MLKL trafficking and accumulation at the plasma membrane control the kinetics and threshold for necroptosis
暂无分享,去创建一个
K. Rogers | Michael J. Mlodzianoski | L. Whitehead | Cheree Fitzgibbon | J. Hildebrand | J. Silke | G. Lessene | E. Hawkins | A. Samson | James M. Murphy | S. N. Young | A. Jacobsen | K. Davies | M. Faux | S. Garnish | N. Lalaoui | Ying Zhang | Daniel Frank | E. Petrie | N. Geoghegan | Anne Hempel | Wayne Cawthorne | Kristy Shield-Artin | X. Gavin | Niall D. Geoghegan | Annette V. Jacobsen | Joanne M. Hildebrand | Samuel N. Young
[1] K. Rogers,et al. MLKL trafficking and accumulation at the plasma membrane control the kinetics and threshold for necroptosis , 2020, Nature Communications.
[2] W. Patrick,et al. Distinct pseudokinase domain conformations underlie divergent activation mechanisms among vertebrate MLKL orthologues , 2020, Nature Communications.
[3] Victoria E. Jackson,et al. A missense mutation in the MLKL brace region promotes lethal neonatal inflammation and hematopoietic dysfunction , 2020, Nature Communications.
[4] A. Koide,et al. Identification of MLKL membrane translocation as a checkpoint in necroptotic cell death using Monobodies , 2020, Proceedings of the National Academy of Sciences.
[5] She Chen,et al. Necroptosis-blocking compound NBC1 targets heat shock protein 70 to inhibit MLKL polymerization and necroptosis , 2020, Proceedings of the National Academy of Sciences.
[6] J. Lieberman,et al. Knocking 'em Dead: Pore-Forming Proteins in Immune Defense. , 2020, Annual review of immunology.
[7] Junying Yuan,et al. A dominant autoinflammatory disease caused by non-cleavable variants of RIPK1 , 2019, Nature.
[8] James M. Murphy. The Killer Pseudokinase Mixed Lineage Kinase Domain-Like Protein (MLKL). , 2019, Cold Spring Harbor perspectives in biology.
[9] J. Mullikin,et al. Mutations that prevent caspase cleavage of RIPK1 cause autoinflammatory disease , 2019, Nature.
[10] G. Manning,et al. Viral MLKL Homologs Subvert Necroptotic Cell Death by Sequestering Cellular RIPK3. , 2019, Cell reports.
[11] J. Qin,et al. K63-linked ubiquitination regulates RIPK1 kinase activity to prevent cell death during embryogenesis and inflammation , 2019, Nature Communications.
[12] L. Komuves,et al. Cleavage of RIPK1 by caspase-8 is crucial for limiting apoptosis and necroptosis , 2019, Nature.
[13] N. Bidère,et al. Pannexin-1 limits the production of proinflammatory cytokines during necroptosis. , 2019, EMBO reports.
[14] Junying Yuan,et al. TAM Kinases Promote Necroptosis by Regulating Oligomerization of MLKL. , 2019, Molecular cell.
[15] M. van Lookeren Campagne,et al. Autophagy regulates inflammatory programmed cell death via turnover of RHIM-domain proteins , 2019, eLife.
[16] K. Aziz,et al. The AMPK-Parkin axis negatively regulates necroptosis and tumorigenesis by inhibiting the necrosome , 2019, Nature Cell Biology.
[17] Xiaodong Wang,et al. Flotillin-mediated endocytosis and ALIX–syntenin-1–mediated exocytosis protect the cell membrane from damage caused by necroptosis , 2019, Science Signaling.
[18] S. Uemura,et al. Addendum: A FRET biosensor for necroptosis uncovers two different modes of the release of DAMPs , 2018, Nature Communications.
[19] U. Pannicke,et al. Human RIPK1 deficiency causes combined immunodeficiency and inflammatory bowel diseases , 2018, Proceedings of the National Academy of Sciences.
[20] S. Uemura,et al. A FRET biosensor for necroptosis uncovers two different modes of the release of DAMPs , 2018, Nature Communications.
[21] S. Nejentsev,et al. Biallelic RIPK1 mutations in humans cause severe immunodeficiency, arthritis, and intestinal inflammation , 2018, Science.
[22] Brian J. Smith,et al. Conformational switching of the pseudokinase domain promotes human MLKL tetramerization and cell death by necroptosis , 2018, Nature Communications.
[23] A. Hale,et al. MLKL Requires the Inositol Phosphate Code to Execute Necroptosis. , 2018, Molecular cell.
[24] P. Vandenabeele,et al. Nuclear RIPK3 and MLKL contribute to cytosolic necrosome formation and necroptosis , 2018, Communications Biology.
[25] L. Stronati,et al. RIP3 AND pMLKL promote necroptosis-induced inflammation and alter membrane permeability in intestinal epithelial cells. , 2017, Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver.
[26] D. Green,et al. Biological events and molecular signaling following MLKL activation during necroptosis , 2017, Cell cycle.
[27] Junying Yuan,et al. Regulation of RIPK1 activation by TAK1-mediated phosphorylation dictates apoptosis and necroptosis , 2017, Nature Communications.
[28] Se-Jin Yoon,et al. MLKL, the Protein that Mediates Necroptosis, Also Regulates Endosomal Trafficking and Extracellular Vesicle Generation , 2017, Immunity.
[29] G. Brumatti,et al. MK2 Phosphorylates RIPK1 to Prevent TNF-Induced Cell Death , 2017, Molecular cell.
[30] B. Stockwell,et al. Necroptosis and ferroptosis are alternative cell death pathways that operate in acute kidney failure , 2017, Cellular and Molecular Life Sciences.
[31] D. Green,et al. ESCRT-III Acts Downstream of MLKL to Regulate Necroptotic Cell Death and Its Consequences , 2017, Cell.
[32] Johannes Schindelin,et al. TrackMate: An open and extensible platform for single-particle tracking. , 2017, Methods.
[33] J. Hildebrand,et al. Combination of IAP antagonist and IFNγ activates novel caspase-10- and RIPK1-dependent cell death pathways , 2017, Cell Death and Differentiation.
[34] Laura F. Dagley,et al. EspL is a bacterial cysteine protease effector that cleaves RHIM proteins to block necroptosis and inflammation , 2017, Nature Microbiology.
[35] M. Ohmuraya,et al. Short form FLICE-inhibitory protein promotes TNFα-induced necroptosis in fibroblasts derived from CFLARs transgenic mice. , 2016, Biochemical and biophysical research communications.
[36] A. Prince,et al. Necroptosis Promotes Staphylococcus aureus Clearance by Inhibiting Excessive Inflammatory Signaling. , 2016, Cell reports.
[37] J. Lieberman,et al. Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores , 2016, Nature.
[38] M. Balda,et al. Tight junctions: from simple barriers to multifunctional molecular gates , 2016, Nature Reviews Molecular Cell Biology.
[39] T. Luedde,et al. The necroptosis-inducing kinase RIPK3 dampens adipose tissue inflammation and glucose intolerance , 2016, Nature Communications.
[40] N. van Bruggen,et al. RIPK3 deficiency or catalytically inactive RIPK1 provides greater benefit than MLKL deficiency in mouse models of inflammation and tissue injury , 2016, Cell Death and Differentiation.
[41] Ulrich Schraermeyer,et al. Bax assembly into rings and arcs in apoptotic mitochondria is linked to membrane pores , 2016, The EMBO journal.
[42] J. Murray,et al. The potential utility of tight junction regulation in celiac disease: focus on larazotide acetate , 2016, Therapeutic advances in gastroenterology.
[43] J. Murphy,et al. HSP90 activity is required for MLKL oligomerisation and membrane translocation and the induction of necroptotic cell death , 2016, Cell Death and Disease.
[44] M. Sweet,et al. Analysis of the N-terminal region of human MLKL, as well as two distinct MLKL isoforms, reveals new insights into necroptotic cell death , 2015, Bioscience reports.
[45] J. Vince,et al. Post-translational control of RIPK3 and MLKL mediated necroptotic cell death , 2015, F1000Research.
[46] James M. Murphy. Faculty Opinions recommendation of Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha. , 2015 .
[47] W. Alexander,et al. Necroptosis signalling is tuned by phosphorylation of MLKL residues outside the pseudokinase domain activation loop. , 2015, The Biochemical journal.
[48] J. Murray,et al. Larazotide acetate for persistent symptoms of celiac disease despite a gluten-free diet: a randomized controlled trial. , 2015, Gastroenterology.
[49] Tobias Pietzsch,et al. BigDataViewer: visualization and processing for large image data sets , 2015, Nature Methods.
[50] Xiaodong Wang,et al. A cytosolic heat shock protein 90 and cochaperone CDC37 complex is required for RIP3 activation during necroptosis , 2015, Proceedings of the National Academy of Sciences.
[51] Wesley R. Legant,et al. Lattice light-sheet microscopy: Imaging molecules to embryos at high spatiotemporal resolution , 2014, Science.
[52] D. Vaux,et al. TNFR1-dependent cell death drives inflammation in Sharpin-deficient mice , 2014, eLife.
[53] W. Alexander,et al. Activation of the pseudokinase MLKL unleashes the four-helix bundle domain to induce membrane localization and necroptotic cell death , 2014, Proceedings of the National Academy of Sciences.
[54] D. Vaux,et al. RIPK1 Regulates RIPK3-MLKL-Driven Systemic Inflammation and Emergency Hematopoiesis , 2014, Cell.
[55] Xiaodong Wang,et al. Mixed lineage kinase domain-like protein MLKL causes necrotic membrane disruption upon phosphorylation by RIP3. , 2014, Molecular cell.
[56] J. Bertin,et al. Necroptosis Is Active in Children With Inflammatory Bowel Disease and Contributes to Heighten Intestinal Inflammation , 2014, The American Journal of Gastroenterology.
[57] Jiahuai Han,et al. Translocation of mixed lineage kinase domain-like protein to plasma membrane leads to necrotic cell death , 2013, Cell Research.
[58] Ling-gang Wu,et al. Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis , 2013, Nature Cell Biology.
[59] Toru Okamoto,et al. The pseudokinase MLKL mediates necroptosis via a molecular switch mechanism. , 2013, Immunity.
[60] Kerstin Pingel,et al. 50 Years of Image Analysis , 2012 .
[61] Kevin W Eliceiri,et al. NIH Image to ImageJ: 25 years of image analysis , 2012, Nature Methods.
[62] J. Murray,et al. Larazotide acetate regulates epithelial tight junctions in vitro and in vivo , 2012, Peptides.
[63] Xiaodong Wang,et al. Mixed Lineage Kinase Domain-like Protein Mediates Necrosis Signaling Downstream of RIP3 Kinase , 2012, Cell.
[64] Helmut Neumann,et al. Caspase-8 regulates TNF-alpha induced epithelial necroptosis and terminal ileitis , 2011, Nature.
[65] Kenneth W Dunn,et al. A practical guide to evaluating colocalization in biological microscopy. , 2011, American journal of physiology. Cell physiology.
[66] J. Whisstock,et al. The structural basis for membrane binding and pore formation by lymphocyte perforin , 2010, Nature.
[67] W. Kaiser,et al. Virus inhibition of RIP3-dependent necrosis. , 2010, Cell host & microbe.
[68] Na Zhang,et al. RIP3, an Energy Metabolism Regulator That Switches TNF-Induced Cell Death from Apoptosis to Necrosis , 2009, Science.
[69] F. Chan,et al. Phosphorylation-Driven Assembly of the RIP1-RIP3 Complex Regulates Programmed Necrosis and Virus-Induced Inflammation , 2009, Cell.
[70] Tao Wang,et al. Receptor Interacting Protein Kinase-3 Determines Cellular Necrotic Response to TNF-α , 2009, Cell.
[71] Alexei Degterev,et al. Identification of RIP1 kinase as a specific cellular target of necrostatins. , 2008, Nature chemical biology.
[72] K. Madsen,et al. Reducing small intestinal permeability attenuates colitis in the IL10 gene-deficient mouse , 2008, Gut.
[73] David L. Vaux,et al. IAP Antagonists Target cIAP1 to Induce TNFα-Dependent Apoptosis , 2007, Cell.
[74] J. Marchant,et al. Tight junction targeting and intracellular trafficking of occludin in polarized epithelial cells. , 2007, American journal of physiology. Cell physiology.
[75] Vinay Tergaonkar,et al. IAP antagonists target cIAP1 to induce TNFalpha-dependent apoptosis. , 2007, Cell.
[76] R. Shoemaker. The NCI60 human tumour cell line anticancer drug screen , 2006, Nature Reviews Cancer.
[77] J. Tschopp,et al. Interactions of Tumor Necrosis Factor (TNF) and TNF Receptor Family Members in the Mouse and Human* , 2006, Journal of Biological Chemistry.
[78] A. Sanabria,et al. Randomized controlled trial. , 2005, World journal of surgery.
[79] Alexei Degterev,et al. Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury , 2005, Nature chemical biology.
[80] Brian Seed,et al. Fas triggers an alternative, caspase-8–independent cell death pathway using the kinase RIP as effector molecule , 2000, Nature Immunology.
[81] Michael Unser,et al. A pyramid approach to subpixel registration based on intensity , 1998, IEEE Trans. Image Process..