Homozygous MTAP deletion in primary human glioblastoma is not associated with elevation of methylthioadenosine
The metabolite methylthioadenosine (MTA) inhibits PRMT5. Therefore, MTA accumulation due to MTA phosphorylase (MTAP) deletion has been proposed as a vulnerability for PRMT5-targeted therapy in cancer. Here, the authors show that MTA does not accumulate in MTAP-deficient cancer cells but is secreted...
Main Authors: | , , , , , , , , , , , , , , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Nature Publishing Group
2021-07-01
|
Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-021-24240-3 |