorticotropin-induced activation of erk 1/2 map kinase in the human H295R adrenal cell lineen_US
dc.typeThesisen_US
dc.rights.holderThe copyright of this thesis rests with the author and no quotation from it or information derived from it may be published without the prior written consent of the author


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    Theses Awarded by Queen Mary University of London

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