IKBKE-driven_TPL2_and_MEK1_phosphorylations_sustain_constitutive_ERK1_2_activation_in_tumor_cells

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buir.contributor.authorGöktuna, Serkan İsmail
buir.contributor.orcidGöktuna, Serkan İsmail |0000-0001-6169-768X
dc.citation.epage453en_US
dc.citation.spage436en_US
dc.citation.volumeNumber21en_US
dc.contributor.authorGöktuna, Serkan İsmail
dc.date.accessioned2023-02-25T14:05:21Z
dc.date.available2023-02-25T14:05:21Z
dc.date.issued2022-02-17
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.description.abstractIKBKE have been associated with numerous cancers. As a result, IKBKE have emerged as potential target for cancer therapy. Accumulating evidence support that IKBKE orchestrate tumor cell survival in cancers. Here we evaluated the possible link between IKBKE and ERK phosphorylation. The effects of IKBKE silencing on MAPK activation in tumor vs. normal cells were evaluated via WB and RT-PCR. Ectopically expressed IKBKE, TPL2 or MEK1 constructs were used to examine the possible interactions among them via co-IP. In vitro kinase assays were performed to understand nature of the observed interactions. In tumors, IKBKE regulates MEK/ERK constitutive activations in vitro and in vivo. IKBKE and TPL2 physically interact and this interaction leads to TPL2 phosphorylation. We describe here a novel regulatory link between IKBKE and constitutive ERK1/2 activation in tumor cells. This new circuitry may be relevant for tumor cell survival in various malignancies.en_US
dc.identifier.doi10.17179/excli2021-4578en_US
dc.identifier.eissn1611-2156
dc.identifier.urihttp://hdl.handle.net/11693/111742
dc.language.isoEnglishen_US
dc.publisherEXCLI Journalen_US
dc.relation.isversionofhttps://dx.doi.org/10.17179/excli2021-4578en_US
dc.source.titleEXCLI Journalen_US
dc.subjectCancer cellsen_US
dc.subjectSignal transductionen_US
dc.subjectIKKɛ (IKBKE)en_US
dc.subjectTPL2 (MAP3K8)en_US
dc.subjectMEK1 (MAP2K1)en_US
dc.subjectERK1/2 (MAPK1/2)en_US
dc.titleIKBKE-driven_TPL2_and_MEK1_phosphorylations_sustain_constitutive_ERK1_2_activation_in_tumor_cellsen_US
dc.typeArticleen_US

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Department of Molecular Biology and Genetics
Institute of Materials Science and Nanotechnology (UNAM)