Kristijan Ramadan

This study identifies nucleophagy as the mechanism by which trapped PARP1 is cleared, showing that inhibiting this process re-sensitizes PARPi-resistant cells to PARPi.

This study reveals how DNA-induced conformational changes in SPRTN relieve its auto-inhibitory effect on protease activity, enabling efficient DPC proteolysis.

The paper shows that skull bone marrow is vulnerable to age-related decline, contradicting previous claims of resilience, and highlights its role in blood and immune health.

This study identifies a ubiquitin-binding domain in SPRTN that enhances its proteolytic activity towards polyubiquitinated DNA-protein crosslinks.

The paper identifies p97 ATPase as a key player in removing trapped PARP1 from chromatin, enhancing PARPi-induced cytotoxicity in homologous recombination-defective cells.