Auswahl der wissenschaftlichen Literatur zum Thema „RPC7α“
Geben Sie eine Quelle nach APA, MLA, Chicago, Harvard und anderen Zitierweisen an
Inhaltsverzeichnis
Machen Sie sich mit den Listen der aktuellen Artikel, Bücher, Dissertationen, Berichten und anderer wissenschaftlichen Quellen zum Thema "RPC7α" bekannt.
Neben jedem Werk im Literaturverzeichnis ist die Option "Zur Bibliographie hinzufügen" verfügbar. Nutzen Sie sie, wird Ihre bibliographische Angabe des gewählten Werkes nach der nötigen Zitierweise (APA, MLA, Harvard, Chicago, Vancouver usw.) automatisch gestaltet.
Sie können auch den vollen Text der wissenschaftlichen Publikation im PDF-Format herunterladen und eine Online-Annotation der Arbeit lesen, wenn die relevanten Parameter in den Metadaten verfügbar sind.
Zeitschriftenartikel zum Thema "RPC7α"
Cheng, Ruiying, Sihang Zhou, Rajendra K C, Simon Lizarazo, Leela Mouli, Anshita Jayanth, Qing Liu und Kevin Van Bortle. „A Combinatorial Regulatory Platform Determines Expression of RNA Polymerase III Subunit RPC7α (POLR3G) in Cancer“. Cancers 15, Nr. 20 (15.10.2023): 4995. http://dx.doi.org/10.3390/cancers15204995.
Der volle Inhalt der QuelleKessler, Alan C., und Richard J. Maraia. „The nuclear and cytoplasmic activities of RNA polymerase III, and an evolving transcriptome for surveillance“. Nucleic Acids Research 49, Nr. 21 (26.11.2021): 12017–34. http://dx.doi.org/10.1093/nar/gkab1145.
Der volle Inhalt der QuelleCheng, Ruiying, und Kevin Van Bortle. „RNA polymerase III transcription and cancer: A tale of two RPC7 subunits“. Frontiers in Molecular Biosciences 9 (12.01.2023). http://dx.doi.org/10.3389/fmolb.2022.1073795.
Der volle Inhalt der QuelleVan Bortle, Kevin, David P. Marciano, Qing Liu, Tristan Chou, Andrew M. Lipchik, Sanjay Gollapudi, Benjamin S. Geller, Emma Monte, Rohinton T. Kamakaka und Michael P. Snyder. „A cancer-associated RNA polymerase III identity drives robust transcription and expression of snaR-A noncoding RNA“. Nature Communications 13, Nr. 1 (30.05.2022). http://dx.doi.org/10.1038/s41467-022-30323-6.
Der volle Inhalt der QuelleDissertationen zum Thema "RPC7α"
Lata, Elisabeth. „L’isoforme embryonnaire de l’ARN polymérase III humaine : son rôle dans la transformation tumorale et l’établissement de métastases“. Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0168.
Der volle Inhalt der QuelleRNA polymerase (Pol) III transcribes small non coding RNAs that are essential for the cell. There are two Pol III isoforms containing either RPC7α or RPC7β subunit. RPC7β is ubiquitously expressed whereas RPC7α is only expressed in embryonic stem cells and some tumor cells. Particularly, RPC7α is overexpressed in triple negative breast cancer (TNBC) clinical samples and cell lines. RPC7α deletion in the TNBC cell line MDA-MB-231 reduces tumor growth and metastases formation in a xenograft mouse model. However, the molecular mechanisms by which Pol IIIα regulates tumorigenesis and metastasis are still unknown. In this thesis, I show that the suppression of RPC7α in MDA-MB-231 cells alters the expression of several messenger RNAs, some of which are involved in the regulation of cancer and gene expression. Analysis of RPC7α localization indicates that, in addition to occupying Pol III genes, RPC7α also colocalizes with Pol II on coding genes. These genes are among the most highly expressed in MDA-MB-231 cells and are involved in important mechanisms for tumors and metastasis such as translation and cell interaction with the extracellular matrix. Unlike RPC7α, RPC7β is only localized on Pol III genes. Thus, these results suggest that RPC7α acts directly with Pol II on coding genes, possibly to promote their expression, which would explain its important role in tumor growth and metastasis generation in TNBC
Buchteile zum Thema "RPC7α"
„RPC7 Specification relating to the execution of the isothermal relaxation test on prestressing steel“. In RILEM Technical Recommendations for the testing and use of construction materials, 706–11. CRC Press, 1994. http://dx.doi.org/10.1201/9781482271362-174.
Der volle Inhalt der Quelle