Primary Antibodies & Antigens
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Gene Symbol Gene Description ACVR1B Activin a Receptor, Type IB
Table S1. Kinase clones included in human kinase cDNA library for yeast two-hybrid screening Gene Symbol Gene Description ACVR1B activin A receptor, type IB ADCK2 aarF domain containing kinase 2 ADCK4 aarF domain containing kinase 4 AGK multiple substrate lipid kinase;MULK AK1 adenylate kinase 1 AK3 adenylate kinase 3 like 1 AK3L1 adenylate kinase 3 ALDH18A1 aldehyde dehydrogenase 18 family, member A1;ALDH18A1 ALK anaplastic lymphoma kinase (Ki-1) ALPK1 alpha-kinase 1 ALPK2 alpha-kinase 2 AMHR2 anti-Mullerian hormone receptor, type II ARAF v-raf murine sarcoma 3611 viral oncogene homolog 1 ARSG arylsulfatase G;ARSG AURKB aurora kinase B AURKC aurora kinase C BCKDK branched chain alpha-ketoacid dehydrogenase kinase BMPR1A bone morphogenetic protein receptor, type IA BMPR2 bone morphogenetic protein receptor, type II (serine/threonine kinase) BRAF v-raf murine sarcoma viral oncogene homolog B1 BRD3 bromodomain containing 3 BRD4 bromodomain containing 4 BTK Bruton agammaglobulinemia tyrosine kinase BUB1 BUB1 budding uninhibited by benzimidazoles 1 homolog (yeast) BUB1B BUB1 budding uninhibited by benzimidazoles 1 homolog beta (yeast) C9orf98 chromosome 9 open reading frame 98;C9orf98 CABC1 chaperone, ABC1 activity of bc1 complex like (S. pombe) CALM1 calmodulin 1 (phosphorylase kinase, delta) CALM2 calmodulin 2 (phosphorylase kinase, delta) CALM3 calmodulin 3 (phosphorylase kinase, delta) CAMK1 calcium/calmodulin-dependent protein kinase I CAMK2A calcium/calmodulin-dependent protein kinase (CaM kinase) II alpha CAMK2B calcium/calmodulin-dependent -
Binding and Uptake of H-Ferritin Are Mediated by Human Transferrin Receptor-1
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Caltech Authors Binding and uptake of H-ferritin are mediated by human transferrin receptor-1 Li Lia, Celia J. Fanga,b, James C. Ryana,b, Eréne C. Niemib, José A. Lebrónc,1, Pamela J. Björkmanc,d,2, Hisashi Arasee, Frank M. Tortif, Suzy V. Tortig, Mary C. Nakamuraa,b, and William E. Seamana,b,h,2 aDepartment of Medicine, Veterans Administration Medical Center, San Francisco, CA 94121; bDepartment of Medicine, University of California, San Francisco, CA 94143; cDivision of Biology, California Institute of Technology, Pasadena, CA 91125; dHoward Hughes Medical Institute, California Institute of Technology, Pasadena, CA 91125; eDepartment of Immunochemistry, World Premier International Immunology Frontier Research Center and Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan; fDepartment of Cancer Biology, Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157; gDepartment of Biochemistry, Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157; and hDepartment of Microbiology and Immunology, University of California, San Francisco, CA 94143 Contributed by Pamela J. Björkman, November 18, 2009 (sent for review October 5, 2009) − Ferritin is a spherical molecule composed of 24 subunits of two constant of ∼6.5 × 10 7 L/mol and ∼10,000 receptors sites per cell; types, ferritin H chain (FHC) and ferritin L chain (FLC). Ferritin stores subsequently, they endocytose HFt (13). Activated fresh lympho- iron within cells, but it also circulates and binds specifically and cytes also bind HFt (16), as do erythroid precursors, in which the saturably to a variety of cell types. -
High Efficiency Blood-Brain Barrier Transport Using a VNAR Targeting the Transferrin Receptor 1 (Tfr1)
bioRxiv preprint doi: https://doi.org/10.1101/816900; this version posted October 30, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Title: High efficiency blood-brain barrier transport using a VNAR targeting the Transferrin Receptor 1 (TfR1) Authors: Pawel Stocki§, Jaroslaw M Szary§, Charlotte LM Jacobsen¶, Mykhaylo Demydchuk§, Leandra Northall§, Torben Moos¶, Frank S Walsh§ and J Lynn Rutkowski§* §Ossianix, Inc, Stevenage Bioscience Catalyst, Gunnels Wood Rd, Stevenage, Herts, SG1 2FX, UK and 3675 Market St, Philadelphia, PA 19104, USA ¶Laboratory of Neurobiology, Department of Health Science and Technology, Aalborg University, Fredrik Bajers Vej 3, 9220 Aalborg, Denmark Address correspondence to: *J. Lynn Rutkowski, PhD Ossianix, Inc, 3675 Market St., Philadelphia, PA 19104, USA Email: [email protected] Tel: +1(610)291-1724 A one-sentence summary: Development of highly efficient, TfR1 specific, cross-species reactive blood-brain barrier (BBB) shuttle based on shark single domain VNAR antibody. Definitions of all symbols, abbreviations, and acronyms: Transferrin Receptor 1 (TfR1), blood-brain barrier (BBB), Transferrin (Tf), central nervous system (CNS), Variable domain of New Antigen Receptors (VNAR), complementarity-determining region 3 (CDR3), room temperature (RT), size exclusion chromatography (SEC), human serum albumin (HSA), Neurotensin (NT), Immunohistochemistry (IHC), next generation sequencing (NGS), Pharmacokinetic (PK), blood-CSF barrier (BCSFB), Percentage injected dose (%ID), Area under the curve (AUC), attenuated effector function (AEF), sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS- PAGE), Western blot (WB), intravenous (IV) 1 bioRxiv preprint doi: https://doi.org/10.1101/816900; this version posted October 30, 2019. -
Redox-Mediated Regulation of the Tyrosine Kinase Zap70
Redox-mediated regulation of the tyrosine kinase Zap70 DISSERTATION zur Erlangung des akademischen Grades doctor rerum naturalium (Dr. rer. nat.) genehmigt durch die Fakultät für Naturwissenschaften der Otto-von-Guericke-Universität von M.Sc. Christoph Thurm geb. am 27.06.1988 in Borna Gutachter: apl. Prof. Dr. Luca Simeoni PD Dr. rer. nat. Marcus Lettau eingereicht am: 02.02.2018 verteidigt am: 06.06.2018 Eigenständigkeitserklärung I. Eigenständigkeitserklärung Christoph Thurm Halberstädter Straße 29 39112 Magdeburg Hiermit erkläre ich, dass ich die von mir eingereichte Dissertation zu dem Thema Redox-mediated regulation of the tyrosine kinase Zap70 selbständig verfasst, nicht schon als Dissertation verwendet habe und die benutzten Hilfsmittel und Quellen vollständig angegeben wurden. Weiterhin erkläre ich, dass ich weder diese noch eine andere Arbeit zur Erlangung des akademischen Grades doctor rerum naturalium (Dr. rer. nat.) an anderen Einrichtungen eingereicht habe. Magdeburg, den 02.02.2018 ____________________________________ M.Sc. Christoph Thurm II ACKNOWLEDGEMENTS II. Acknowledgements Firstly, I would like to express my sincere gratitude to my supervisor Prof. Dr. Luca Simeoni. His extraordinary support during my PhD thesis together with his motivation and knowledge enabled me to pursue my dream. I could not have imagined having a better mentor. Furthermore, I would like to thank Prof. Dr. Burkhart Schraven for giving me the opportunity to work in his institute. His support, ideas, and the lively discussions promoted me to develop as a scientist. Special thanks go also to the whole AG Simeoni/Schraven - Ines, Camilla, Matthias, and Andreas - for the help with experiments, the discussions, and the fun we had. This helped to sustain also the longest days. -
FLRT Proteins Are Endogenous Latrophilin Ligands and Regulate Excitatory Synapse Development
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Neuron Report FLRT Proteins Are Endogenous Latrophilin Ligands and Regulate Excitatory Synapse Development Matthew L. O’Sullivan,1,5 Joris de Wit,1,5 Jeffrey N. Savas,2 Davide Comoletti,3 Stefanie Otto-Hitt,1,6 John R. Yates III,2 and Anirvan Ghosh1,4,* 1Neurobiology Section, Division of Biology, University of California San Diego, La Jolla, CA 92093, USA 2Department of Chemical Physiology, The Scripps Research Institute, La Jolla, CA 92037, USA 3Child Health Institute of New Jersey and Department of Neuroscience and Cell Biology, UMDNJ/Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA 4CNS Discovery, F. Hoffmann-La Roche, 4070 Basel, Switzerland 5These authors contributed equally to this work 6Present address: Department of Natural Sciences, Carroll College, Helena, MT 59625, USA *Correspondence: [email protected] DOI 10.1016/j.neuron.2012.01.018 SUMMARY much effort has been expended investigating the mechanisms of a-latrotoxin action (Su¨ dhof, 2001), nothing is known about Latrophilins (LPHNs) are a small family of G protein- the endogenous function of latrophilins in vertebrates. Further coupled receptors known to mediate the massive evidence for the importance of latrophilins in the proper synaptic exocytosis caused by the black widow functioning of neural circuits comes from recent human spider venom a-latrotoxin, but their endogenous genetics studies that have linked LPHN3 mutations to attention ligands and function remain unclear. Mutations in deficit hyperactivity disorder (ADHD), a common and highly LPHN3 are strongly associated with attention deficit heritable developmental psychiatric disorder (Arcos-Burgos et al., 2010; Domene´ et al., 2011; Jain et al., 2011; Ribase´ s hyperactivity disorder, suggesting a role for latrophi- et al., 2011). -
Role of Negative Regulation of Immune Signaling Pathways in Neutrophil Function
Role of negative regulation of immune signaling pathways in neutrophil function Veronica Azcutia *, Charles A. Parkos *, Jennifer C. Brazil * *Department of Pathology, University of Michigan, Ann Arbor, MI 48109 USA. Summary statement: Review on how PMN functions are negatively regulated by immune signaling pathways. Running title: Negative regulation of PMN function. Send correspondence to V.A and J.C.B, and the Editorial and Production Office information to V.A.: *Veronica Azcutia, Ph.D. Department of Pathology, University of Michigan. Biomedical Science Research Building (BSRB),109 Zina Pitcher Place, Ann Arbor, MI 48109 USA. This is the author manuscript accepted for publication and has undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1002/JLB.3MIR0917-374R. This article is protected by copyright. All rights reserved. Tel: (734)-936-1856, Fax: (734)-615-2331, e-Mail: [email protected] *Jennifer C. Brazil, Ph.D. Department of Pathology, University of Michigan. Biomedical Science Research Building (BSRB),109 Zina Pitcher Place, Ann Arbor, MI 48109 USA. Tel: (734)-936-1856, Fax: (734)-615-2331, e-Mail: [email protected] Key words: neutrophils, ITIM, inflammation. Total character count: 43,451; 2 Figures: Figure 1 and 2 are in color; 89 references; 144 words in Abstract; 12 words in summary statement. Abbreviations A(A2)AR = adenosine receptor BM = bone marrow CEACAM = carcinoembryonic antigen-related cell adhesion molecule Csk = C-terminal Scr kinase fMLF = formyl-methionyl-leucyl phenylalanine peptide GAP = GTPase activating proteins GEF = guanine nucleotide exchange factor G-CSF = Granulocyte colony stimulating factor G-CSFR = Granulocyte colony stimulating factor receptor GPCR = G protein coupled receptor GRK = G protein coupled receptor kinase IBD = Inflammatory bowel disease ICAM-1 = Intracellular Adhesion molecule-1 2 This article is protected by copyright. -
Edinburgh Research Explorer
Edinburgh Research Explorer International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list Citation for published version: Davenport, AP, Alexander, SPH, Sharman, JL, Pawson, AJ, Benson, HE, Monaghan, AE, Liew, WC, Mpamhanga, CP, Bonner, TI, Neubig, RR, Pin, JP, Spedding, M & Harmar, AJ 2013, 'International Union of Basic and Clinical Pharmacology. LXXXVIII. G protein-coupled receptor list: recommendations for new pairings with cognate ligands', Pharmacological reviews, vol. 65, no. 3, pp. 967-86. https://doi.org/10.1124/pr.112.007179 Digital Object Identifier (DOI): 10.1124/pr.112.007179 Link: Link to publication record in Edinburgh Research Explorer Document Version: Publisher's PDF, also known as Version of record Published In: Pharmacological reviews Publisher Rights Statement: U.S. Government work not protected by U.S. copyright General rights Copyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights. Take down policy The University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorer content complies with UK legislation. If you believe that the public display of this file breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 1521-0081/65/3/967–986$25.00 http://dx.doi.org/10.1124/pr.112.007179 PHARMACOLOGICAL REVIEWS Pharmacol Rev 65:967–986, July 2013 U.S. -
The 'C3ar Antagonist' SB290157 Is a Partial C5ar2 Agonist
bioRxiv preprint doi: https://doi.org/10.1101/2020.08.01.232090; this version posted August 3, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. The ‘C3aR antagonist’ SB290157 is a partial C5aR2 agonist Xaria X. Li1, Vinod Kumar1, John D. Lee1, Trent M. Woodruff1* 1School of Biomedical Sciences, The University of Queensland, St Lucia, 4072 Australia. * Correspondence: Prof. Trent M. Woodruff School of Biomedical Sciences, The University of Queensland, St Lucia, 4072 Australia. Ph: +61 7 3365 2924; Fax: +61 7 3365 1766; E-mail: [email protected] Keywords: Complement C3a, C3aR, SB290157, C5aR1, C5aR2 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.08.01.232090; this version posted August 3, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Abbreviations used in this article: BRET, bioluminescence resonance energy transfer; BSA, bovine serum albumin; C3aR, C3a receptor C5aR1, C5a receptor 1; CHO-C3aR, Chinese hamster ovary cells stably expressing C3aR; CHO-C5aR1, Chinese hamster ovary cells stably expressing C5aR1; DMEM, Dulbecco's Modified Eagle's Medium; ERK1/2, extracellular signal-regulated kinase 1/2; FBS, foetal bovine serum; HEK293, human embryonic kidney 293 cells; HMDM, human monocyte-derived macrophage; i.p., intraperitoneal; i.v., intravenous; rhC5a, recombinant human C5a; RT, room temperature; S.E.M. -
Neutrophil Chemoattractant Receptors in Health and Disease: Double-Edged Swords
Cellular & Molecular Immunology www.nature.com/cmi REVIEW ARTICLE Neutrophil chemoattractant receptors in health and disease: double-edged swords Mieke Metzemaekers1, Mieke Gouwy1 and Paul Proost 1 Neutrophils are frontline cells of the innate immune system. These effector leukocytes are equipped with intriguing antimicrobial machinery and consequently display high cytotoxic potential. Accurate neutrophil recruitment is essential to combat microbes and to restore homeostasis, for inflammation modulation and resolution, wound healing and tissue repair. After fulfilling the appropriate effector functions, however, dampening neutrophil activation and infiltration is crucial to prevent damage to the host. In humans, chemoattractant molecules can be categorized into four biochemical families, i.e., chemotactic lipids, formyl peptides, complement anaphylatoxins and chemokines. They are critically involved in the tight regulation of neutrophil bone marrow storage and egress and in spatial and temporal neutrophil trafficking between organs. Chemoattractants function by activating dedicated heptahelical G protein-coupled receptors (GPCRs). In addition, emerging evidence suggests an important role for atypical chemoattractant receptors (ACKRs) that do not couple to G proteins in fine-tuning neutrophil migratory and functional responses. The expression levels of chemoattractant receptors are dependent on the level of neutrophil maturation and state of activation, with a pivotal modulatory role for the (inflammatory) environment. Here, we provide an overview -
Non-Redundant Dual Functions of the ZAP70 Catalytic and Scaffolding
ical C lin as C e Isakov, J Clinic Case Reports 2012, 2:6 f R o l e DOI: 10.4172/2165-7920.1000e113 a p n o r r t u s o J Journal of Clinical Case Reports ISSN: 2165-7920 Editorial Open Access ZAP70-Related SCID: Non-Redundant Dual Functions of the ZAP70 Catalytic and Scaffolding Regions Noah Isakov* The Shraga Segal Department of Microbiology and Immunology, Faculty of Health Sciences and the Cancer Research Center, Ben Gurion University of the Negev, P.O.B. 653, Beer Sheva 84105, Israel Primary Severe Combined Immunodeficiency (SCID) is a form rearrangement of the actin cytoskeleton. These transient intracellular of heritable immunodeficiency, characterized by impaired adaptive signals permit the activation of selected transcription factors that immune responses [1]. It includes a group of genetic disorders promote the proliferation and differentiation of T cells. originated by defects in one of several different genes that are critical Analysis of the phosphorylation sites of ZAP-70 and their impact for T lymphocyte production and/or function and involve defects in B on the function of the molecule demonstrated that phosphorylation lymphocytes as a primary or secondary cause [2]. of Tyr319, Tyr492 and Tyr493 serves to regulate the ZAP70 catalytic The most common type of SCID is linked to the X chromosome activity [23-25]. However, in vivo activation of T cells results in ZAP70 (X-SCID), and therefore affects only males [3,4]. The X-SCID males phosphorylation on additional tyrosine residues [26,27] which may possess mutations in the interleukin-2 (IL-2) receptor gamma chain also function as putative docking sites for SH2-containing proteins. -
Profiling Data
Compound Name DiscoveRx Gene Symbol Entrez Gene Percent Compound Symbol Control Concentration (nM) JNK-IN-8 AAK1 AAK1 69 1000 JNK-IN-8 ABL1(E255K)-phosphorylated ABL1 100 1000 JNK-IN-8 ABL1(F317I)-nonphosphorylated ABL1 87 1000 JNK-IN-8 ABL1(F317I)-phosphorylated ABL1 100 1000 JNK-IN-8 ABL1(F317L)-nonphosphorylated ABL1 65 1000 JNK-IN-8 ABL1(F317L)-phosphorylated ABL1 61 1000 JNK-IN-8 ABL1(H396P)-nonphosphorylated ABL1 42 1000 JNK-IN-8 ABL1(H396P)-phosphorylated ABL1 60 1000 JNK-IN-8 ABL1(M351T)-phosphorylated ABL1 81 1000 JNK-IN-8 ABL1(Q252H)-nonphosphorylated ABL1 100 1000 JNK-IN-8 ABL1(Q252H)-phosphorylated ABL1 56 1000 JNK-IN-8 ABL1(T315I)-nonphosphorylated ABL1 100 1000 JNK-IN-8 ABL1(T315I)-phosphorylated ABL1 92 1000 JNK-IN-8 ABL1(Y253F)-phosphorylated ABL1 71 1000 JNK-IN-8 ABL1-nonphosphorylated ABL1 97 1000 JNK-IN-8 ABL1-phosphorylated ABL1 100 1000 JNK-IN-8 ABL2 ABL2 97 1000 JNK-IN-8 ACVR1 ACVR1 100 1000 JNK-IN-8 ACVR1B ACVR1B 88 1000 JNK-IN-8 ACVR2A ACVR2A 100 1000 JNK-IN-8 ACVR2B ACVR2B 100 1000 JNK-IN-8 ACVRL1 ACVRL1 96 1000 JNK-IN-8 ADCK3 CABC1 100 1000 JNK-IN-8 ADCK4 ADCK4 93 1000 JNK-IN-8 AKT1 AKT1 100 1000 JNK-IN-8 AKT2 AKT2 100 1000 JNK-IN-8 AKT3 AKT3 100 1000 JNK-IN-8 ALK ALK 85 1000 JNK-IN-8 AMPK-alpha1 PRKAA1 100 1000 JNK-IN-8 AMPK-alpha2 PRKAA2 84 1000 JNK-IN-8 ANKK1 ANKK1 75 1000 JNK-IN-8 ARK5 NUAK1 100 1000 JNK-IN-8 ASK1 MAP3K5 100 1000 JNK-IN-8 ASK2 MAP3K6 93 1000 JNK-IN-8 AURKA AURKA 100 1000 JNK-IN-8 AURKA AURKA 84 1000 JNK-IN-8 AURKB AURKB 83 1000 JNK-IN-8 AURKB AURKB 96 1000 JNK-IN-8 AURKC AURKC 95 1000 JNK-IN-8 -
ILC2 Activation by Protozoan Commensal Microbes
International Journal of Molecular Sciences Review ILC2 Activation by Protozoan Commensal Microbes Kyle Burrows 1 , Louis Ngai 1 , Flora Wong 1,2, David Won 1 and Arthur Mortha 1,* 1 University of Toronto, Department of Immunology, Toronto, ON M5S 1A8, Canada; [email protected] (K.B.) [email protected] (L.N.); fl[email protected] (F.W.); [email protected] (D.W.) 2 Ranomics, Inc. Toronto, ON M5G 1X5, Canada * Correspondence: [email protected] Received: 3 September 2019; Accepted: 27 September 2019; Published: 30 September 2019 Abstract: Group 2 innate lymphoid cells (ILC2s) are a member of the ILC family and are involved in protective and pathogenic type 2 responses. Recent research has highlighted their involvement in modulating tissue and immune homeostasis during health and disease and has uncovered critical signaling circuits. While interactions of ILC2s with the bacterial microbiome are rather sparse, other microbial members of our microbiome, including helminths and protozoans, reveal new and exciting mechanisms of tissue regulation by ILC2s. Here we summarize the current field on ILC2 activation by the tissue and immune environment and highlight particularly new intriguing pathways of ILC2 regulation by protozoan commensals in the intestinal tract. Keywords: ILC2; protozoa; Trichomonas; Tritrichomonas musculis; mucosal immunity; taste receptors; succinate; intestinal immunity; type 2 immunity; commensals 1. The ILC Lineage 1.1. The Family of Innate Lymphoid Cells Research over the last decade has redirected focus away from classical immune cell interactions within lymphoid tissues towards immunity within non-lymphoid tissues. Within these tissues, immune interactions involve local adaptation and rapid responses by tissue-resident immune cells.