Publication Date:
2014-01-05
Description:
Article The majority of ovarian granulosa tumours harbour the C134W mutation in FOXL2 but the mechanism of tumorigenesis is largely unknown. Here, Kim et al . show that mutant FOXL2 is hyperphosphorylated by GSK3β, which targets the protein for degradation, and find that GSK3β inhibition represses the growth of ovarian granulosa cells. Nature Communications doi: 10.1038/ncomms3936 Authors: Jae-Hong Kim, Yong-Hak Kim, Hong-Man Kim, Ho-Oak Park, Nam-Chul Ha, Tae Heon Kim, Mira Park, Kangseok Lee, Jeehyeon Bae
Electronic ISSN:
2041-1723
Topics:
Biology
,
Chemistry and Pharmacology
,
Natural Sciences in General
,
Physics
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