RIPK1 ensures intestinal homeostasis by protecting the epithelium against apoptosis

[1]  M. Pasparakis,et al.  RIPK1 maintains epithelial homeostasis by inhibiting apoptosis and necroptosis , 2014, Nature.

[2]  Michelle C. Schaeffer,et al.  Cutting Edge: RIP1 kinase activity is dispensable for normal development but is a key regulator of inflammation in SHARPIN-deficient mice. , 2014, Journal of immunology.

[3]  D. Vaux,et al.  RIPK1 Regulates RIPK3-MLKL-Driven Systemic Inflammation and Emergency Hematopoiesis , 2014, Cell.

[4]  D. Green,et al.  RIPK1 Blocks Early Postnatal Lethality Mediated by Caspase-8 and RIPK3 , 2014, Cell.

[5]  J. Bertin,et al.  RIP1 suppresses innate immune necrotic as well as apoptotic cell death during mammalian parturition , 2014, Proceedings of the National Academy of Sciences.

[6]  L. Komuves,et al.  Activity of Protein Kinase RIPK3 Determines Whether Cells Die by Necroptosis or Apoptosis , 2014, Science.

[7]  Junying Yuan,et al.  Regulation of RIP1 kinase signalling at the crossroads of inflammation and cell death , 2013, Nature Reviews Molecular Cell Biology.

[8]  A. Strasser,et al.  The pseudokinase MLKL mediates necroptosis via a molecular switch mechanism. , 2013, Immunity.

[9]  P. Vandenabeele,et al.  RIPK3 contributes to TNFR1-mediated RIPK1 kinase-dependent apoptosis in conditions of cIAP1/2 depletion or TAK1 kinase inhibition , 2013, Cell Death and Differentiation.

[10]  J. Tschopp,et al.  Inhibitor of apoptosis proteins limit RIP3 kinase-dependent interleukin-1 activation. , 2012, Immunity.

[11]  Xiaodong Wang,et al.  Mixed Lineage Kinase Domain-like Protein Mediates Necrosis Signaling Downstream of RIP3 Kinase , 2012, Cell.

[12]  D. Vaux,et al.  In mouse embryonic fibroblasts, neither caspase-8 nor cellular FLICE-inhibitory protein (FLIP) is necessary for TNF to activate NF-κB, but caspase-8 is required for TNF to cause cell death, and induction of FLIP by NF-κB is required to prevent it , 2011, Cell Death and Differentiation.

[13]  Vanesa Fernández-Majada,et al.  FADD prevents RIP3-mediated epithelial cell necrosis and chronic intestinal inflammation , 2011, Nature.

[14]  Helmut Neumann,et al.  Caspase-8 regulates TNF-alpha induced epithelial necroptosis and terminal ileitis , 2011, Nature.

[15]  G. Häcker,et al.  cIAPs Block Ripoptosome Formation, a RIP1/Caspase-8 Containing Intracellular Cell Death Complex Differentially Regulated by cFLIP Isoforms , 2011, Molecular cell.

[16]  T. Tenev,et al.  The Ripoptosome, a signaling platform that assembles in response to genotoxic stress and loss of IAPs. , 2011, Molecular cell.

[17]  M. Bertrand,et al.  cIAP1 and TAK1 protect cells from TNF-induced necrosis by preventing RIP1/RIP3-dependent reactive oxygen species production , 2011, Cell Death and Differentiation.

[18]  R. Hakem,et al.  RIP3 mediates the embryonic lethality of caspase-8-deficient mice , 2011, Nature.

[19]  D. Vaux,et al.  In TNF-stimulated Cells, RIPK1 Promotes Cell Survival by Stabilizing TRAF2 and cIAP1, which Limits Induction of Non-canonical NF-κB and Activation of Caspase-8* , 2011, The Journal of Biological Chemistry.

[20]  Guy S. Salvesen,et al.  Catalytic activity of the caspase-8-FLIPL complex inhibits RIPK3-dependent necrosis , 2011, Nature.

[21]  J. Ninomiya-Tsuji,et al.  TGF-β–Activated Kinase 1 Signaling Maintains Intestinal Integrity by Preventing Accumulation of Reactive Oxygen Species in the Intestinal Epithelium , 2010, The Journal of Immunology.

[22]  P. Vandenabeele,et al.  RIP Kinases at the Crossroads of Cell Death and Survival , 2009, Cell.

[23]  Na Zhang,et al.  RIP3, an Energy Metabolism Regulator That Switches TNF-Induced Cell Death from Apoptosis to Necrosis , 2009, Science.

[24]  Xiaodong Wang,et al.  Receptor Interacting Protein Kinase-3 Determines Cellular Necrotic Response to TNF-α , 2009, Cell.

[25]  F. Chan,et al.  Phosphorylation-Driven Assembly of the RIP1-RIP3 Complex Regulates Programmed Necrosis and Virus-Induced Inflammation , 2009, Cell.

[26]  H. Clevers,et al.  Single Lgr5 stem cells build crypt–villus structures in vitro without a mesenchymal niche , 2009, Nature.

[27]  M. Bertrand,et al.  cIAP1 and cIAP2 facilitate cancer cell survival by functioning as E3 ligases that promote RIP1 ubiquitination. , 2008, Molecular cell.

[28]  M. Neurath,et al.  Epithelial NEMO links innate immunity to chronic intestinal inflammation , 2007, Nature.

[29]  W. Yeh,et al.  Ubiquitination of RIP1 Regulates an NF-κB-Independent Cell-Death Switch in TNF Signaling , 2007, Current Biology.

[30]  M. Neurath,et al.  High resolution colonoscopy in live mice , 2006, Nature Protocols.

[31]  Gabriel Pineda,et al.  Activation of IKK by TNFalpha requires site-specific ubiquitination of RIP1 and polyubiquitin binding by NEMO. , 2006, Molecular cell.

[32]  Daniel Metzger,et al.  Tissue‐specific and inducible Cre‐mediated recombination in the gut epithelium , 2004, Genesis.

[33]  V. Dixit,et al.  Kinase RIP3 Is Dispensable for Normal NF-κBs, Signaling by the B-Cell and T-Cell Receptors, Tumor Necrosis Factor Receptor 1, and Toll-Like Receptors 2 and 4 , 2004, Molecular and Cellular Biology.

[34]  L. Schoonjans,et al.  Improved Generation of Germline‐Competent Embryonic Stem Cell Lines from Inbred Mouse Strains , 2003, Stem cells.

[35]  D. Gumucio,et al.  cis Elements of the Villin Gene Control Expression in Restricted Domains of the Vertical (Crypt) and Horizontal (Duodenum, Cecum) Axes of the Intestine* , 2002, The Journal of Biological Chemistry.

[36]  P Chambon,et al.  Site- and time-specific gene targeting in the mouse. , 2001, Methods.

[37]  Reynaldo Sequerra,et al.  High-efficiency deleter mice show that FLPe is an alternative to Cre-loxP , 2000, Nature Genetics.

[38]  S. Akira,et al.  Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function. , 1998, Immunity.

[39]  Stefan Grimm,et al.  The Death Domain Kinase RIP Mediates the TNF-Induced NF-κB Signal , 1998 .

[40]  Werner Müller,et al.  Bypass of lethality with mosaic mice generated by Cre–loxP-mediated recombination , 1996, Current Biology.

[41]  R. Zinkernagel,et al.  Mice lacking the tumour necrosis factor receptor 1 are resistant to IMF-mediated toxicity but highly susceptible to infection by Listeria monocytogenes , 1993, Nature.

[42]  Hans Clevers,et al.  Primary mouse small intestinal epithelial cell cultures. , 2013, Methods in molecular biology.