N. Bidere

Necrosulfonamide causes oxidation of PCM1 and impairs ciliogenesis and autophagy

This study shows that necrosulfonamide oxidizes PCM1, disrupts ciliogenesis, and impairs autophagy, highlighting PCM1 as a redox sensor.

The paracaspase MALT1 controls cholesterol homeostasis in glioblastoma stem-like cells through lysosome proteome shaping

This study shows that MALT1 regulates cholesterol homeostasis in glioblastoma stem-like cells by shaping the lysosome proteome, leading to cell death when disrupted.

SARS-CoV-2 E and 3a proteins are inducers of pannexin currents

This paper investigates whether SARS-CoV-2 E and 3a proteins act as viroporins and finds they instead induce cell shape changes and death, indirectly activating pannexin channels.

The von Willebrand Factor stamps Plasmatic Extracellular Vesicles from Glioblastoma Patients

The paper demonstrates that extracellular vesicles from glioblastoma patients can be reliably measured and show differential protein cargos, with von Willebrand Factor as a selective hallmark.

The Necroptosis Effector MLKL drives Small Extracellular Vesicle Release and Tumour Growth in Glioblastoma

This study identifies MLKL as a regulator of EV release from GSCs, showing its role in promoting tumour growth and suggesting EV targeting as a therapeutic strategy.

Serine 165 Phosphorylation of SHARPIN regulates the Activation of NF-κB

The paper shows that phosphorylation of SHARPIN at serine 165 is required for optimal NF-κB activation, despite not affecting linear ubiquitin chain formation.

The LUBAC participates in Lysophosphatidic Acid-induced NF-κB Activation

This study shows that LUBAC is essential for LPA-induced NF-κB activation through MALT1-mediated cleavage of HOIL1 and GEF-H1-dependent regulation.

Control of the Endo-Lysosome Homeostasis by the Paracaspase MALT1 regulates Glioma Cell Survival

This study shows that MALT1 regulates endo-lysosome homeostasis and glioma cell survival, with MALT1 inhibition leading to lysosomal-mediated cell death.

Pannexin-1 Channels govern the Generation of Necroptotic small Extracellular Vesicles

The paper identifies MLKL-induced activation of PANX1 channels as a mechanism driving necroptosis-associated small extracellular vesicle generation.