Bitte benutzen Sie diese Kennung, um auf die Ressource zu verweisen: http://dx.doi.org/10.18419/opus-13070
Autor(en): Schneider, Lucas
Herkt, Stefanie
Wang, Lei
Feld, Christine
Wesely, Josephine
Kuvardina, Olga N.
Meyer, Annekarin
Oellerich, Thomas
Häupl, Björn
Seifried, Erhard
Bonig, Halvard
Lausen, Joern
Titel: PRMT6 activates cyclin D1 expression in conjunction with the transcription factor LEF1
Erscheinungsdatum: 2021
Dokumentart: Zeitschriftenartikel
Seiten: 14
Erschienen in: Oncogenesis 10 (2021), No. 42
URI: http://nbn-resolving.de/urn:nbn:de:bsz:93-opus-ds-130899
http://elib.uni-stuttgart.de/handle/11682/13089
http://dx.doi.org/10.18419/opus-13070
ISSN: 2157-9024
Zusammenfassung: The establishment of cell type specific gene expression by transcription factors and their epigenetic cofactors is central for cell fate decisions. Protein arginine methyltransferase 6 (PRMT6) is an epigenetic regulator of gene expression mainly through methylating arginines at histone H3. This way it influences cellular differentiation and proliferation. PRMT6 lacks DNA-binding capability but is recruited by transcription factors to regulate gene expression. However, currently only a limited number of transcription factors have been identified, which facilitate recruitment of PRMT6 to key cell cycle related target genes. Here, we show that LEF1 contributes to the recruitment of PRMT6 to the central cell cycle regulator CCND1 (Cyclin D1). We identified LEF1 as an interaction partner of PRMT6. Knockdown of LEF1 or PRMT6 reduces CCND1 expression. This is in line with our observation that knockdown of PRMT6 increases the number of cells in G1 phase of the cell cycle and decreases proliferation. These results improve the understanding of PRMT6 activity in cell cycle regulation. We expect that these insights will foster the rational development and usage of specific PRMT6 inhibitors for cancer therapy.
Enthalten in den Sammlungen:04 Fakultät Energie-, Verfahrens- und Biotechnik

Dateien zu dieser Ressource:
Datei Beschreibung GrößeFormat 
s41389-021-00332-z.pdf1,97 MBAdobe PDFÖffnen/Anzeigen


Diese Ressource wurde unter folgender Copyright-Bestimmung veröffentlicht: Lizenz von Creative Commons Creative Commons