Discriminating Between Apoptosis, Necrosis, Necroptosis, and Ferroptosis by Microscopy and Flow Cytometry

Funding Information: The Martin laboratory is supported by an ERC Advanced grant (101020534, DESTRESS) as well as an Irish Research Council Advanced Laureate Award (IRCLA/2019/133). The Hollville laboratory is supported by a Royal Society Research grant (RG16955).Peer reviewedPublisher PD

Differential role of FL-BID and t-BID during verotoxin-1-induced apoptosis in Burkitt's lymphoma cells

Funding Information: Acknowledgements We thank Yann Lécluse (Imaging and Cytometry Platform, Institut Gustave Roussy) for expert technical assistance in performing flow cytometry analyses. We are very grateful to Hana Raslova and Julie Rivière (INSERM UMR 1170, Institut Gustave-Roussy) for their help in producing lentivirus and to Evelyne May and Martine Raphaël (UMR 8126 CNRS) for helpful discussions and suggestions. This work was supported by grants from the Fondation de France 2014 00047509 (JW), the Ligue National Contre le Cancer (doctoral fellowship to JD) and the Fondation ARC (doctoral fellowship to EH).Peer reviewe

Aberrant miR-29 is a predictive feature of severe phenotypes in pediatric Crohn’s disease

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Rôle de l'antigène GB3/CD77 dans les cellules de lymphome de Burkitt (Relation fonctionnelle avec le BCR et transduction d'un signale apoptotique)

LE KREMLIN-B.- PARIS 11-BU Méd (940432101) / SudocSudocFranceF

Parkin Sensitizes toward Apoptosis Induced by Mitochondrial Depolarization through Promoting Degradation of Mcl-1

SummaryMitochondrial depolarization promotes Parkin- and PTEN-induced kinase 1 (PINK1)-dependent polyubiquitination of multiple proteins on mitochondrial outer membranes, resulting in the removal of defective mitochondria via mitophagy. Because Parkin mutations occur in Parkinson’s disease, a condition associated with the death of dopaminergic neurons in the midbrain, wild-type Parkin is thought to promote neuronal survival. However, here we show that wild-type Parkin greatly sensitized toward apoptosis induced by mitochondrial depolarization but not by proapoptotic stimuli that failed to activate Parkin. Parkin-dependent apoptosis required PINK1 and was efficiently blocked by prosurvival members of the Bcl-2 family or knockdown of Bax and Bak. Upon mitochondrial depolarization, the Bcl-2 family member Mcl-1 underwent rapid Parkin- and PINK1-dependent polyubiquitination and degradation, which sensitized toward apoptosis via opening of the Bax/Bak channel. These data suggest that similar to other sensors of cell stress, such as p53, Parkin has cytoprotective (mitophagy) or cytotoxic modes (apoptosis), depending on the degree of mitochondrial damage

Characterization of a Cul9–Parkin double knockout mouse model for Parkinson’s disease

Acknowledgements We thank Viktoriya Nikolova at the UNC Mouse Behavioural Phenotyping Laboratory for her technical assistance. This work was supported by a Rapid Response Innovation Award (ID 9056) from the Michael J Fox Foundation for Parkinson’s Research and by the NIH Grant GM118331 to M.D. V.J. was supported by Training in translational Research in Neurology NIH Fellowship 2T32NS007480. The Tansey laboratory is supported by NIH/NIA 1R01 AG057247, NIH/NINDS 5R01 NS092122, NIH/NIA 3RF1 AG051514-01, and the Norman Fixel Institute for Neurological Diseases to M.G.T. The UNC Mouse Behavioural Phenotyping Laboratory is supported by a grant from the National Institute of Child Health and Human Development (NICHD), U54-HD079124. The Neuroscience Microscopy Core Facility is supported, in part, by funding from the NIH-NINDS Neuroscience Center Support Grant P30 NS045892 and the NIH-NICHD Intellectual and Developmental Disabilities Research Center Support Grant U54 HD079124. Contributions E.H. conducted the in vitro experiments and prepared the mice cohorts. V.S. and A.N. helped with generating the Cul9, Parkin double KO mice. V.J and M.J.T. performed the stereological analysis and quantification of dopaminergic neurons. S.M. conducted and analysed the neurobehavioral assessments. M.D. outlined and supervised the project. E.H. and M.D. produced the final version of the manuscript.Peer reviewedPublisher PD