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5. Protein citrullination and NET formation do not contribute to the pathology of A20/TNFAIP3 mutant mice

Author

Karel F. A. Van Damme, Pieter Hertens, Arne Martens, Elisabeth Gilis, Dario Priem, Inge Bruggeman, Amelie Fossoul, Jozefien Declercq, Helena Aegerter, Andy Wullaert, Tino Hochepied, Esther Hoste, Lieselotte Vande Walle, Mohamed Lamkanfi, Savvas N. Savvides, Dirk Elewaut, Bart N. Lambrecht, and Geert van Loo

Subjects
Medicine, Science
Abstract

Abstract A20 serves as a critical brake on NF-κB-dependent inflammation. In humans, polymorphisms in or near the TNFAIP3/A20 gene have been linked to various inflammatory disorders, including systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Experimental gene knockout studies in mice have confirmed A20 as a susceptibility gene for SLE and RA. Here, we examine the significance of protein citrullination and NET formation in the autoimmune pathology of A20 mutant mice because autoimmunity directed against citrullinated antigens released by neutrophil extracellular traps (NETs) is central to the pathogenesis of RA and SLE. Furthermore, genetic variants impairing the deubiquitinase (DUB) function of A20 have been shown to contribute to autoimmune susceptibility. Our findings demonstrate that genetic disruption of A20 DUB function in A20 C103R knockin mice does not result in autoimmune pathology. Moreover, we show that PAD4 deficiency, which abolishes protein citrullination and NET formation, does not prevent the development of autoimmunity in A20 deficient mice. Collectively, these findings provide experimental confirmation that PAD4-dependent protein citrullination and NET formation do not serve as pathogenic mechanisms in the development of RA and SLE pathology in mice with A20 mutations.

Published
2023
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10. Ym1 protein crystals promote type 2 immunity

Author

Ines Heyndrickx, Kim Deswarte, Kenneth Verstraete, Koen HG Verschueren, Ursula Smole, Helena Aegerter, Ann Dansercoer, Hamida Hammad, Savvas N Savvides, and Bart N Lambrecht

Subjects
adjuvanticity, protein crystals, Ym1, Ym2, chitinase-like proteins, Charcot-Leyden crystals, Medicine, Science, Biology (General), QH301-705.5
Abstract

Spontaneous protein crystallization is a rare event, yet protein crystals are frequently found in eosinophil-rich inflammation. In humans, Charcot-Leyden crystals (CLCs) are made from galectin-10 (Gal10) protein, an abundant protein in eosinophils. Although mice do not encode Gal10 in their genome, they do form pseudo-CLCs, made from the chitinase-like proteins Ym1 and/or Ym2, encoded by Chil3 and Chil4 and made by myeloid and epithelial cells respectively. Here, we investigated the biological effects of pseudo-CLCs since their function is currently unknown. We produced recombinant Ym1 crystals which were shown to have identical crystal packing and structure by X-ray crystallography as in vivo native crystals derived from murine lung. When administered to the airways of mice, crystalline but not soluble Ym1 stimulated innate and adaptive immunity and acted as a type 2 immune adjuvant for eosinophilic inflammation via triggering of dendritic cells (DCs). Murine Ym1 protein crystals found at sites of eosinophilic inflammation reinforce type 2 immunity and could serve as a surrogate model for studying the biology of human CLCs.

Published
2024
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11. Improving de novo protein binder design with deep learning

Author

Nathaniel R. Bennett, Brian Coventry, Inna Goreshnik, Buwei Huang, Aza Allen, Dionne Vafeados, Ying Po Peng, Justas Dauparas, Minkyung Baek, Lance Stewart, Frank DiMaio, Steven De Munck, Savvas N. Savvides, and David Baker

Subjects
Science
Abstract

Abstract Recently it has become possible to de novo design high affinity protein binding proteins from target structural information alone. There is, however, considerable room for improvement as the overall design success rate is low. Here, we explore the augmentation of energy-based protein binder design using deep learning. We find that using AlphaFold2 or RoseTTAFold to assess the probability that a designed sequence adopts the designed monomer structure, and the probability that this structure binds the target as designed, increases design success rates nearly 10-fold. We find further that sequence design using ProteinMPNN rather than Rosetta considerably increases computational efficiency.

Published
2023
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12. Towards Clinical Development of Scandium Radioisotope Complexes for Use in Nuclear Medicine: Encouraging Prospects with the Chelator 1,4,7,10-Tetraazacyclododecane-1,4,7,10-tetraacetic Acid (DOTA) and Its Analogues

Author

Ioannis Ioannidis, George Lefkaritis, Savvas N. Georgiades, Ioannis Pashalidis, and George J. Kontoghiorghes

Subjects
scandium radiopharmaceuticals, scandium theranostic pair, scandium radiolabeled complexes production and development, scandium imaging and diagnostic agents, chelating agents, DOTA, Biology (General), QH301-705.5, Chemistry, QD1-999
Abstract

Scandium (Sc) isotopes have recently attracted significant attention in the search for new radionuclides with potential uses in personalized medicine, especially in the treatment of specific cancer patient categories. In particular, Sc-43 and Sc-44, as positron emitters with a satisfactory half-life (3.9 and 4.0 h, respectively), are ideal for cancer diagnosis via Positron Emission Tomography (PET). On the other hand, Sc-47, as an emitter of beta particles and low gamma radiation, may be used as a therapeutic radionuclide, which also allows Single-Photon Emission Computed Tomography (SPECT) imaging. As these scandium isotopes follow the same biological pathway and chemical reactivity, they appear to fit perfectly into the “theranostic pair” concept. A step-by-step description, initiating from the moment of scandium isotope production and leading up to their preclinical and clinical trial applications, is presented. Recent developments related to the nuclear reactions selected and employed to produce the radionuclides Sc-43, Sc-44, and Sc-47, the chemical processing of these isotopes and the main target recovery methods are also included. Furthermore, the radiolabeling of the leading chelator, 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA), and its structural analogues with scandium is also discussed and the advantages and disadvantages of scandium complexation are evaluated. Finally, a review of the preclinical studies and clinical trials involving scandium, as well as future challenges for its clinical uses and applications, are presented.

Published
2024
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13. The Fab region of IgG impairs the internalization pathway of FcRn upon Fc engagement

Author

Maximilian Brinkhaus, Erwin Pannecoucke, Elvera J. van der Kooi, Arthur E. H. Bentlage, Ninotska I. L. Derksen, Julie Andries, Bianca Balbino, Magdalena Sips, Peter Ulrichts, Peter Verheesen, Hans de Haard, Theo Rispens, Savvas N. Savvides, and Gestur Vidarsson

Subjects
Science
Abstract

Disrupting the association between the Immunoglobulin G constant fragment (Fc) and the neonatal Fc receptor (FcRn) by engineered antibodies is a promising strategy to reduce autoantibody levels in autoimmune diseases. Here authors show that the variable fragment (Fab) of immunoglobulins could disturb the Fc-FcRn interaction, therefore the therapeutic effect of Fc-only fragments might surpass that of Fc-engineered antibodies with enhanced binding to FcRn.

Published
2022
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15. Pathophysiology and inhibition of IL-23 signaling in psoriatic arthritis: A molecular insight

Author

Nguyen, Cuong Thach, Bloch, Yehudi, Składanowska, Katarzyna, Savvides, Savvas N, and Adamopoulos, Iannis E

Subjects
Rare Diseases, Autoimmune Disease, Psoriasis, Arthritis, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Antibodies, Monoclonal, Humanized, Arthritis, Psoriatic, Dermatologic Agents, Humans, Interleukin-23, Signal Transduction, Ustekinumab, Psoriatic arthritis, Skin and joint inflammation, Cytokines, IL-23/IL-23R pathways, Human monoclonal IL-23 antibodies, Therapeutics, Immunology
Abstract

Psoriatic arthritis (PsA) is a chronic inflammatory arthritis of unknown etiology, and currently the cellular and molecular interactions that dictate its pathogenesis remain elusive. A role of the interleukin-23 (IL-23)/IL-23R (IL-23 receptor) interaction in the development of psoriasis and PsA is well established. As IL-23 regulates the differentiation and activation of innate and adaptive immunity, it pertains to a very complex pathophysiology involving a plethora of effectors and transducers. In this review, we will discuss recent advances on the cellular and molecular pathophysiological mechanisms that regulate the initiation and progression of PsA as well as new therapeutic approaches for IL-23/IL-23R targeted therapeutics.

Published
2019

17. Design of protein-binding proteins from the target structure alone

Author

Cao, Longxing, Coventry, Brian, Goreshnik, Inna, Huang, Buwei, Sheffler, William, Park, Joon Sung, Jude, Kevin M., Marković, Iva, Kadam, Rameshwar U., Verschueren, Koen H. G., Verstraete, Kenneth, Walsh, Scott Thomas Russell, Bennett, Nathaniel, Phal, Ashish, Yang, Aerin, Kozodoy, Lisa, DeWitt, Michelle, Picton, Lora, Miller, Lauren, Strauch, Eva-Maria, DeBouver, Nicholas D., Pires, Allison, Bera, Asim K., Halabiya, Samer, Hammerson, Bradley, Yang, Wei, Bernard, Steffen, Stewart, Lance, Wilson, Ian A., Ruohola-Baker, Hannele, Schlessinger, Joseph, Lee, Sangwon, Savvides, Savvas N., Garcia, K. Christopher, and Baker, David

Published
2022
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19. Clostridium perfringens chitinases, key enzymes during early stages of necrotic enteritis in broiler chickens.

Author

Dierick, Evelien, Callens, Chana, Bloch, Yehudi, Savvides, Savvas N., Hark, Sarah, Pelzer, Stefan, Ducatelle, Richard, Van Immerseel, Filip, and Goossens, Evy

Subjects
NECROTIC enteritis, BACTERIAL adhesion, BROILER chickens, CLOSTRIDIUM perfringens, SUBSTRATES (Materials science)
Abstract

The interaction between bacteria and the intestinal mucus is crucial during the early pathogenesis of many enteric diseases in mammals. A critical step in this process employed by both commensal and pathogenic bacteria focuses on the breakdown of the protective layer presented by the intestinal mucus by mucolytic enzymes. C. perfringens type G, the causative agent of necrotic enteritis in broilers, produces two glycosyl hydrolase family 18 chitinases, ChiA and ChiB, which display distinct substrate preferences. Whereas ChiB preferentially processes linear substrates such as chitin, ChiA prefers larger and more branched substrates, such as carbohydrates presented by the chicken intestinal mucus. Here, we show via crystal structures of ChiA and ChiB in the apo and ligand-bound forms that the two enzymes display structural features that explain their substrate preferences providing a structural blueprint for further interrogation of their function and inhibition. This research focusses on the roles of ChiA and ChiB in bacterial proliferation and mucosal attachment, two processes leading to colonization and invasion of the gut. ChiA and ChiB, either supplemented or produced by the bacteria, led to a significant increase in C. perfringens growth. In addition to nutrient acquisition, the importance of chitinases in bacterial attachment to the mucus layer was shown using an in vitro binding assay of C. perfringens to chicken intestinal mucus. Both an in vivo colonization trial and a necrotic enteritis trial were conducted, demonstrating that a ChiA chitinase mutant strain was less capable to colonize the intestine and was hampered in its disease-causing ability as compared to the wild-type strain. Our findings reveal that the pathogen-specific chitinases produced by C. perfringens type G strains play a fundamental role during colonization, suggesting their potential as vaccine targets. Author summary: The intestinal mucus layer protects the intestinal mucosa from invasion by pathogenic bacteria. However, it is precisely this first line of protection that invading bacteria aim to break down en route to colonizing the gut. Clostridium perfringens type G, the causative agent of necrotic enteritis in broiler chickens, an enteric disease characterised by ulcers in the small intestine, employs such a pathogenic strategy. In addition to the well-studied NetB toxin, this bacterium can produce other pathogen-specific enzymes, some of which could play a central role during disease development. Two of these enzymes were identified as putative chitinases, ChiA and ChiB. We have demonstrated that ChiA and ChiB are indeed functional enzymes that can hydrolyze a wide variety of substrates, with ChiA preferring mucus as a substrate. Mucus breakdown by the chitinases induces both bacterial proliferation and attachment to mucus, two processes that are crucial in the first steps of the pathogenesis. In addition, we have shown that a ChiA mutant strain does not efficiently colonize the intestine and causes less severe lesions as compared to the wild-type strain. Thus, we conclude that chitinases provide an advantage to the pathogen to facilitate colonization of the intestine of broiler chickens. [ABSTRACT FROM AUTHOR]

Published
2024
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22. Structural Activation of Pro-inflammatory Human Cytokine IL-23 by Cognate IL-23 Receptor Enables Recruitment of the Shared Receptor IL-12Rβ1

Author

Bloch, Yehudi, Bouchareychas, Laura, Merceron, Romain, Składanowska, Katarzyna, Van den Bossche, Lien, Detry, Sammy, Govindarajan, Srinath, Elewaut, Dirk, Haerynck, Filomeen, Dullaers, Melissa, Adamopoulos, Iannis E, and Savvides, Savvas N

Subjects
Autoimmune Disease, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Animals, Calorimetry, Cell Line, Humans, Interferometry, Interleukin-12 Receptor beta 1 Subunit, Interleukin-12 Subunit p40, Interleukin-23, Male, Mice, Protein Binding, Real-Time Polymerase Chain Reaction, Receptors, Interleukin, Signal Transduction, Crohn’s disease, IL-12Rβ1, IL-23, IL-23 receptor, cytokine-receptor complex, inflammation, inflammatory bowel disease, psoriasis, rheumatoid arthritis, structure, Immunology
Abstract

Interleukin-23 (IL-23), an IL-12 family cytokine, plays pivotal roles in pro-inflammatory T helper 17 cell responses linked to autoimmune and inflammatory diseases. Despite intense therapeutic targeting, structural and mechanistic insights into receptor complexes mediated by IL-23, and by IL-12 family members in general, have remained elusive. We determined a crystal structure of human IL-23 in complex with its cognate receptor, IL-23R, and revealed that IL-23R bound to IL-23 exclusively via its N-terminal immunoglobulin domain. The structural and functional hotspot of this interaction partially restructured the helical IL-23p19 subunit of IL-23 and restrained its IL-12p40 subunit to cooperatively bind the shared receptor IL-12Rβ1 with high affinity. Together with structural insights from the interaction of IL-23 with the inhibitory antibody briakinumab and by leveraging additional IL-23:antibody complexes, we propose a mechanistic paradigm for IL-23 and IL-12 whereby cognate receptor binding to the helical cytokine subunits primes recruitment of the shared receptors via the IL-12p40 subunit.

Published
2018

26. Catalysis of a Diels–Alder Reaction between Azachalcones and Cyclopentadiene by a Recyclable Copper(II)-PEIP Metal-Organic Framework

Author

Eleni Hadjikyprianou, Sotiris Petrides, Andreas Kourtellaris, Anastasios J. Tasiopoulos, and Savvas N. Georgiades

Subjects
MOF, Diels–Alder cycloaddition, heterogeneous catalysis, green solvent, sustainability, Technology, Electrical engineering. Electronics. Nuclear engineering, TK1-9971, Engineering (General). Civil engineering (General), TA1-2040, Microscopy, QH201-278.5, Descriptive and experimental mechanics, QC120-168.85
Abstract

Metal-organic frameworks (MOFs) have attracted considerable interest as emerging heterogeneous catalysts for organic transformations of synthetic utility. Herein, a Lewis-acidic MOF, {[Cu3(PEIP)2(5-NH2-mBDC)(DMF)]·7DMF}∞, denoted as Cu(ΙΙ)-PEIP, has been synthesized via a one-pot process and deployed as an efficient heterogeneous catalyst for a Diels–Alder cycloaddition. Specifically, the [4 + 2] cycloaddition of 13 substituted azachalcone dienophiles with cyclopentadiene has been investigated. MOF-catalyzed reaction conditions were optimized, leading to the selection of water as the solvent, in the presence of 10% mol sodium dodecyl sulfate (SDS) to address substrate solubility. The Cu(II)-PEIP catalyst showed excellent activity under these green and mild conditions, exhibiting comparable or, in some cases, superior efficiency to a homogeneous catalyst often employed in Diels–Alder reactions, namely, Cu(OTf)2. The nature of the azachalcone substituent played a significant role in the reactivity of the dienophiles, with electron-withdrawing (EW) substituents enhancing conversion and electron-donating (ED) ones exhibiting the opposite effect. Coordinating substituents appeared to enhance the endo selectivity. Importantly, the Cu(II)-PEIP catalyst can be readily isolated from the reaction mixture and recycled up to four times without any significant reduction in conversion or selectivity.

Published
2023
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28. Ym1 protein crystals promote type 2 immunity

Author

Heyndrickx, Ines, Deswarte, Kim, Verstraete, Kenneth, Verschueren, Koen H.G., Smole, Ursula, Aegerter, Helena, Dansercoer, Ann, Hammad, Hamida, Savvides, Savvas N., Lambrecht, Bart N., Heyndrickx, Ines, Deswarte, Kim, Verstraete, Kenneth, Verschueren, Koen H.G., Smole, Ursula, Aegerter, Helena, Dansercoer, Ann, Hammad, Hamida, Savvides, Savvas N., and Lambrecht, Bart N.

Abstract

Spontaneous protein crystallization is a rare event, yet protein crystals are frequently found in eosinophil-rich inflammation. In humans, Charcot-Leyden crystals (CLCs) are made from galectin-10 (Gal10) protein, an abundant protein in eosinophils. Although mice do not encode Gal10 in their genome, they do form pseudo-CLCs, made from the chitinase-like proteins Ym1 and/or Ym2, encoded by Chil3 and Chil4 and made by myeloid and epithelial cells respectively. Here, we investigated the biological effects of pseudo-CLCs since their function is currently unknown. We produced recombinant Ym1 crystals which were shown to have identical crystal packing and structure by X-ray crystallography as in vivo native crystals derived from murine lung. When administered to the airways of mice, crystalline but not soluble Ym1 stimulated innate and adaptive immunity and acted as a type 2 immune adjuvant for eosinophilic inflammation via triggering of dendritic cells (DCs). Murine Ym1 protein crystals found at sites of eosinophilic inflammation reinforce type 2 immunity and could serve as a surrogate model for studying the biology of human CLCs.

Published
2024

29. Distinct EH domains of the endocytic TPLATE complex confer lipid and protein binding

Author

Klaas Yperman, Anna C. Papageorgiou, Romain Merceron, Steven De Munck, Yehudi Bloch, Dominique Eeckhout, Qihang Jiang, Pieter Tack, Rosa Grigoryan, Thomas Evangelidis, Jelle Van Leene, Laszlo Vincze, Peter Vandenabeele, Frank Vanhaecke, Martin Potocký, Geert De Jaeger, Savvas N. Savvides, Konstantinos Tripsianes, Roman Pleskot, and Daniel Van Damme

Subjects
Science
Abstract

AtEH/Pan1 proteins contain two N-terminal Eps15 homology (EH) domains and are subunits of the endocytic TPLATE complex present in plants. Here, the authors combine X-ray crystallography, NMR and MD simulations with biochemical and in planta analysis to characterize the two AtEH1/Pan1 EH domains and reveal their structural differences and complementary functional roles.

Published
2021
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30. Towards Clinical Development of Scandium Radioisotope Complexes for Use in Nuclear Medicine: Encouraging Prospects with the Chelator 1,4,7,10-Tetraazacyclododecane-1,4,7,10-tetraacetic Acid (DOTA) and Its Analogues †.

Author

Ioannidis, Ioannis, Lefkaritis, George, Georgiades, Savvas N., Pashalidis, Ioannis, and Kontoghiorghes, George J.

Subjects
RADIOISOTOPES, SINGLE-photon emission computed tomography, NUCLEAR medicine, SCANDIUM, POSITRON emission tomography, BETA rays, MOMENTS method (Statistics)
Abstract

Scandium (Sc) isotopes have recently attracted significant attention in the search for new radionuclides with potential uses in personalized medicine, especially in the treatment of specific cancer patient categories. In particular, Sc-43 and Sc-44, as positron emitters with a satisfactory half-life (3.9 and 4.0 h, respectively), are ideal for cancer diagnosis via Positron Emission Tomography (PET). On the other hand, Sc-47, as an emitter of beta particles and low gamma radiation, may be used as a therapeutic radionuclide, which also allows Single-Photon Emission Computed Tomography (SPECT) imaging. As these scandium isotopes follow the same biological pathway and chemical reactivity, they appear to fit perfectly into the "theranostic pair" concept. A step-by-step description, initiating from the moment of scandium isotope production and leading up to their preclinical and clinical trial applications, is presented. Recent developments related to the nuclear reactions selected and employed to produce the radionuclides Sc-43, Sc-44, and Sc-47, the chemical processing of these isotopes and the main target recovery methods are also included. Furthermore, the radiolabeling of the leading chelator, 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA), and its structural analogues with scandium is also discussed and the advantages and disadvantages of scandium complexation are evaluated. Finally, a review of the preclinical studies and clinical trials involving scandium, as well as future challenges for its clinical uses and applications, are presented. [ABSTRACT FROM AUTHOR]

Published
2024
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31. Attenuated CSF‐1R signalling drives cerebrovascular pathology

Author

Conor Delaney, Michael Farrell, Colin P Doherty, Kiva Brennan, Eoin O’Keeffe, Chris Greene, Kieva Byrne, Eoin Kelly, Niamh Birmingham, Paula Hickey, Simon Cronin, Savvas N Savvides, Sarah L Doyle, and Matthew Campbell

Subjects
adult‐onset leucoencephalopathy with axonal spheroids and pigmented glia (ALSP), blood, brain barrier, CSF‐1, CSF‐1R, IL‐34, Medicine (General), R5-920, Genetics, QH426-470
Abstract

Abstract Cerebrovascular pathologies occur in up to 80% of cases of Alzheimer's disease; however, the underlying mechanisms that lead to perivascular pathology and accompanying blood–brain barrier (BBB) disruption are still not fully understood. We have identified previously unreported mutations in colony stimulating factor‐1 receptor (CSF‐1R) in an ultra‐rare autosomal dominant condition termed adult‐onset leucoencephalopathy with axonal spheroids and pigmented glia (ALSP). Cerebrovascular pathologies such as cerebral amyloid angiopathy (CAA) and perivascular p‐Tau were some of the primary neuropathological features of this condition. We have identified two families with different dominant acting alleles with variants located in the kinase region of the CSF‐1R gene, which confer a lack of kinase activity and signalling. The protein product of this gene acts as the receptor for 2 cognate ligands, namely colony stimulating factor‐1 (CSF‐1) and interleukin‐34 (IL‐34). Here, we show that depletion in CSF‐1R signalling induces BBB disruption and decreases the phagocytic capacity of peripheral macrophages but not microglia. CSF‐1R signalling appears to be critical for macrophage and microglial activation, and macrophage localisation to amyloid appears reduced following the induction of Csf‐1r heterozygosity in macrophages. Finally, we show that endothelial/microglial crosstalk and concomitant attenuation of CSF‐1R signalling causes re‐modelling of BBB‐associated tight junctions and suggest that regulating BBB integrity and systemic macrophage recruitment to the brain may be therapeutically relevant in ALSP and other Alzheimer’s‐like dementias.

Published
2020
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33. Ym1 protein crystals promote type 2 immunity

Author

Heyndrickx, Ines, primary, Deswarte, Kim, additional, Verstraete, Kenneth, additional, Verschueren, Koen HG, additional, Smole, Ursula, additional, Aegerter, Helena, additional, Dansercoer, Ann, additional, Hammad, Hamida, additional, Savvides, Savvas N, additional, and Lambrecht, Bart N, additional

Published
2024
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35. Author Response: Ym1 protein crystals promote type 2 immunity

Author

Heyndrickx, Ines, primary, Deswarte, Kim, additional, Verstraete, Kenneth, additional, Verschueren, Koen H. G., additional, Smole, Ursula, additional, Aegerter, Helena, additional, Dansercoer, Ann, additional, Hammad, Hamida, additional, Savvides, Savvas N., additional, and Lambrecht, Bart N., additional

Published
2023
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36. Ym1 protein crystals promote type 2 immunity

Author

Heyndrickx, Ines, primary, Deswarte, Kim, additional, Verstraete, Kenneth, additional, Verschueren, Koen H. G., additional, Smole, Ursula, additional, Aegerter, Helena, additional, Dansercoer, Ann, additional, Hammad, Hamida, additional, Savvides, Savvas N., additional, and Lambrecht, Bart N., additional

Published
2023
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38. The Physics of the B Factories

Author

Bevan, A. J., Golob, B., Mannel, Th., Prell, S., Yabsley, B. D., Abe, K., Aihara, H., Anulli, F., Arnaud, N., Aushev, T., Beneke, M., Beringer, J., Bianchi, F., Bigi, I. I., Bona, M., Brambilla, N., rodzicka, J. B, Chang, P., Charles, M. J., Cheng, C. H., Cheng, H. -Y., Chistov, R., Colangelo, P., Coleman, J. P., Drutskoy, A., Druzhinin, V. P., Eidelman, S., Eigen, G., Eisner, A. M., Faccini, R., Flood, K. T ., Gambino, P., Gaz, A., Gradl, W., Hayashii, H., Higuchi, T., Hulsbergen, W. D., Hurth, T., Iijima, T., Itoh, R., Jackson, P. D., Kass, R., Kolomensky, Yu. G., Kou, E., Križan, P., Kronfeld, A., Kumano, S., Kwon, Y. J., Latham, T. E., Leith, D. W. G. S., Lüth, V., Martinez-Vidal, F., Meadows, B. T., Mussa, R., Nakao, M., Nishida, S., Ocariz, J., Olsen, S. L., Pakhlov, P., Pakhlova, G., Palano, A., Pich, A., Playfer, S., Poluektov, A., Porter, F. C., Robertson, S. H., Roney, J. M., Roodman, A., Sakai, Y., Schwanda, C., Schwartz, A. J., Seidl, R., Sekula, S. J., Steinhauser, M., Sumisawa, K., Swanson, E. S., Tackmann, F., Trabelsi, K., Uehara, S., Uno, S., van der Water, R., Vasseur, G., Verkerke, W., Waldi, R., Wang, M. Z., Wilson, F. F., Zupan, J., Zupanc, A., Adachi, I., Albert, J., Banerjee, Sw., Bellis, M., Ben-Haim, E., Biassoni, P., Cahn, R. N., Cartaro, C., Chauveau, J., Chen, C., Chiang, C. C., Cowan, R., Dalseno, J., Davier, M., Davies, C., Dingfelder, J. C., nard, B. Eche, Epifanov, D., Fulsom, B. G., Gabareen, A. M., Gary, J. W., Godang, R., Graham, M. T., Hafner, A., Hamilton, B., Hartmann, T., Hayasaka, K., Hearty, C., Iwasaki, Y., Khodjamirian, A., Kusaka, A., Kuzmin, A., Lafferty, G. D., Lazzaro, A., Li, J., Lindemann, D., Long, O., Lusiani, A., Marchiori, G., Martinelli, M., Miyabayashi, K., Mizuk, R., Mohanty, G. B., Muller, D. R., Nakazawa, H., Ongmongkolkul, P., Pacetti, S., Palombo, F., Pedlar, T. K., Piilonen, L. E., Pilloni, A., Poireau, V., Prothmann, K., Pulliam, T., Rama, M., Ratcliff, B. N., Roudeau, P., Schrenk, S., Schroeder, T., Schubert, K. R., Shen, C. P., Shwartz, B., Soffer, A., Solodov, E. P., Somov, A., Starič, M., Stracka, S., Telnov, A. V., Todyshev, K. Yu., Tsuboyama, T., Uglov, T., Vinokurova, A., Walsh, J. J., Watanabe, Y., Won, E., Wormser, G., Wright, D. H., Ye, S., Zhang, C. C., Abachi, S., Abashian, A., Abe, N., Abe, R., Abe, T., Abrams, G. S., Adam, I., Adamczyk, K., Adametz, A., Adye, T., Agarwal, A., Ahmed, H., Ahmed, M., Ahmed, S., Ahn, B. S., Ahn, H. S., Aitchison, I. J. R., Akai, K., Akar, S., Akatsu, M., Akemoto, M., Akhmetshin, R., Akre, R., Alam, M. S., Albert, J. N., Aleksan, R., Alexander, J. P., Alimonti, G., Allen, M. T., Allison, J., Allmendinger, T., Alsmiller, J. R. G., Altenburg, D., Alwyn, K. E., An, Q., Anderson, J., Andreassen, R., Andreotti, D., Andreotti, M., Andress, J. C., Angelini, C., Anipko, D., Anjomshoaa, A., Anthony, P. L., Antillon, E. A., Antonioli, E., Aoki, K., Arguin, J. 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G., Piatenko, T., Piccolo, D., Piccolo, M., Piemontese, L., Piemontese, M., Pierini, M., Pierson, S., Pioppi, M., Piredda, G., Pivk, M., Plaszczynski, S., Polci, F., Pompili, A., Poropat, P., Posocco, M., Potter, C. T., Potter, R. J. L., Prasad, V., Prebys, E., Prencipe, E., Prendki, J., Prepost, R., Prest, M., Prim, M., Pripstein, M., Prudent, X., Pruvot, S., Puccio, E. M. T., Purohit, M. V., Qi, N. D., Quinn, H., Raaf, J., Rabberman, R., Raffaelli, F., Ragghianti, G., Rahatlou, S., Rahimi, A. M., Rahmat, R., Rakitin, A. Y., Randle-Conde, A., Rankin, P., Rashevskaya, I., Ratkovsky, S., Raven, G., Re, V., Reep, M., Regensburger, J. J., Reidy, J., Reif, R., Reisert, B., Renard, C., Renga, F., Ricciardi, S., Richman, J. D., Ritchie, J. L., Ritter, M., Rivetta, C., Rizzo, G., Roat, C., Robbe, P., Roberts, D. A., Robertson, A. I., Robutti, E., Rodier, S., Rodriguez, D. M., Rodriguez, J. L., Rodriguez, R., Roe, N. A., Röhrken, M., Roethel, W., Rolquin, J., Romanov, L., Romosan, A., Ronan, M. T., Rong, G., Ronga, F. J., Roos, L., Root, N., Rosen, M., Rosenberg, E. I., Rossi, A., Rostomyan, A., Rotondo, M., Roussot, E., Roy, J., Rozanska, M., Rozen, Y., Rubin, A. E., Ruddick, W. O., Ruland, A. M., Rybicki, K., Ryd, A., Ryu, S., Ryuko, J., Sabik, S., Sacco, R., Saeed, M. A., Tehrani, F. Safai, Sagawa, H., Sahoo, H., Sahu, S., Saigo, M., Saito, T., Saitoh, S., Sakai, K., Sakamoto, H., Sakaue, H., Saleem, M., Salnikov, A. A., Salvati, E., Salvatore, F., Samuel, A., Sanders, D. A., Sanders, P., Sandilya, S., Sandrelli, F., Sands, W., Sands, W. R., Sanpei, M., Santel, D., Santelj, L., Santoro, V., Santroni, A., Sanuki, T., Sarangi, T. R., Saremi, S., Sarti, A., Sasaki, T., Sasao, N., Satapathy, M., Sato, Nobuhiko, Sato, Noriaki, Sato, Y., Satoyama, N., Satpathy, A., Savinov, V., Savvas, N., Saxton, O. H., Sayeed, K., Schaffner, S. F., Schalk, T., Schenk, S., Schieck, J. R., Schietinger, T., Schilling, C. J., Schindler, R. H., Schmid, S., Schmitz, R. E., Schmuecker, H., Schneider, O., Schnell, G., Schönmeier, P., Schofield, K. C., Schott, G., Schröder, H., Schram, M., Schubert, J., Schümann, J., Schultz, J., Schumm, B. A., Schune, M. H., Schwanke, U., Schwarz, H., Schwiening, J., Schwierz, R., Schwitters, R. F., Sciacca, C., Sciolla, G., Scott, I. J., Seeman, J., Seiden, A., Seitz, R., Seki, T., Sekiya, A. I., Semenov, S., Semmler, D., Sen, S., Senyo, K., Seon, O., Serbo, V. V., Serednyakov, S. I., Serfass, B., Serra, M., Serrano, J., Settai, Y., Seuster, R., Sevior, M. E., Shakhova, K. V., Shang, L., Shapkin, M., Sharma, V., Shebalin, V., Shelkov, V. G., Shen, B. C., Shen, D. Z., Shen, Y. T., Sherwood, D. J., Shibata, T., Shibata, T. A., Shibuya, H., Shidara, T., Shimada, K., Shimoyama, M., Shinomiya, S., Shiu, J. G., Shorthouse, H. W., Shpilinskaya, L. I., Sibidanov, A., Sicard, E., Sidorov, A., Sidorov, V., Siegle, V., Sigamani, M., Simani, M. C., Simard, M., Simi, G., Simon, F., Simonetto, F., Sinev, N. B., Singh, H., Singh, J. B., Sinha, R., Sitt, S., Skovpen, Yu. I., Sloane, R. J., Smerkol, P., Smith, A. J. S., Smith, D., Smith, D. S., Smith, J. G., Smol, A., Snoek, H. L., Snyder, A., So, R. Y., Sobie, R. J., Soderstrom, E., Soha, A., Sohn, Y. S., Sokoloff, M. D., Sokolov, A., Solagna, P., Solovieva, E., Soni, N., Sonnek, P., Sordini, V., Spaan, B., Spanier, S. M., Spencer, E., Speziali, V., Spitznagel, M., Spradlin, P., Staengle, H., Stamen, R., Stanek, M., Stanič, S., Stark, J., Steder, M., Steininger, H., Steinke, M., Stelzer, J., Stevanato, E., Stocchi, A., Stock, R., Stoeck, H., Stoker, D. P., Stroili, R., Strom, D., Strother, P., Strube, J., Stugu, B., Stypula, J., Su, D., Suda, R., Sugahara, R., Sugi, A., Sugimura, T., Sugiyama, A., Suitoh, S., Sullivan, M. K., Sumihama, M., Sumiyoshi, T., Summers, D. J., Sun, L., Sun, S., Sundermann, J. E., Sung, H. F., Susaki, Y., Sutcliffe, P., Suzuki, A., Suzuki, J., Suzuki, J. I., Suzuki, K., Suzuki, S., Suzuki, S. Y., Swain, J. E., Swain, S. K., T'Jampens, S., Tabata, M., Tackmann, K., Tajima, H., Tajima, O., Takahashi, K., Takahashi, S., Takahashi, T., Takasaki, F., Takayama, T., Takita, M., Tamai, K., Tamponi, U., Tamura, N., Tan, N., Tan, P., Tanabe, K., Tanabe, T., Tanaka, H. A., Tanaka, J., Tanaka, M., Tanaka, S., Tanaka, Y., Tanida, K., Taniguchi, N., Taras, P., Tasneem, N., Tatishvili, G., Tatomi, T., Tawada, M., Taylor, F., Taylor, G. N., Taylor, G. P., Telnov, V. I., Teodorescu, L., Ter-Antonyan, R., Teramoto, Y., Teytelman, D., Thérin, G., Thiebaux, Ch., Thiessen, D., Thomas, E. W., Thompson, J. M., Thorne, F., Tian, X. C., Tibbetts, M., Tikhomirov, I., Tinslay, J. S., Tiozzo, G., Tisserand, V., Tocut, V., Toki, W. H., Tomassini, E. W., Tomoto, M., Tomura, T., Torassa, E., Torrence, E., Tosi, S., Touramanis, C., Toussaint, J. C., Tovey, S. N., Trapani, P. P., Treadwell, E., Triggiani, G., Trincaz-Duvoid, S., Trischuk, W., Troost, D., Trunov, A., Tsai, K. L., Tsai, Y. T., Tsujita, Y., Tsukada, K., Tsukamoto, T., Tuggle, J. M., Tumanov, A., Tung, Y. W., Turnbull, L., Turner, J., Turri, M., Uchida, K., Uchida, M., Uchida, Y., Ueki, M., Ueno, K., Ujiie, N., Ulmer, K. A., Unno, Y., Urquijo, P., Ushiroda, Y., Usov, Y., Usseglio, M., Usuki, Y., Uwer, U., Va'vra, J., Vahsen, S. E., Vaitsas, G., Valassi, A., Vallazza, E., Vallereau, A., Vanhoefer, P., van Hoek, W. C., Van Hulse, C., van Winkle, D., Varner, G., Varnes, E. W., Varvell, K. E., Vasileiadis, G., Velikzhanin, Y. S., Verderi, M., Versillé, S., Vervink, K., Viaud, B., Vidal, P. B., Villa, S., Villanueva-Perez, P., Vinograd, E. L., Vitale, L., Vitug, G. M., Voß, C., Voci, C., Voena, C., Volk, A., von Wimmersperg-Toeller, J. H., Vorobyev, V., Vossen, A., Vuagnin, G., Vuosalo, C. O., Wacker, K., Wagner, A. P., Wagner, D. L., Wagner, G., Wagner, M. N., Wagner, S. R., Wagoner, D. E., Walker, D., Walkowiak, W., Wallom, D., Wang, C. C., Wang, C. H., Wang, J., Wang, J. G., Wang, K., Wang, L., Wang, L. L., Wang, P., Wang, T. J., Wang, W. F., Wang, X. L., Wang, Y. F., Wappler, F. R., Watanabe, M., Watson, A. T., Watson, J. E., Watson, N. K., Watt, M., Weatherall, J. H., Weaver, M., Weber, T., Wedd, R., Wei, J. T., Weidemann, A. W., Weinstein, A. J. R., Wenzel, W. A., West, C. A., West, C. G., West, T. J., White, E., White, R. M., Wicht, J., Widhalm, L., Wiechczynski, J., Wienands, U., Wilden, L., Wilder, M., Williams, D. C., Williams, G., Williams, J. C., Williams, K. M., Williams, M. I., Willocq, S. Y., Wilson, J. R., Wilson, M. G., Wilson, R. J., Winklmeier, F., Winstrom, L. O., Winter, M. A., Wisniewski, W. J., Wittgen, M., Wittlin, J., Wittmer, W., Wixted, R., Woch, A., Wogsland, B. J., Wong, Q. K., Wray, B. C., Wren, A. C., Wright, D. M., Wu, C. H., Wu, J., Wu, S. L., Wulsin, H. W., Xella, S. M., Xie, Q. L., Xie, Y., Xu, Z. Z., Yèche, Ch., Yamada, Y., Yamaga, M., Yamaguchi, A., Yamaguchi, H., Yamaki, T., Yamamoto, H., Yamamoto, N., Yamamoto, R. K., Yamamoto, S., Yamanaka, T., Yamaoka, H., Yamaoka, J., Yamaoka, Y., Yamashita, Y., Yamauchi, M., Yan, D. S., Yan, Y., Yanai, H., Yanaka, S., Yang, H., Yang, R., Yang, S., Yarritu, A. K., Yashchenko, S., Yashima, J., Yasin, Z., Yasu, Y., Ye, S. W., Yeh, P., Yi, J. I., Yi, K., Yi, M., Yin, Z. W., Ying, J., Yocky, G., Yokoyama, K., Yokoyama, M., Yokoyama, T., Yoshida, K., Yoshida, M., Yoshimura, Y., Young, C. C., Yu, C. X., Yu, Z., Yuan, C. Z., Yuan, Y., Yumiceva, F. X., Yusa, Y., Yushkov, A. N., Yuta, H., Zacek, V., Zain, S. B., Zallo, A., Zambito, S., Zander, D., Zang, S. L., Zanin, D., Zaslavsky, B. G., Zeng, Q. L., Zghiche, A., Zhang, B., Zhang, J., Zhang, L., Zhang, L. M., Zhang, S. Q., Zhang, Z. P., Zhao, H. W., Zhao, M., Zhao, Z. G., Zheng, Y., Zheng, Y. H., Zheng, Z. P., Zhilich, V., Zhou, P., Zhu, R. Y., Zhu, Y. S., Zhu, Z. M., Zhulanov, V., Ziegler, T., Ziegler, V., Zioulas, G., Zisman, M., Zito, M., Zürcher, D., Zwahlen, N., Zyukova, O., Živko, T., and Žontar, D.

Subjects
High Energy Physics - Experiment, High Energy Physics - Phenomenology
Abstract

This work is on the Physics of the B Factories. Part A of this book contains a brief description of the SLAC and KEK B Factories as well as their detectors, BaBar and Belle, and data taking related issues. Part B discusses tools and methods used by the experiments in order to obtain results. The results themselves can be found in Part C. Please note that version 3 on the archive is the auxiliary version of the Physics of the B Factories book. This uses the notation alpha, beta, gamma for the angles of the Unitarity Triangle. The nominal version uses the notation phi_1, phi_2 and phi_3. Please cite this work as Eur. Phys. J. C74 (2014) 3026., Comment: 928 pages, version 3 (arXiv:1406.6311v3) corresponds to the alpha, beta, gamma version of the book, the other versions use the phi1, phi2, phi3 notation

Published
2014
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39. DNA methylation repels binding of hypoxia-inducible transcription factors to maintain tumor immunotolerance

Author

Flora D’Anna, Laurien Van Dyck, Jieyi Xiong, Hui Zhao, Rebecca V. Berrens, Junbin Qian, Pawel Bieniasz-Krzywiec, Vikas Chandra, Luc Schoonjans, Jason Matthews, Julie De Smedt, Liesbeth Minnoye, Ricardo Amorim, Sepideh Khorasanizadeh, Qian Yu, Liyun Zhao, Marie De Borre, Savvas N. Savvides, M. Celeste Simon, Peter Carmeliet, Wolf Reik, Fraydoon Rastinejad, Massimiliano Mazzone, Bernard Thienpont, and Diether Lambrechts

Subjects
DNA methylation, Hypoxia, HIF, Cryptic transcripts, Immunotherapy, Cancer, Biology (General), QH301-705.5, Genetics, QH426-470
Abstract

Abstract Background Hypoxia is pervasive in cancer and other diseases. Cells sense and adapt to hypoxia by activating hypoxia-inducible transcription factors (HIFs), but it is still an outstanding question why cell types differ in their transcriptional response to hypoxia. Results We report that HIFs fail to bind CpG dinucleotides that are methylated in their consensus binding sequence, both in in vitro biochemical binding assays and in vivo studies of differentially methylated isogenic cell lines. Based on in silico structural modeling, we show that 5-methylcytosine indeed causes steric hindrance in the HIF binding pocket. A model wherein cell-type-specific methylation landscapes, as laid down by the differential expression and binding of other transcription factors under normoxia, control cell-type-specific hypoxia responses is observed. We also discover ectopic HIF binding sites in repeat regions which are normally methylated. Genetic and pharmacological DNA demethylation, but also cancer-associated DNA hypomethylation, expose these binding sites, inducing HIF-dependent expression of cryptic transcripts. In line with such cryptic transcripts being more prone to cause double-stranded RNA and viral mimicry, we observe low DNA methylation and high cryptic transcript expression in tumors with high immune checkpoint expression, but not in tumors with low immune checkpoint expression, where they would compromise tumor immunotolerance. In a low-immunogenic tumor model, DNA demethylation upregulates cryptic transcript expression in a HIF-dependent manner, causing immune activation and reducing tumor growth. Conclusions Our data elucidate the mechanism underlying cell-type-specific responses to hypoxia and suggest DNA methylation and hypoxia to underlie tumor immunotolerance.

Published
2020
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41. Exploring Adaptation and Satisfaction in Copied Complete Dentures Regarding Two Different Occlusal Schemes.

Author

Kamalakidis, Savvas N., Anastassiadou, Vassiliki, and Pissiotis, Argirios L.

Subjects
DENTURES, PATIENT satisfaction, PATIENTS' attitudes, DENTAL occlusion, DENTAL research
Abstract

Purpose: To compare patient adaptation to and satisfaction with new complete dentures fabricated via a duplication construction protocol (DCP) using two different occlusal schemes: bilateral balanced (BBO) and lingualized (LO). Materials and Methods: A total of 20 complete denture wearers who received replacement DCP dentures participated in this study. Of these, 10 participants received complete dentures with a BBO scheme, while the other 10 received DCP dentures with an LO scheme. All of them evaluated their prostheses subjectively through the Oral Health Impact Profile-20 (OHIP-20) and the Complete Denture Satisfaction (CDS) questionnaires before treatment and at 3- and 6-month posttreatment intervals. The new prostheses were also normatively evaluated by recording the location and number of sore spots present at the scheduled early adjustment visits. Data were analyzed with nonparametric tests to identify differences in patient response both between groups and within each group at each evaluation interval (α = .05). Results: The within-group comparisons revealed statistically significant improvement for both denture groups (P < .05), while the between-group comparisons did not show statistically significant differences at the overall evaluation period (P > .05). Significant within-group differences were recorded in the pain, functional limitation, and psychologic disability domains of the OHIP-20 questionnaire, as well as the comfort, esthetics, and stability domains of the CDS questionnaire. Conclusion: Patient adaptation to and satisfaction with newly constructed DCP dentures improved significantly for both BBO and LO denture groups throughout the evaluation period. The mean number of early adjustment visits was equal for both the BBO and LO denture groups. [ABSTRACT FROM AUTHOR]

Published
2023
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42. Distinct EH domains of the endocytic TPLATE complex confer lipid and protein binding

Author

Yperman, Klaas, Papageorgiou, Anna C., Merceron, Romain, De Munck, Steven, Bloch, Yehudi, Eeckhout, Dominique, Jiang, Qihang, Tack, Pieter, Grigoryan, Rosa, Evangelidis, Thomas, Van Leene, Jelle, Vincze, Laszlo, Vandenabeele, Peter, Vanhaecke, Frank, Potocký, Martin, De Jaeger, Geert, Savvides, Savvas N., Tripsianes, Konstantinos, Pleskot, Roman, and Van Damme, Daniel

Published
2021
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43. Activating mutations in CSF1R and additional receptor tyrosine kinases in histiocytic neoplasms

Author

Durham, Benjamin H., Lopez Rodrigo, Estibaliz, Picarsic, Jennifer, Abramson, David, Rotemberg, Veronica, De Munck, Steven, Pannecoucke, Erwin, Lu, Sydney X., Pastore, Alessandro, Yoshimi, Akihide, Mandelker, Diana, Ceyhan-Birsoy, Ozge, Ulaner, Gary A., Walsh, Michael, Yabe, Mariko, Petrova-Drus, Kseniya, Arcila, Maria E., Ladanyi, Marc, Solit, David B., Berger, Michael F., Hyman, David M., Lacouture, Mario E., Erickson, Caroline, Saganty, Ruth, Ki, Michelle, Dunkel, Ira J., Santa-María López, Vicente, Mora, Jaume, Haroche, Julien, Emile, Jean-Francois, Decaux, Olivier, Geissmann, Frederic, Savvides, Savvas N., Drilon, Alexander, Diamond, Eli L., and Abdel-Wahab, Omar

Published
2019
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46. Serine 25 phosphorylation inhibits RIPK1 kinase-dependent cell death in models of infection and inflammation

Author

Yves Dondelinger, Tom Delanghe, Dario Priem, Meghan A. Wynosky-Dolfi, Daniel Sorobetea, Diego Rojas-Rivera, Piero Giansanti, Ria Roelandt, Julia Gropengiesser, Klaus Ruckdeschel, Savvas N. Savvides, Albert J. R. Heck, Peter Vandenabeele, Igor E. Brodsky, and Mathieu J. M. Bertrand

Subjects
Science
Abstract

RIPK1 kinase activity is known to transduce a death signal, but the molecular mechanisms that normally prevent RIPK1 activation are unclear. Here, the authors report that IKK-mediated phosphorylation on RIPK1 Ser25 directly represses its enzymatic activity and thus RIPK1-dependent cell death.

Published
2019
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47. Physical and functional interaction between A20 and ATG16L1-WD40 domain in the control of intestinal homeostasis

Author

Karolina Slowicka, Inmaculada Serramito-Gómez, Emilio Boada-Romero, Arne Martens, Mozes Sze, Ioanna Petta, Hanna K. Vikkula, Riet De Rycke, Eef Parthoens, Saskia Lippens, Savvas N. Savvides, Andy Wullaert, Lars Vereecke, Felipe X. Pimentel-Muiños, and Geert van Loo

Subjects
Science
Abstract

Maintaining the intestinal barrier function requires a balance of multiple signalling pathways. Here the authors show that A20, an anti-inflammatory and anti-apoptotic protein, and Atg1611, an autophagy regulator, cross-regulate their respective protein levels and function to serve compensatory and redundant roles in fine-tuning gut barrier homeostasis.

Published
2019
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49. Nonselective Chemical Inhibition of Sec7 Domain-Containing ARF GTPase Exchange Factors

Author

Mishev, Kiril, Lu, Qing, BramDenoo, Peurois, François, WimDejonghe, JanHullaert, RietDeRycke, Boeren, Sjef, Bretou, Marine, De Munck, Steven, Sharma, Isha, Goodman, Kaija, Kalinowska, Kamila, Storme, Veronique, Nguyen, Le Son Long, Drozdzecki, Andrzej, Martins, Sara, Nerinckx, Wim, Audenaert, Dominique, AnnemiekeMadder, Isono, Erika, Savvides, Savvas N., Annaert, Wim, De Vries, Sacco, Cherfils, Jacqueline, JohanWinne, and Russinova, Eugenia

Published
2018

50. Stabilization of cytokine mRNAs in iNKT cells requires the serine-threonine kinase IRE1alpha

Author

Srinath Govindarajan, Djoere Gaublomme, Renée Van der Cruyssen, Eveline Verheugen, Sofie Van Gassen, Yvan Saeys, Simon Tavernier, Takao Iwawaki, Yehudi Bloch, Savvas. N. Savvides, Bart N. Lambrecht, Sophie Janssens, Dirk Elewaut, and Michael B. Drennan

Subjects
Science
Abstract

Invariant natural killer T (iNKT) cells rapidly enhance cytokine secretion and effector function following activation, but the underlying mechanism is still unclear. Here the authors show that an endoplasmic reticulum stress sensor, inositol-requiring enzyme 1α, activates the p38 kinase to stabilize cytokine mRNA for enhanced iNKT functions.

Published
2018
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