dc.contributor.author
Xiao, Yi
dc.contributor.author
Meierhofer, David
dc.date.accessioned
2019-09-12T12:14:22Z
dc.date.available
2019-09-12T12:14:22Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/25540
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-25310
dc.description.abstract
A significantly increased level of the reactive oxygen species (ROS) scavenger glutathione (GSH) has been identified as a hallmark of renal cell carcinoma (RCC). The proposed mechanism for increased GSH levels is to counteract damaging ROS to sustain the viability and growth of the malignancy. Here, we review the current knowledge about the three main RCC subtypes, namely clear cell RCC (ccRCC), papillary RCC (pRCC), and chromophobe RCC (chRCC), at the genetic, transcript, protein, and metabolite level and highlight their mutual influence on GSH metabolism. A further discussion addresses the question of how the manipulation of GSH levels can be exploited as a potential treatment strategy for RCC.
en
dc.format.extent
20 Seiten
dc.rights.uri
https://creativecommons.org/licenses/by/4.0/
dc.subject
renal cell carcinoma
en
dc.subject
reactive oxygen species
en
dc.subject
glutathione metabolism
en
dc.subject.ddc
500 Naturwissenschaften und Mathematik::540 Chemie::547 Organische Chemie
dc.title
Glutathione Metabolism in Renal Cell Carcinoma Progression and Implications for Therapies
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation.articlenumber
3672
dcterms.bibliographicCitation.doi
10.3390/ijms20153672
dcterms.bibliographicCitation.journaltitle
International journal of molecular sciences
dcterms.bibliographicCitation.number
15
dcterms.bibliographicCitation.originalpublishername
Molecular Diversity Preservation International
dcterms.bibliographicCitation.originalpublisherplace
Basel
dcterms.bibliographicCitation.volume
20
dcterms.bibliographicCitation.url
https://doi.org/10.3390/ijms20153672
refubium.affiliation
Biologie, Chemie, Pharmazie
refubium.affiliation.other
Institut für Chemie und Biochemie
refubium.resourceType.isindependentpub
no
dcterms.accessRights.openaire
open access
dcterms.isPartOf.eissn
1422-0067
refubium.resourceType.provider
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