Apolist – june 2012

Death receptor pathway

A Death Effector Domain Chain DISC Model Reveals a Crucial Role for Caspase-8 Chain Assembly in Mediating Apoptotic Cell Death
Laura S. Dickens, Robert S. Boyd, Rebekah Jukes-Jones, Michelle A. Hughes, Gemma L. Robinson, Louise Fairall, John W.R. Schwabe, Kelvin Cain, and Marion MacFarlane

Stoichiometry of the CD95 Death-Inducing Signaling Complex: Experimental and Modeling Evidence for a Death Effector Domain Chain Model
Kolja Schleich, Uwe Warnken, Nicolai Fricker, Selcen Öztürk, Petra Richter, Kerstin Kammerer, Martina Schnölzer, Peter H. Krammer, and Inna N. Lavrik

Cleavage of Atg3 protein by caspase-8 regulates autophagy during receptor-activated cell death
Ozlem Oral, Devrim Oz-Arslan, Zeynep Itah, Atabak Naghavi, Remziye Deveci, Sabire Karacali & Devrim Gozuacik

A novel role for RIP1 kinase in mediating TNFα production
D E Christofferson, Y Li, J Hitomi, W Zhou, C Upperman, H Zhu, S A Gerber, S Gygi and J Yuan

NF-B directly regulates Fas transcription to modulate Fas-mediated apoptosis and tumor suppression
Feiyan Liu, Kankana Bardhan, Dafeng Yang, Muthusamy Thangaraju, Vadivel Ganapathy, Georgia Liles, Jeffrey Lee, and Kebin Liu

A series of Fas receptor agonist antibodies that demonstrate an inverse correlation between affinity and potency
M Chodorge, S Züger, C Stirnimann, C Briand, L Jermutus, M G Grütter and R R Minter

Caspases and downstream

Survival Function of the FADD-CASPASE-8-cFLIPL Complex
Christopher P. Dillon, Andrew Oberst, Ricardo Weinlich, Laura J. Janke, Tae-Bong Kang, Tehila Ben-Moshe, Tak W. Mak, David Wallach, Douglas R. Green

Ubiquitylation of the initiator caspase DREDD is required for innate immune signalling
Annika Meinander, Christopher Runchel, Tencho Tenev, Li Chen, Chan-Hee Kim, Paulo S Ribeiro, Meike Broemer, Francois Leulier, Marketa Zvelebil, Neal Silverman and Pascal Meier

zVAD-fmk upregulates caspase-9 cleavage and activity in etoposide-induced cell death of mouse embryonic fibroblasts
Aida Rodríguez-Enfedaque, Elisabeth Delmas, Arnaud Guillaume, Sébastien Gaumer, Bernard Mignotte, Jean-Luc Vayssière, Flore Renaud

Neuronal caspase 2 activity and function requires RAIDD, but not PIDD
Elena M. Ribe, Ying Y. Jean, Rebecca L. Goldstein, Claudia Manzl, Leonidas Stefanis, Andreas Villunger and Carol M. Troy

The Core Apoptotic Executioner Proteins CED-3 and CED-4 Promote Initiation of Neuronal Regeneration in Caenorhabditis elegans
Berangere Pinan-Lucarre, Christopher V. Gabel, Christopher P. Reina, S. Elizabeth Hulme, Sergey S. Shevkoplyas, R. Daniel Slone, Jian Xue, Yujie Qiao, Sarah Weisberg, Kevin Roodhouse, Lin Sun, George M. Whitesides, Aravinthan Samuel, Monica Driscoll

Structural study of TTR-52 reveals the mechanism by which a bridging molecule mediates apoptotic cell engulfment
Yanyong Kang, Dongfeng Zhao, Huanhuan Liang, Bin Liu, Yan Zhang, Qinwen Liu, Xiaochen Wang, and Yingfang Liu

Bcl-2 family proteins

Bim Inhibits Autophagy by Recruiting Beclin 1 to Microtubules
Shouqing Luo, Moises Garcia-Arencibia, Rui Zhao, Claudia Puri, Pearl P.C. Toh, Oana Sadiq, and David C. Rubinsztein

Targeting antiapoptotic A1/Bfl-1 by in vivo RNAi reveals multiple roles in leukocyte development in mice
Eleonora Ottina, Francesca Grespi, Denise Tischner, Claudia Soratroi, Stephan Geley, Andreas Ploner, Holger M. Reichardt, Andreas Villunger, and Marco J. Herold

Bcl-2, Bcl-xL, and Bcl-w are not equivalent targets of ABT-737 and navitoclax (ABT-263) in lymphoid and leukemic cells
Delphine Mérino, Seong L. Khaw, Stefan P. Glaser, Daniel J. Anderson, Lisa D. Belmont, Chihunt Wong, Peng Yue, Mikara Robati, Belinda Phipson, Walter D. Fairlie, Erinna F. Lee, Kirsteen J. Campbell, Cassandra J. Vandenberg, Suzanne Cory, Andrew W. Roberts, Mary J. C. Ludlam, David C. S. Huang, and Philippe Bouillet

2-Deoxyglucose-induced toxicity is regulated by Bcl-2 family members and is enhanced by antagonizing Bcl-2 in lymphoma cell lines
O Zagorodna, S M Martin, D T Rutkowski, T Kuwana, D R Spitz and C M Knudson

Mcl-1 and Bcl-xL coordinately regulate megakaryocyte survival
Marlyse A. Debrincat, Emma C. Josefsson, Chloé James, Katya J. Henley, Sarah Ellis, Marion Lebois, Kelly L. Betterman, Rachael M. Lane, Kelly L. Rogers, Michael J. White, Andrew W. Roberts, Natasha L. Harvey, Donald Metcalf, and Benjamin T. Kile

Mcl-1 Phosphorylation Defines ABT-737 Resistance That Can Be Overcome by Increased NOXA Expression in Leukemic B cells
Suparna Mazumder, Gaurav S. Choudhary, Sayer Al-harbi, and Alexandru Almasan

Predominant requirement of Bax for apoptosis in HCT116 cells is determined by Mcl-1’s inhibitory effect on Bak
C Wang and R J Youle

Bax and Bcl-xL exert their regulation on different sites of the ceramide channel
Meenu N. Perera, Shang H. Lin, Yuri K. Peterson, Alicja Bielawska, Zdzislaw M. Szulc, Robert Bittman and Marco Colombini

Charge Profile Analysis Reveals That Activation of Pro-apoptotic Regulators Bax and Bak Relies on Charge Transfer Mediated Allosteric Regulation
Crina-Maria Ionescu1,2, Radka Svobodová Vařeková1,2, Jochen H. M. Prehn3,4, Heinrich J. Huber3,4, Jaroslav Koča

µ-Calpain Conversion of Antiapoptotic Bfl-1 (BCL2A1) into a Prodeath Factor Reveals Two Distinct alpha-Helices Inducing Mitochondria-Mediated Apoptosis
Juan García Valero, Aurélie Cornut-Thibaut, Romain Jugé, Anne-Laure Debaud, Diana Giménez, Germain Gillet, Nathalie Bonnefoy-Bérard, Jesús Salgado, Gilles Salles, Abdel Aouacheria, Jérôme Kucharczak

The anti-apoptotic Bcl-B protein inhibits BECN1-dependent autophagic cell death
Guillaume Robert, Cecile Gastaldi, Alexandre Puissant, Amine Hamouda, Arnaud Jacquel, Maeva Dufies, Nathalie Belhacene, Pascal Colosetti, John C. Reed, Patrick Auberger and Fréderic Luciano

Perk-dependent repression of miR-106b-25 cluster is required for ER stress-induced apoptosis
S Gupta, D E Read, A Deepti, K Cawley, A Gupta, D Oommen, T Verfaillie, S Matus, M A Smith, J L Mott, P Agostinis, C Hetz and A Samali

Charge Profile Analysis Reveals That Activation of Pro-apoptotic Regulators Bax and Bak Relies on Charge Transfer Mediated Allosteric Regulation
Crina-Maria Ionescu, Radka Svobodová Vařeková, Jochen H. M. Prehn, Heinrich J. Huber, Jaroslav Koča


Mitochondria and cell death

A BAX/BAK and Cyclophilin D-Independent Intrinsic Apoptosis Pathway
Sebastián Zamorano, Diego Rojas-Rivera, Fernanda Lisbona, Valentina Parra, Felipe A. Court, Rosario Villegas, Emily H. Cheng, Stanley J. Korsmeyer, Sergio Lavandero, Claudio Hetz

p53 Opens the Mitochondrial Permeability Transition Pore to Trigger Necrosis
Angelina V. Vaseva, Natalie D. Marchenko, Kyungmin Ji, Stella E. Tsirka, Sonja Holzmann, Ute M. Moll

Structure-based analysis of VDAC1: N-terminus location, translocation, channel gating and association with anti-apoptotic proteins
Shay Geula, Danya Ben Hail and Varda Shoshan Barmatz

Reviews / Comments / Previews

The flick of a switch: which death program to choose?
P Vandenabeele and G Melino

Caspase-3 and prostaglandins signal for tumor regrowth in cancer therapy
L Galluzzi, O Kepp and G Kroemer

Innate immunity: regulation of caspases by IAP-dependent ubiquitylation
DIAP2-mediated ubiquitylation of the pro-apoptotic initiator caspase Dredd converts it to an activator of the NfκB pathway required for innate immune signalling in Drosophila.
Christina Falschlehner and Michael Boutros

When Death Was Young: An Ancestral Apoptotic Network in Bacteria
D. Carmona-Gutierrez, G. Kroemer, and F. Madeo

Stemming Danger with Golgified BAX
L.D. Walensky

Death regulates platelet birth and life
Karin M. Hoffmeister

Cancer drug’s survivin suppression called into question
David Holmes

Channeling Death
Nancy R. Gough
Caspase-mediated cleavage of the channel TRPM7 enhances its activity and promotes Fas-mediated cell death.

p53 Opens the Gates to Necrosis
Ernesto Andrianantoandro
p53 induces necrosis in response to oxidative stress by opening the mitochondrial permeability transition pore.

Cell death: 1+1≠2
Michael Yaffe and colleagues show that pretreatment with one targeted drug for a specific period of time can increase the sensitivity of triple-negative breast cancer cells to standard chemotherapy.