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Campo DC | Valor | Lengua/Idioma |
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dc.contributor.author | Meng, Xueqiong | - |
dc.contributor.author | Chen, Yixiang | - |
dc.contributor.author | Macip, Salvador | - |
dc.contributor.author | Leppard, Keith | - |
dc.contributor.other | Universitat Oberta de Catalunya (UOC) | - |
dc.date.accessioned | 2022-02-10T17:39:43Z | - |
dc.date.available | 2022-02-10T17:39:43Z | - |
dc.date.issued | 2021-07-02 | - |
dc.identifier.citation | Meng, X., Chen, Y., Macip, S. et al. PML-II regulates ERK and AKT signal activation and IFNa-induced cell death. Cell Commun Signal 19, 70 (2021). https://doi.org/10.1186/s12964-021-00756-5 | - |
dc.identifier.issn | 1478-811XMIAR | - |
dc.identifier.uri | http://hdl.handle.net/10609/139238 | - |
dc.description.abstract | Background: The requirement of promyelocytic leukaemia protein (PML) in interferon (IFN)-induced cell apoptosis is well-established. However, the exact mechanisms by which the multiple isoforms of PML protein participate in this process remain not well-understood. We previously demonstrated that PML isoform II (PML-II) positively regulates induced gene expression during a type I IFN response and evaluate here how PML-II contributes to IFNa-induced cell death. Methods: HeLa cells were transiently depleted of PML-II by siRNA treatment and the response of these cells to treatment with IFNa assessed by molecular assays of mRNA and proteins associated with IFN and apoptosis responses. Results: In HeLa cells, death during IFNa stimulation was reduced by prior PML-II depletion. PML-II removal also considerably decreased the induced expression of pro-apoptotic ISGs such as ISG54 (IFIT2), and substantially impaired or prevented expression of PUMA and TRAIL, proteins that are associated with the intrinsic and extrinsic apoptotic pathways respectively. Thirdly, PML-II depletion enhanced ERK and AKT pro-survival signaling activation suggesting that PML-II normally suppresses signaling via these pathways, and that lack of PML-II hence led to greater than normal activation of AKT signaling upon IFNa stimulation and consequently increased resistance to IFNa-induced apoptosis. Conclusions: The positive contribution of PML-II to the expression of various IFNa-induced pro-apoptotic proteins and its inhibition of pro-survival signaling together provide a mechanistic explanation for reduced apoptosis under conditions of PML deficiency and may account for at least part of the role of PML as a tumor suppressor gene. | en |
dc.language.iso | eng | - |
dc.publisher | Cell Communication and Signaling | - |
dc.relation.ispartofseries | 19;1 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | - |
dc.subject | promyelocytic leukemia protein | en |
dc.subject | PML-II | en |
dc.subject | IFNa | en |
dc.subject | apoptotic signaling | en |
dc.subject | ERK | en |
dc.subject | AKT | en |
dc.title | PML-II regulates ERK and AKT signal activation and IFN alpha-induced cell death | - |
dc.type | info:eu-repo/semantics/article | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.doi | https://doi.org/10.1186/s12964-021-00756-5 | - |
dc.gir.id | AR/0000009063 | - |
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