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dc.contributor.authorKim, H.R.
dc.contributor.authorSanthakumar, K.
dc.contributor.authorMarkham, E.
dc.contributor.authorBaldera, D.
dc.contributor.authorGreenald, D.
dc.contributor.authorBryant, H.E.
dc.contributor.authorEl-Khamisy, Sherif
dc.contributor.authorvan Eeden, F.J.
dc.date.accessioned2020-08-25T15:28:50Z
dc.date.accessioned2020-09-22T13:51:23Z
dc.date.available2020-08-25T15:28:50Z
dc.date.available2020-09-22T13:51:23Z
dc.date.issued2020-03
dc.identifier.citationKim HR, Santhakumar K, Markham E et al (2020) Investigation of the role of VHL-HIF signaling in DNA repair and apoptosis in zebrafish. Oncotarget. 11(13): 1109-1130.
dc.identifier.urihttp://hdl.handle.net/10454/18019
dc.descriptionYes
dc.description.abstractpVHL is a tumor suppressor. The lack of its function leads to various tumors, among which ccRCC (clear cell renal cell carcinoma) has the most serious outcome due to its resistance to chemotherapies and radiotherapies. Although HIF promotes the progression of ccRCC, the precise mechanism by which the loss of VHL leads to tumor initiation remains unclear. We exploited two zebrafish vhl mutants, vhl and vll, and Tg(phd3
dc.description.sponsorshipThe work was supported by two BBSRC Grants: BB/R015457/1 and BB/M02332X/1.
dc.language.isoen
dc.rightsCopyright: Kim et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
dc.subjectHif
dc.subjectVhl
dc.subjectDNA repair
dc.subjectApoptosis
dc.subjectChemo/radio-resistance
dc.titleInvestigation of the role of VHL-HIF signaling in DNA repair and apoptosis in zebrafish
dc.status.refereedYes
dc.date.Accepted2020-02-17
dc.date.application2020-03-31
dc.typeArticle
dc.type.versionPublished version
dc.identifier.doihttps://doi.org/10.18632/oncotarget.27521
dc.rights.licenseCC-BY
dc.date.updated2020-08-25T14:28:54Z
refterms.dateFOA2020-09-22T13:52:10Z
dc.openaccess.statusopenAccess


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