Carboxy-terminal fragment of fibroblast growth factor 23 induces heart hypertrophy in sickle cell disease

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Calpain mobilizes Atg9/Bif-1 vesicles from Golgi stacks upon autophagy induction by thapsigargin

CAPNS1 is essential for stability and function of the ubiquitous calcium-dependent proteases micro- and milli-calpain. Upon inhibition of the endoplasmic reticulum Ca2+ ATPase by 100 nM thapsigargin, both micro-calpain and autophagy are activated in human U2OS osteosarcoma cells in a CAPNS1-dependent manner. As reported for other autophagy triggers, thapsigargin treatment induces Golgi fragmentation and fusion of Atg9/Bif-1-containing vesicles with LC3 bodies in control cells. By contrast, CAPNS1 depletion is coupled with an accumulation of LC3 bodies and Rab5 early endosomes. Moreover, Atg9 and Bif-1 remain in the GM130- positive Golgi stacks and Atg9 fails to interact with the endocytic route marker transferrin receptor and with the core autophagic protein Vps34 in CAPNS1-depleted cells. Ectopic expression of a Bif-1 point mutant resistant to calpain processing is coupled to endogenous p62 and LC3-II accumulation. Altogether, these data indicate that calpain allows dynamic flux of Atg9/Bif-1 vesicles from the Golgi toward the budding autophagosome.Peer reviewe

Beta 1-integrin-c-Met cooperation reveals an inside-in survival signalling on autophagy-related endomembranes

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/R.B.M. was a recipient of a UK Medical Research Council (MRC) studentship, MRC Centenary Award, Barts and The London Charity (472/1711) and Rosetrees Trust (M314), N.K. was a recipient of an MRC studentship (MR/J500409/1), C.J. was a recipient of the Barts and The London Charitable Foundation Scholarship (RAB 05/PJ/07), L.M. was supported by CR-UK, Breast Cancer Now (2008NovPR10) and Rosetrees Trust (M346), A.H. was a recipient of a CR-UK studentship (C236/A11795). P.J.P. was supported by CR-UK. J.I. was supported by grants from the Academy of Finland, ERC Starting grant, Finnish Cancer Organisations and Sigrid Juselius Foundation. S.K. was supported by the MRC (G0501003) and The British Lung Foundation (CAN09-4)

Autophagie et adhérence cellulaire (régulation par la matrice extracellulaire et rôle au cours de la migration)

L autophagie est régulée par l adhérence cellulaire. Dans les cellules adhérentes sur le collagène IV, l autophagie basale est élevée mais non inductible par la carence, contrairement aux cellules adhérentes sur le collagène I qui présentent une autophagie basale faible mais inductible. Cette régulation dépend de l activation de la protéine kinase FAK par l adhérence des cellules au collagène IV. La survie à la carence nutritionnelle des cellules adhérentes sur le collagène IV ne dépend pas de l autophagie. Nous avons également étudié le rôle de l autophagie au cours de la migration : l autophagie modifie le recyclage des intégrines en convergeant avec la voie d endocytose et freine la migration des cellules. De plus, deux comportements différents au sein de notre population de cellules migrantes ont été décelés : les cellules situées en front de migration forment peu d autophagosomes et présentent une faible activité pour la kinase mTOR comparativement aux cellules qui les suiventPARIS-BIUSJ-Biologie recherche (751052107) / SudocSudocFranceF

Carboxy-terminal fragment of fibroblast growth factor 23 induces heart hypertrophy in sickle cell disease

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