G. Ichim

Lysosomal MLKL is balanced by ESCRT to control cell death

The paper shows lysosomal MLKL is activated independently of RIPK3 and necroptosis, leading to cell death, which is counteracted by ESCRT machinery through lysosomal repair and sequestration of MLKL.

An optogenetic approach to control and monitor inflammasome activation.

This paper introduces an optogenetic method to control ASC oligomerization, enabling the study of inflammasome activation without PAMPs or DAMPs.

Targeting the cell and non-cell autonomous regulation of 47S synthesis by GCN2 in colon cancer.

This study shows GCN2 regulates 47S rRNA synthesis in colon cancer cells under different nutrient conditions, affecting cell survival and response to chemotherapy.

Live-cell imaging and mathematical analysis of the "community effect" in apoptosis

The paper analyzes the community effect in apoptosis using live-cell imaging and mathematical modeling, showing apoptosis is density-insensitive but proximity to apoptotic cells increases apoptosis probability.

Mitochondrial dynamics regulate genome stability via control of caspase-dependent DNA damage

This study shows mitochondrial dysfunction promotes DNA damage through caspase-dependent mechanisms regulated by mitochondrial dynamics.

Confined migration promotes cancer metastasis through resistance to anoikis and increased invasiveness

This study shows that confined migration in breast cancer cells increases metastatic potential by promoting resistance to anoikis and enhancing invasiveness.

Increased apoptotic priming of glioblastoma enables therapeutic targeting by BH3-mimetics

This study shows that glioblastoma (GBM) is highly sensitive to BH3-mimetics due to elevated anti-apoptotic BCL-xL and MCL-1 expression, which can be therapeutically targeted.

Profiling anti-apoptotic protein BCL-xL expression in U-87 MG glioblastoma cells and patient-derived tumorspheres

This study shows that BCL-xL is overexpressed in glioblastoma tumorspheres and that modulating its expression affects cell survival and response to BH3 mimetics.

Failed apoptosis enhances melanoma cancer cells aggressiveness

The paper shows that failed apoptosis in melanoma cells leads to increased aggressiveness through transcriptomic changes and JNK pathway activation, observed in vitro and in vivo.