about
An autoinflammatory disease with deficiency of the interleukin-1-receptor antagonistHorror autoinflammaticus: the molecular pathophysiology of autoinflammatory disease (*)The familial Mediterranean fever protein, pyrin, is cleaved by caspase-1 and activates NF-kappaB through its N-terminal fragmentSPRY domain-containing SOCS box protein 2: crystal structure and residues critical for protein bindingActivation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1β in type 2 diabetes.RIPK3 promotes cell death and NLRP3 inflammasome activation in the absence of MLKLPyrin Modulates the Intracellular Distribution of PSTPIP1.Succinate is an inflammatory signal that induces IL-1β through HIF-1α.Adipose tissue macrophages promote myelopoiesis and monocytosis in obesityThe SPRY domain-containing SOCS box protein SPSB2 targets iNOS for proteasomal degradation.Regulation of interleukin-1beta by interferon-gamma is species specific, limited by suppressor of cytokine signalling 1 and influences interleukin-17 productionDeficiency of 5-hydroxyisourate hydrolase causes hepatomegaly and hepatocellular carcinoma in mice.Transcriptional analysis of the three Nlrp1 paralogs in mice.The B30.2 domain of pyrin, the familial Mediterranean fever protein, interacts directly with caspase-1 to modulate IL-1beta productionNLRP1 inflammasome activation induces pyroptosis of hematopoietic progenitor cells.A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases.Activation of the NLRP3 inflammasome complex is not required for stress-induced death of pancreatic islets.Aberrant actin depolymerization triggers the pyrin inflammasome and autoinflammatory disease that is dependent on IL-18, not IL-1β.Dynamics of the SPRY domain-containing SOCS box protein 2: flexibility of key functional loopsAn aspartyl protease defines a novel pathway for export of Toxoplasma proteins into the host cell.Recent advances in the molecular pathogenesis of hereditary recurrent fevers.Plasmacytoid dendritic cells are short-lived: reappraising the influence of migration, genetic factors and activation on estimation of lifespan.STAT4 and the risk of rheumatoid arthritis and systemic lupus erythematosus.Familial Mediterranean fever with a single MEFV mutation: where is the second hit?Dual role for inflammasome sensors NLRP1 and NLRP3 in murine resistance to Toxoplasma gondii.The pathogen Candida albicans hijacks pyroptosis for escape from macrophagesDisease-associated amyloid and misfolded protein aggregates activate the inflammasome.Specific inflammasomes in complex diseases.ATF3 Is a Key Regulator of Macrophage IFN Responses.Monogenic autoinflammatory diseases: Cytokinopathies.Myeloid-derived miR-223 regulates intestinal inflammation via repression of the NLRP3 inflammasome.NLRP3 inflammasome activation downstream of cytoplasmic LPS recognition by both caspase-4 and caspase-5.Cutting edge: miR-223 and EBV miR-BART15 regulate the NLRP3 inflammasome and IL-1β production.Posttranslational Modification as a Critical Determinant of Cytoplasmic Innate Immune Recognition.Familial autoinflammation with neutrophilic dermatosis reveals a regulatory mechanism of pyrin activation.Regulation of Starch Stores by a Ca(2+)-Dependent Protein Kinase Is Essential for Viable Cyst Development in Toxoplasma gondii.The SPRY domain of SSB-2 adopts a novel fold that presents conserved Par-4-binding residues.Deficient NLRP3 and AIM2 Inflammasome Function in Autoimmune NZB Mice.Fas regulates neutrophil lifespan during viral and bacterial infection.Release of the mitochondrial endosymbiont helps explain sterile inflammation.
P50
Q24606097-BBDE48C6-272C-4C7D-9B6B-8B2052210D4CQ24631660-51D1F983-CC51-4BB7-B902-33C679B60074Q24642151-5C085C81-A7B2-4997-B87A-101ADD7FB5E7Q27653472-C0D18303-06F2-4C2A-9962-EE1AE3B89BF0Q29615593-CBCB715B-0C24-4DD4-9815-1A4E88F7D3DDQ30623992-3A79E0E2-AE2F-43F9-AFC9-55EA1D6E0EECQ33479535-6DBC5CEA-E49B-4B08-941D-94FE8D33D44FQ33652731-38A2ACC6-6EA7-4A92-BF36-7A78B3304F60Q33724394-75159CC3-F6B4-4431-A04D-F5A6993BE578Q34026690-A58626D8-0ED9-4353-B519-5C421E08F1BFQ34061498-7D283549-BAF3-4604-A8AE-9BB50ABDB832Q34151625-C9ECB2E7-F2EE-4721-A946-28DFAB51FA3FQ34626353-F4359C9F-CD97-4C10-862A-EA25C1C43B45Q34684433-E1DEB029-BFA1-45BD-A1DE-87EA2F4D2461Q34764912-D46D6F58-9101-4BD8-A50B-4E263D2D6F97Q35350543-43470249-E519-4828-BCA4-8890FE7B7FFDQ35432420-9C483146-D5B4-419D-9B97-1ADA30E2B001Q35671251-28D0F255-3AFB-4741-8BAC-3E72846EF61CQ36458177-132269DE-CD99-4EDA-A075-A3D01B81AD41Q36609991-996BBEA9-7A94-4BE0-A290-AC324CC15044Q36646672-E3C0E0F5-DCCD-4D51-8974-C8166D446E35Q36835494-D59ABC8C-C5B0-4735-AAD5-5E7A295B0FAEQ37070948-7D16BE5D-C693-4742-AC23-125FB4D99A6FQ37366257-E2E5F4D8-EDF2-425A-8B02-A76287328EF6Q37621648-BDDD44FA-C68E-4B41-86A1-EABF2B5A920FQ37687805-6159DFFE-FB72-4EE3-A715-92C7C246036AQ37849966-9C0C1008-F3E2-4116-AACE-214CA459D2D6Q38072155-265DD4F7-6F84-41A9-83D9-21AAEB5C48A9Q38296292-C9295D8F-E414-46EC-B3E1-93CAEAC7E617Q38392859-26E33ED0-ACA7-42DA-BC9B-C2B6041E9A37Q38795315-CF6CCC1B-CE0E-42D2-911F-0A0CBD093C0DQ38853111-46F0AFFA-4431-494C-A537-57091D677D6CQ39277512-AC4DB19A-EE84-401B-80AC-8820159BA300Q39374120-A13E74BA-FEF0-4C29-9097-5A6FDD6A1E8BQ40111903-7F1219E8-8AD4-4FCF-B314-F6AFA0BEA0D5Q40227747-7DDD6AF4-847C-4A2D-A1F3-BFDB204636E5Q40337569-CD25E8C1-00FD-4CE1-8AAA-46B5FD2603D7Q41136957-6E0DB262-ED68-4728-A6DE-A542144418ECQ41619299-0F156AAA-7EF5-4C77-917E-F9586991CBB9Q42865565-A9538C77-4E4D-48AE-9048-9B44ACFC70B1
P50
description
onderzoeker
@nl
researcher
@en
researcher
@en-gb
հետազոտող
@hy
name
Seth L Masters
@ast
Seth L Masters
@en
Seth L Masters
@en-gb
Seth L Masters
@es
Seth L Masters
@nl
Seth L Masters
@sl
type
label
Seth L Masters
@ast
Seth L Masters
@en
Seth L Masters
@en-gb
Seth L Masters
@es
Seth L Masters
@nl
Seth L Masters
@sl
prefLabel
Seth L Masters
@ast
Seth L Masters
@en
Seth L Masters
@en-gb
Seth L Masters
@es
Seth L Masters
@nl
Seth L Masters
@sl
P106
P1153
8618391900
P21
P31
P496
0000-0003-4763-576X