DJ-1/PARK7 Determines miRNA Network Plasticity During Genotoxic Stress
This study shows DJ-1/PARK7 influences miRNA network plasticity during genotoxic stress by altering miRNA abundance and regulatory machinery.
Author
Hebrew University of JerusalemORCID 0009-0006-0407-9969Unclaimed ORCID profile · follow to get notified of new preprints
8 papers
Recent·Most cited
This study shows DJ-1/PARK7 influences miRNA network plasticity during genotoxic stress by altering miRNA abundance and regulatory machinery.
Keren Zohar, Haya Obied Zoubi, Michal Goldberg…·Michal Linial B
This study shows that altering DJ-1 levels changes non-coding RNA expression and cellular homeostasis after X-ray exposure.
Isra Sadiya, Irina Nekrasova, Meirav Avital‐Shacham…·Mickey Kosloff
The paper investigates the molecular mechanism of the Gαo E246K mutation in neurodevelopmental disorders, showing it disrupts the GTPase cycle by impairing Gβγ dissociation, leading to dominant-negative effects.
Keren Zohar, Elyad Lezmi, Fanny Reichert…·Michal Linial B
This study identifies miRNA expression changes in activated microglia, showing their role in inflammation and potential as biomarkers for neurodegenerative diseases.
Marco Strecker, Keren Zohar, Martin Böttcher…·Ulf D. Kahlert
This study identifies xCT regulation pathways in colon cancer using patient-specific models and reveals potential therapeutic targets for chemotherapy resistance.
This study shows that knocking down DJ-1 in HEK293 cells activates an antiviral innate immune response and affects RNA metabolism and mitochondrial functions.
Keren Zohar, Thomas Wartmann, Marco Strecker…·Michal Linial
The paper analyzes RNA-seq data from CRC patients to identify SLC7A11's role in metabolic regulation and cell proliferation, linking it to clinical outcomes and therapeutic responses.
Keren Zohar, Elyad Lezmi, Fanny Reichert…·Michal Linial B
This study examines how microglia respond to LPS and bzATP activation, finding that only combined treatment leads to a sustained inflammatory gene expression profile.