Publications by authors named "Johanna Ruemenapp"
Article Synopsis
- ZFP36L1 and ZFP36L2 are proteins that help regulate cell quiescence and are important in the context of blood cancers, acting mainly as tumor suppressors by lowering oncogene expression.
- In chronic myeloid leukemia (CML), researchers found that the expression of ZFP36L1 and ZFP36L2 was altered, especially in cases of drug resistance to imatinib, indicating their potential role in disease progression.
- Knocking out ZFP36L1 in imatinib-sensitive cells reduced cell proliferation and affected the expression of cell cycle regulators, with findings suggesting that ZFP36L1 directly targets the tumor suppressor gene CDKN1A, complicating its classification solely as
BCR-ABL-independent resistance against tyrosine kinase inhibitor is an emerging problem in therapy of chronic myeloid leukemia. Such drug resistance can be linked to dysregulation of ATP-binding cassette (ABC)-transporters leading to increased tyrosine kinase inhibitor efflux, potentially caused by changes in microRNA expression or DNA-methylation. In an -imatinib-resistance model using K-562 cells, microRNA-212 was found to be dysregulated and inversely correlated to ABC-transporter ABCG2 expression, targeting its 3'-UTR.
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