G. Bossis

The SUMOylation inhibitor TAK-981 (Subasumstat) triggers IFN-I-dependent activation of Natural Killer cells against Acute Myeloid Leukemias.

This paper shows that TAK-981 activates NK cells against AML by inducing IFN-I secretion, enhancing their cytotoxicity and cytokine production.

Bidirectional regulation between AP-1 and SUMO genes modulates inflammatory signaling during Salmonella Typhimurium infection

This study shows that Salmonella Typhimurium modulates SUMOylation by regulating AP-1 transcription factors, affecting inflammatory responses and infection outcomes.

Loss of SUMO-specific protease 2 causes isolated glucocorticoid deficiency by blocking adrenal cortex zonal transdifferentiation

This study shows that loss of SENP2 causes adrenal cortex zonal defects and glucocorticoid deficiency by disrupting transdifferentiation and signaling pathways.

Discovery and mechanism of action of small molecule inhibitors of ceramidases

The paper discovers small molecule inhibitors of alkaline ceramidase 3 using fluorescent substrates and characterizes their mechanism of action.

The NADPH oxidase NOX2 is a marker of adverse prognosis involved in chemoresistance of Acute Myeloid Leukemias

This study identifies NOX2 as a marker of poor prognosis and a contributor to chemoresistance in AML, showing its upregulation in drug-resistant cells and association with adverse outcomes.

Trim39 regulates neuronal apoptosis by acting as a SUMO-targeted E3 ubiquitin-ligase for the transcription factor NFATc3

This study identifies Trim39 as an E3 ubiquitin-ligase for NFATc3, showing it regulates neuronal apoptosis through SUMO-dependent ubiquitination.

SUMOylation of SAMHD1 at Lysine 595 is required for HIV-1 restriction in non-cycling cells

This study shows that SUMOylation of SAMHD1 at K595 is necessary for its antiviral activity in non-cycling cells, independent of its dNTPase function.

Ubiquitin and SUMO conjugation as biomarkers of Acute Myeloid Leukemias response to chemotherapies

This paper identifies ubiquitin and SUMO conjugation biomarkers to predict AML response to chemotherapy and develops an assay to measure them.

Targeting the SUMO pathway primes all-trans-retinoic acid-induced differentiation of non promyelocytic Acute Myeloid Leukemias

This study shows that inhibiting the SUMO pathway enhances the effectiveness of all-trans-retinoic acid in treating non-APL AMLs by promoting differentiation and reducing proliferation.