Özgen Deniz

The paper develops TEgment, a tool to analyze transposable element transcriptional modalities, showing that CDK9 inhibition leads to TE activation in AML through non-autonomous expression patterns.

This study identifies IRF2BP2 as a critical regulator of transposable element silencing in AML, showing its loss leads to TE activation and leukemia cell death.

This study identifies DEK::NUP214 as an XPO1-dependent transcriptional activator of leukemia genes, showing selective response to XPO1 inhibitors in t(6;9) AML cases.

The paper identifies endogenous retroviruses (ERVs) as a source of oncogenic enhancers in acute myeloid leukemia (AML) and shows their role in altering gene expression and promoting cell growth.

This study shows TET2 regulates microglial inflammatory responses through NF-κB-dependent pathways and metabolic changes, suggesting it as a target for neurodegenerative diseases.

The paper evaluates the role of transposable elements as enhancers in mouse embryonic and trophoblast stem cells using bioinformatics and genetic editing, finding that only a minority significantly regulate gene expression.

This study shows that SETDB1 prevents TET2 from demethylating H4R3 in IAP retroelements in naive ESCs, maintaining their silencing.