TY  - JOUR
A1  - Galluzzi, L.
A1  - Bravo-San Pedro, J. M.
A1  - Vitale, I.
A1  - Aaronson, S. A.
A1  - Abrams, J. M.
A1  - Adam, D.
A1  - Alnemri, E. S.
A1  - Altucci, L.
A1  - Andrews, D.
A1  - Annicchiarico-Petruzelli, M.
A1  - Baehrecke, E. H.
A1  - Bazan, N. G.
A1  - Bertrand, M. J.
A1  - Bianchi, K.
A1  - Blagosklonny, M. V.
A1  - Blomgren, K.
A1  - Borner, C.
A1  - Bredesen, D. E.
A1  - Brenner, C.
A1  - Campanella, M.
A1  - Candi, E.
A1  - Cecconi, F.
A1  - Chan, F. K.
A1  - Chandel, N. S.
A1  - Cheng, E. H.
A1  - Chipuk, J. E.
A1  - Cidlowski, J. A.
A1  - Ciechanover, A.
A1  - Dawson, T. M.
A1  - Dawson, V. L.
A1  - De Laurenzi, V.
A1  - De Maria, R.
A1  - Debatin, K. M.
A1  - Di Daniele, N.
A1  - Dixit, V. M.
A1  - Dynlacht, B. D.
A1  - El-Deiry, W. S.
A1  - Fimia, G. M.
A1  - Flavell, R. A.
A1  - Fulda, S.
A1  - Garrido, C.
A1  - Gougeon, M. L.
A1  - Green, D. R.
A1  - Gronemeyer, H.
A1  - Hajnoczky, G.
A1  - Hardwick, J. M.
A1  - Hengartner, M. O.
A1  - Ichijo, H.
A1  - Joseph, B.
A1  - Jost, P. J.
A1  - Kaufmann, T.
A1  - Kepp, O.
A1  - Klionsky, D. J.
A1  - Knight, R. A.
A1  - Kumar, S.
A1  - Lemasters, J. J.
A1  - Levine, B.
A1  - Linkermann, A.
A1  - Lipton, S. A.
A1  - Lockshin, R. A.
A1  - López-Otín, C.
A1  - Lugli, E.
A1  - Madeo, F.
A1  - Malorni, W.
A1  - Marine, J. C.
A1  - Martin, S. J.
A1  - Martinou, J. C.
A1  - Medema, J. P.
A1  - Meier, P.
A1  - Melino, S.
A1  - Mizushima, N.
A1  - Moll, U.
A1  - Muñoz-Pinedo, C.
A1  - Nuñez, G.
A1  - Oberst, A.
A1  - Panaretakis, T.
A1  - Penninger, J. M.
A1  - Peter, M. E.
A1  - Piacentini, M.
A1  - Pinton, P.
A1  - Prehn, J. H.
A1  - Puthalakath, H.
A1  - Rabinovich, G. A.
A1  - Ravichandran, K. S.
A1  - Rizzuto, R.
A1  - Rodrigues, C. M.
A1  - Rubinsztein, D. C.
A1  - Rudel, T.
A1  - Shi, Y.
A1  - Simon, H. U.
A1  - Stockwell, B. R.
A1  - Szabadkai, G.
A1  - Tait, S. W.
A1  - Tang, H. L.
A1  - Tavernarakis, N.
A1  - Tsujimoto, Y.
A1  - Vanden Berghe, T.
A1  - Vandenabeele, P.
A1  - Villunger, A.
A1  - Wagner, E. F.
A1  - Walczak, H.
A1  - White, E.
A1  - Wood, W. G.
A1  - Yuan, J.
A1  - Zakeri, Z.
A1  - Zhivotovsky, B.
A1  - Melino, G.
A1  - Kroemer, G.
T1  - Essential versus accessory aspects of cell death: recommendations of the NCCD 2015
JF  - Cell Death and Differentiation
N2  - Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as 'accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. 'Regulated cell death' (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.
Y1  - 2015
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-121207
VL  - 22
ER  - 
TY  - JOUR
A1  - Albert, A.
A1  - André, M.
A1  - Anghinolfi, M.
A1  - Anton, G.
A1  - Ardid, M.
A1  - Aubert, J.-J.
A1  - Aublin, J.
A1  - Avgitas, T.
A1  - Baret, B.
A1  - Barrios-Martít, J.
A1  - Basa, S.
A1  - Belhorma, B.
A1  - Bertin, V.
A1  - Biagi, S.
A1  - Bormuth, R.
A1  - Boumaaza, J
A1  - Bourret, S.
A1  - Bouwhuis, M. C.
A1  - Brânzas, H.
A1  - Bruijn, R.
A1  - Brunner, J.
A1  - Busto, J.
A1  - Capone, A.
A1  - Caramete, L.
A1  - Carr, J.
A1  - Celli, S.
A1  - Chabab, M.
A1  - Cherkaoui El Moursli, R.
A1  - Chiarusi, T.
A1  - Circella, M.
A1  - Coelho, J. A. B.
A1  - Coleiro, A.
A1  - Colomer, M
A1  - Coniglione, R.
A1  - Costantini, H.
A1  - Coyle, P.
A1  - Creusot, A.
A1  - Díaz, A. F.
A1  - Deschamps, A.
A1  - Distefano, C.
A1  - Di Palma, I.
A1  - Domi, A.
A1  - Donzaud, C.
A1  - Dornic, D.
A1  - Drouhin, D.
A1  - Eberl, T.
A1  - El Bojaddaini, I.
A1  - El Khayati, N.
A1  - Elsässer, D.
A1  - Enzenhöfer, A.
A1  - Ettahiri, A.
A1  - Fassi, F.
A1  - Felis, I.
A1  - Fermani, P.
A1  - Ferrara, G.
A1  - Fusco, L. A.
A1  - Gay, P.
A1  - Glotin, H.
A1  - Grégoire, T.
A1  - Gracia Ruiz, R.
A1  - Graf, K.
A1  - Hallmann, S.
A1  - van Haren, H.
A1  - Heijboer, A. J.
A1  - Hello, Y.
A1  - Hernández-Rey, J. J.
A1  - Hößl, J.
A1  - Hofestädt, J.
A1  - Illuminati, G.
A1  - de Jong, M.
A1  - Jongen, M.
A1  - Kadler, M.
A1  - Kalekin, O.
A1  - Katz, U.
A1  - Khan-Chowdhury, N. R.
A1  - Kouchner, A.
A1  - Kreter, M.
A1  - Kreykenbohm, I.
A1  - Kulikovskiy, V.
A1  - Lachaud, C.
A1  - Lahmann, R.
A1  - Lefèvre, D.
A1  - Leonora, E.
A1  - Levi, G.
A1  - Lotze, M.
A1  - Loucatos, S.
A1  - Marcelin, M.
A1  - Margiotta, A.
A1  - Marinelli, A.
A1  - Martínez-Mora, J. A.
A1  - Mele, R.
A1  - Melis, K.
A1  - Migliozzi, P.
A1  - Moussa, A.
A1  - Navas, S.
A1  - Nezri, E.
A1  - Nuñez, A.
A1  - Organokov, M.
A1  - Pavalas, G. E.
A1  - Pellegrino, C.
A1  - Piattelli, P.
A1  - Popa, V.
A1  - Pradier, T.
A1  - Quinn, L.
A1  - Racca, C.
A1  - Randazzo, N.
A1  - Riccobene, G.
A1  - Sánchez-Losa, A.
A1  - Saldaña, M.
A1  - Salvadori, I.
A1  - Samtleben, D. F. E.
A1  - Sanguineti, M.
A1  - Sapienza, P.
A1  - Schüssler, F.
A1  - Spurio, M.
A1  - Stolarczyk, Th.
A1  - Taiuti, M.
A1  - Tayalati, Y.
A1  - Trovato, A.
A1  - Vallage, B.
A1  - Van Elewyck, V.
A1  - Versari, F.
A1  - Vivolo, D.
A1  - Wilms, J.
A1  - Zaborov, D.
A1  - Zornoza, J. D.
A1  - Zúñiga, J.
T1  - The cosmic ray shadow of the Moon observed with the ANTARES neutrino telescope
JF  - European Physical Journal C
N2  - One of the main objectives of the ANTARES telescope is the search for point- like neutrino sources. Both the pointing accuracy and the angular resolution of the detector are important in this context and a reliableway to evaluate this performance is needed. In order to measure the pointing accuracy of the detector, one possibility is to study the shadow of the Moon, i. e. the deficit of the atmospheric muon flux from the direction of the Moon induced by the absorption of cosmic rays. Analysing the data taken between 2007 and 2016, theMoon shadow is observed with 3.5s statistical significance. The detector angular resolution for downwardgoing muons is 0.73. +/- 0.14.. The resulting pointing performance is consistent with the expectations. An independent check of the telescope pointing accuracy is realised with the data collected by a shower array detector onboard of a ship temporarily moving around the ANTARES location.
KW  - Atmospheric muons
Y1  - 2019
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-227802
VL  - 78
ER  - 
TY  - JOUR
A1  - Pollitt, Alice Y.
A1  - Poulter, Natalie S.
A1  - Gitz, Eelo
A1  - Navarro-Nuñez, Leyre
A1  - Wang, Ying-Jie
A1  - Hughes, Craig E.
A1  - Thomas, Steven G.
A1  - Nieswandt, Bernhard
A1  - Douglas, Michael R.
A1  - Owen, Dylan M.
A1  - Jackson, David G.
A1  - Dustin, Michael L.
A1  - Watson, Steve P.
T1  - Syk and Src Family Kinases Regulate C-type Lectin Receptor 2 (CLEC-2)-mediated Clustering of Podoplanin and Platelet Adhesion to Lymphatic Endothelial Cells*
JF  - The Journal of Biological Chemistry
N2  - The interaction of CLEC-2 on platelets with Podoplanin on lymphatic endothelial cells initiates platelet signalling events that are necessary for prevention of blood-lymph mixing during development. In the present study, we show that CLEC-2 signalling via Src family and Syk tyrosine kinases promotes platelet adhesion to primary mouse lymphatic endothelial cells at low shear. Using supported lipid bilayers containing mobile Podoplanin, we further show that activation of Src and Syk in platelets promotes clustering of CLEC-2 and Podoplanin. Clusters of CLEC-2-bound Podoplanin migrate rapidly to the centre of the platelet to form a single structure. Fluorescence life-time imaging demonstrates that molecules within these clusters are within 10 nm of one another and that the clusters are disrupted by inhibition of Src and Syk family kinases. CLEC-2 clusters are also seen in platelets adhered to immobilised Podoplanin using direct stochastic optical reconstruction microscopy (dSTORM). These findings provide mechanistic insight by which CLEC-2 signalling promotes adhesion to Podoplanin and regulation of Podoplanin signalling thereby contributing to lymphatic vasculature development.
KW  - endothelial cell
KW  - lipid bilayer
KW  - platelet receptor
KW  - tyrosine-protein kinase
KW  - CLEC-2 ITAM
KW  - podoplanin
KW  - Src family
KW  - kinase Syk
Y1  - 2014
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-120770
VL  - 289
IS  - 52
ER  -