dc.contributor.author | Ruiz, EJ | |
dc.contributor.author | Lan, L | |
dc.contributor.author | Diefenbacher, ME | |
dc.contributor.author | Riising, EM | |
dc.contributor.author | Da Costa, C | |
dc.contributor.author | Chakraborty, A | |
dc.contributor.author | Hoeck, JD | |
dc.contributor.author | Spencer-Dene, B | |
dc.contributor.author | Kelly, G | |
dc.contributor.author | David, J-P | |
dc.contributor.author | Nye, E | |
dc.contributor.author | Downward, J | |
dc.contributor.author | Behrens, A | |
dc.date.accessioned | 2021-09-23T09:49:16Z | |
dc.date.available | 2021-09-23T09:49:16Z | |
dc.date.issued | 2021-07-08 | |
dc.identifier.citation | JCI insight, 2021, 6 (13) | |
dc.identifier.issn | 2379-3708 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/4827 | |
dc.identifier.eissn | 2379-3708 | |
dc.identifier.doi | 10.1172/jci.insight.124985 | |
dc.description.abstract | The AP-1 transcription factor c-Jun is required for Ras-driven tumorigenesis in many tissues and is considered as a classical proto-oncogene. To determine the requirement for c-Jun in a mouse model of K-RasG12D-induced lung adenocarcinoma, we inducibly deleted c-Jun in the adult lung. Surprisingly, we found that inactivation of c-Jun, or mutation of its JNK phosphorylation sites, actually increased lung tumor burden. Mechanistically, we found that protein levels of the Jun family member JunD were increased in the absence of c-Jun. In c-Jun-deficient cells, JunD phosphorylation was increased, and expression of a dominant-active JNKK2-JNK1 transgene further increased lung tumor formation. Strikingly, deletion of JunD completely abolished Ras-driven lung tumorigenesis. This work identifies JunD, not c-Jun, as the crucial substrate of JNK signaling and oncogene required for Ras-induced lung cancer. | |
dc.format | Electronic | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | AMER SOC CLINICAL INVESTIGATION INC | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0 | |
dc.title | JunD, not c-Jun, is the AP-1 transcription factor required for Ras-induced lung cancer. | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2021-05-28 | |
rioxxterms.version | VoR | |
rioxxterms.versionofrecord | 10.1172/jci.insight.124985 | |
rioxxterms.licenseref.uri | https://creativecommons.org/licenses/by/4.0 | |
rioxxterms.licenseref.startdate | 2021-07-08 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | JCI insight | |
pubs.issue | 13 | |
pubs.notes | Not known | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Biology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Biology/Lung Cancer Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology/Lung Cancer Group | |
pubs.organisational-group | /ICR | |
pubs.organisational-group | /ICR/Primary Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Biology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Cancer Biology/Lung Cancer Group | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology | |
pubs.organisational-group | /ICR/Primary Group/ICR Divisions/Molecular Pathology/Lung Cancer Group | |
pubs.publication-status | Published | |
pubs.volume | 6 | |
pubs.embargo.terms | Not known | |
icr.researchteam | Lung Cancer Group | |
icr.researchteam | Lung Cancer Group | |
dc.contributor.icrauthor | Behrens, Axel | |