PILRA Antibody Cat

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PILRA Antibody Cat. No.: 30-252 PILRA Antibody Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human Antibody produced in rabbits immunized with a synthetic peptide corresponding a region IMMUNOGEN: of human PILRA. TESTED APPLICATIONS: ELISA, WB PILRA antibody can be used for detection of PILRA by ELISA at 1:1562500. PILRA antibody APPLICATIONS: can be used for detection of PILRA by western blot at 0.5 μg/mL, and HRP conjugated secondary antibody should be diluted 1:50,000 - 100,000. POSITIVE CONTROL: 1) Cat. No. 1211 - HepG2 Cell Lysate PREDICTED MOLECULAR 18 kDa WEIGHT: Properties PURIFICATION: Antibody is purified by peptide affinity chromatography method. CLONALITY: Polyclonal CONJUGATE: Unconjugated PHYSICAL STATE: Liquid September 25, 2021 1 https://www.prosci-inc.com/pilra-antibody-30-252.html Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% BUFFER: sucrose. CONCENTRATION: batch dependent For short periods of storage (days) store at 4˚C. For longer periods of storage, store PILRA STORAGE CONDITIONS: antibody at -20˚C. As with any antibody avoid repeat freeze-thaw cycles. Additional Info OFFICIAL SYMBOL: PILRA ALTERNATE NAMES: PILRA, FDF03 ACCESSION NO.: NP_840057 PROTEIN GI NO.: 30179907 GENE ID: 29992 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References Cell signaling pathways rely on a dynamic interaction between activating and inhibiting processes. SHP-1-mediated dephosphorylation of protein tyrosine residues is central to the regulation of several cell signaling pathways. Two types of inhibitory receptor superfamily members are immunoreceptor tyrosine-based inhibitory motif (ITIM)-bearing receptors and their non-ITIM-bearing, activating counterparts. Control of cell signaling via SHP-1 is thought to occur through a balance between PILRalpha-mediated inhibition and PILRbeta-mediated activation. This particular gene encodes the ITIM-bearing member of the receptor pair, which functions in the inhibitory role.Cell signaling pathways rely on a dynamic interaction between activating and inhibiting processes. SHP-1-mediated BACKGROUND: dephosphorylation of protein tyrosine residues is central to the regulation of several cell signaling pathways. Two types of inhibitory receptor superfamily members are immunoreceptor tyrosine-based inhibitory motif (ITIM)-bearing receptors and their non- ITIM-bearing, activating counterparts. Control of cell signaling via SHP-1 is thought to occur through a balance between PILRalpha-mediated inhibition and PILRbeta-mediated activation. These paired immunoglobulin-like receptor genes are located in a tandem head-to-tail orientation on chromosome 7. This particular gene encodes the ITIM-bearing member of the receptor pair, which functions in the inhibitory role. Alternative splicing has been observed at this locus and three variants, each encoding a distinct isoform, are described. REFERENCES: 1) Satoh, T., (2008) Cell 132 (6), 935-944. ANTIBODIES FOR RESEARCH USE ONLY. For additional information, visit ProSci's Terms & Conditions Page. September 25, 2021 2 https://www.prosci-inc.com/pilra-antibody-30-252.html.

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Blood Flow Guides Sequential Support of Neutrophil Arrest and Diapedesis
RESEARCH ARTICLE Blood flow guides sequential support of neutrophil arrest and diapedesis by PILR-b 1 and PILR-a Yu-Tung Li, Debashree Goswami†, Melissa Follmer, Annette Artz, Mariana Pacheco-Blanco, Dietmar Vestweber* Vascular Cell Biology, Max Planck Institute of Molecular Biomedicine, Mu¨ nster, Germany Abstract Arrest of rapidly flowing neutrophils in venules relies on capturing through selectins and chemokine-induced integrin activation. Despite a long-established concept, we show here that gene inactivation of activating paired immunoglobulin-like receptor (PILR)-b1 nearly halved the efficiency of neutrophil arrest in venules of the mouse cremaster muscle. We found that this receptor binds to CD99, an interaction which relies on flow-induced shear forces and boosts chemokine-induced b2-integrin-activation, leading to neutrophil attachment to endothelium. Upon arrest, binding of PILR-b1 to CD99 ceases, shifting the signaling balance towards inhibitory PILR-a. This enables integrin deactivation and supports cell migration. Thus, flow-driven shear forces guide sequential signaling of first activating PILR-b1 followed by inhibitory PILR-a to prompt neutrophil arrest and then transmigration. This doubles the efficiency of selectin-chemokine driven neutrophil arrest by PILR-b1 and then supports transition to migration by PILR-a. DOI: https://doi.org/10.7554/eLife.47642.001 *For correspondence: [email protected] Present address: †Center for Global Infectious Disease Introduction Research, Seattle Childrens Host defense against pathogens depends on the recruitment of leukocytes to sites of infections Research Institute, Seattle, (Ley et al., 2007). Selectins capture leukocytes to the endothelial cell surface by binding to glyco- United States conjugates (McEver, 2015).
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Epistatic Interactions of Genetic Loci Associated with Age-Related
www.nature.com/scientificreports OPEN Epistatic interactions of genetic loci associated with age‑related macular degeneration Christina Kiel1,3, Christoph A. Nebauer1,3, Tobias Strunz1,3, Simon Stelzl1 & Bernhard H. F. Weber 1,2* The currently largest genome‑wide association study (GWAS) for age‑related macular degeneration (AMD) defnes disease association with genome‑wide signifcance for 52 independent common and rare genetic variants across 34 chromosomal loci. Overall, these loci contain over 7200 variants and are enriched for genes with functions indicating several shared cellular processes. Still, the precise mechanisms leading to AMD pathology are largely unknown. Here, we exploit the phenomenon of epistatic interaction to identify seemingly independent AMD‑associated variants that reveal joint efects on gene expression. We focus on genetic variants associated with lipid metabolism, organization of extracellular structures, and innate immunity, specifcally the complement cascade. Multiple combinations of independent variants were used to generate genetic risk scores allowing gene expression in liver to be compared between low and high‑risk AMD. We identifed genetic variant combinations correlating signifcantly with expression of 26 genes, of which 19 have not been associated with AMD before. This study defnes novel targets and allows prioritizing further functional work into AMD pathobiology. A frst successful genome-wide association study (GWAS) was reported in 2005 and identifed with genome- wide signifcance genetic variants at the CFH locus associated with age-related macular degeneration (AMD), a complex disease which is a frequent cause of progressive vision loss in the elderly population 1. Since then, the list of AMD-associated genetic variation has grown exponentially, presently bringing the total to 52 independent common and rare variants across 34 chromosomal loci2.
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Distribution of Cellular HSV-1 Receptor Expression in Human Brain
J. Neurovirol. DOI 10.1007/s13365-016-0504-x Distribution of cellular HSV-1 receptor expression in human brain Richard Lathe1 & Juergen G. Haas1 Received: 7 September 2016 /Revised: 23 November 2016 /Accepted: 1 December 2016 # The Author(s) 2016. This article is published with open access at Springerlink.com Abstract Herpes simplex virus type 1 (HSV-1) is a neuro- hippocampus are likely to underlie the susceptibility of this tropic virus linked to a range of acute and chronic neurological brain region to HSV-1 infection. disorders affecting distinct regions of the brain. Unusually, HSV-1 entry into cells requires the interaction of viral proteins Keywords HSV-1 . Brain . Hippocampus . Virus receptor . glycoprotein D (gD) and glycoprotein B (gB) with distinct Glycoprotein D . Glycoprotein B . MAG . MYH9 . PILRA . cellular receptor proteins. Several different gD and gB recep- PVRL1/nectin 1 . TNFRSF14/HVEM tors have been identified, including TNFRSF14/HVEM and PVRL1/nectin 1 as gD receptors and PILRA, MAG, and MYH9 as gB receptors. We investigated the expression of Introduction these receptor molecules in different areas of the adult and developing human brain using online transcriptome data- Infection with herpes simplex virus type 1 and 2 (HSV-1/2) bases. Whereas all HSV-1 receptors showed distinct expres- causes orofacial, genital, cerebral, and ocular disorders. In sion patterns in different brain areas, the Allan Brain Atlas particular, HSV-1 has been implicated in diverse acute and (ABA) reported increased expression of both gD and gB re- chronic neurological diseases including meningitis, encepha- ceptors in the hippocampus. Specifically, for PVRL1, litis, and epilepsy (Gilden et al.
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Engineered Type 1 Regulatory T Cells Designed for Clinical Use Kill Primary
ARTICLE Acute Myeloid Leukemia Engineered type 1 regulatory T cells designed Ferrata Storti Foundation for clinical use kill primary pediatric acute myeloid leukemia cells Brandon Cieniewicz,1* Molly Javier Uyeda,1,2* Ping (Pauline) Chen,1 Ece Canan Sayitoglu,1 Jeffrey Mao-Hwa Liu,1 Grazia Andolfi,3 Katharine Greenthal,1 Alice Bertaina,1,4 Silvia Gregori,3 Rosa Bacchetta,1,4 Norman James Lacayo,1 Alma-Martina Cepika1,4# and Maria Grazia Roncarolo1,2,4# Haematologica 2021 Volume 106(10):2588-2597 1Department of Pediatrics, Division of Stem Cell Transplantation and Regenerative Medicine, Stanford School of Medicine, Stanford, CA, USA; 2Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA, USA; 3San Raffaele Telethon Institute for Gene Therapy, Milan, Italy and 4Center for Definitive and Curative Medicine, Stanford School of Medicine, Stanford, CA, USA *BC and MJU contributed equally as co-first authors #AMC and MGR contributed equally as co-senior authors ABSTRACT ype 1 regulatory (Tr1) T cells induced by enforced expression of interleukin-10 (LV-10) are being developed as a novel treatment for Tchemotherapy-resistant myeloid leukemias. In vivo, LV-10 cells do not cause graft-versus-host disease while mediating graft-versus-leukemia effect against adult acute myeloid leukemia (AML). Since pediatric AML (pAML) and adult AML are different on a genetic and epigenetic level, we investigate herein whether LV-10 cells also efficiently kill pAML cells. We show that the majority of primary pAML are killed by LV-10 cells, with different levels of sensitivity to killing. Transcriptionally, pAML sensitive to LV-10 killing expressed a myeloid maturation signature.
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Human PILR‑Α Alexa Fluor® 750‑Conjugated Antibody
Human PILR‑α Alexa Fluor® 750‑conjugated Antibody Recombinant Monoclonal Rabbit IgG Clone # 2175D Catalog Number: FAB64841S 100 µg DESCRIPTION Species Reactivity Human Specificity Detects human PILR-α in direct ELISAs. Source Recombinant Monoclonal Rabbit IgG Clone # 2175D Purification Protein A or G purified from cell culture supernatant Immunogen Mouse myeloma cell line NS0-derived recombinant human PILR-α with a C-terminal 6-His tag Gln20-Thr196 Accession # Q9UKJ1 Conjugate Alexa Fluor 750 Excitation Wavelength: 749 nm Emission Wavelength: 775 nm Formulation Supplied 0.2 mg/mL in a saline solution containing BSA and Sodium Azide. *Contains <0.1% Sodium Azide, which is not hazardous at this concentration according to GHS classifications. Refer to the Safety Data Sheet (SDS) for additional information and handling instructions. APPLICATIONS Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website. Recommended Sample Concentration Flow Cytometry 0.25-1 µg/106 cells HEK293 Human Cell Line Transfected with Human PILR-alpha and eGFP PREPARATION AND STORAGE Shipping The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below. Stability & Storage Protect from light. Do not freeze. 12 months from date of receipt, 2 to 8 °C as supplied. BACKGROUND Paired immunoglobulin-like type 2 receptor alpha (PILRa; also inhibitory receptor PILR-alpha) are 44-50 kDa paired receptors that consist of highly related activating and inhibitory receptors, and are widely involved in the regulation of the immune system. PILR-α is thought to act as a cellular signaling inhibitory receptor by recruiting cytoplasmic phosphatases like PTPN6/SHP-1 and PTPN11/SHP-2 via their SH2 domains that block signal transduction through dephosphorylation of signaling molecules.
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Manifestations of Genetic Risk for Alzheimer's Disease in the Blood
bioRxiv preprint doi: https://doi.org/10.1101/2021.03.26.437267; this version posted March 28, 2021. 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. Manifestations of genetic risk for Alzheimer’s Disease in the blood: a cross-sectional multi- omic analysis in healthy adults aged 18-90+ Laura Heath1,2,*, John C. Earls1,3, Andrew T. Magis1, Sergey A. Kornilov1, Jennifer C. Lovejoy1, Cory C. Funk1, Noa Rappaport1, Benjamin A. Logsdon2, Lara M. Mangravite2, Brian W. Kunkle4,5, Eden R. Martin4,5, Adam C. Naj6,7, Nilüfer Ertekin-Taner8,9, Todd E. Golde10, Leroy Hood1,10, Nathan D. Price1,3,*, Alzheimer’s Disease Genetics Consortium 1Institute for Systems Biology, Seattle, WA 2Sage Bionetworks, Seattle, WA 3Onegevity, a division of Thorne HealthTech, New York, NY 4John P. Hussman Institute for Human Genomics, University of Miami Miller School of Medicine, Miami, FL 5Dr. John T. Macdonald Foundation Department of Human Genetics, University of Miami Miller School of Medicine, Miami, FL 6Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 7Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 8Mayo Clinic, Department of Neurology, Jacksonville, FL 9Mayo Clinic, Department of Neuroscience, Jacksonville, FL 10Department of Neuroscience, College of Medicine, Center for Translational Research in Neurodegenerative Disease University of Florida, McKnight Brain Institute, Gainesville, FL 11Providence St.
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Alzheimer's Disease Risk Polymorphisms Regulate
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Common Variants in Alzheimer's Disease
medRxiv preprint doi: https://doi.org/10.1101/19012021; this version posted January 17, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license . Common variants in Alzheimer’s disease: Novel association of six genetic variants with AD and risk stratification by polygenic risk scores Itziar de Rojas1,2*, Sonia Moreno-Grau1,2*, Niccolò Tesi3,4*, Benjamin Grenier-Boley5*, Victor Andrade6,7*, Iris Jansen3,8*, Nancy L. Pedersen9, Najada Stringa10, Anna Zettergren11, Isabel Hernández1,2, Laura Montrreal1, Carmen Antúnez12, Anna Antonell13, Rick M. Tankard14, Joshua C. Bis15, Rebecca Sims16,17, Céline Bellenguez5, Inés Quintela18, Antonio González-Perez19, Miguel Calero20,21,2, Emilio Franco22, Juan Macías23, Rafael Blesa24,2, Manuel Menéndez-González25,26, Ana Frank-García27,28,29,2, Jose Luís Royo30, Fermín Moreno31,2, Raquel Huerto32,33, Miquel Baquero34, Mónica Diez-Fairen35, Carmen Lage36,2, Sebastian Garcia-Madrona37, Pablo García1, Emilio Alarcón-Martín30,1, Sergi Valero1,2, Oscar Sotolongo-Grau1, EADB, GR@ACE, DEGESCO, IGAP (ADGC, CHARGE, EADI, GERAD) and PGC- ALZ Consortia, Guillermo Garcia-Ribas37, Pascual Sánchez-Juan36,2, Pau Pastor35, Jordi Pérez-Tur38,34,2, Gerard Piñol-Ripoll32,33, Adolfo Lopez de Munain31,39, Jose María García-Alberca40, María J. Bullido41,28,29,2, Victoria Álvarez25,26, Alberto Lleó24,2, Luis M. Real23,42, Pablo Mir43,2, Miguel Medina2,21, Philip Scheltens10, Henne Holstege10,4, Marta Marquié1, María Eugenia Sáez19, Ángel Carracedo18,44, Philippe Amouyel5, Julie Williams16,17, Sudha Seshadri45,46,47, Cornelia M.
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Enhancer Variants Associated With
Kikuchi et al. BMC Medical Genomics (2019) 12:128 https://doi.org/10.1186/s12920-019-0574-8 RESEARCH ARTICLE Open Access Enhancer variants associated with Alzheimer’s disease affect gene expression via chromatin looping Masataka Kikuchi1* , Norikazu Hara2, Mai Hasegawa1, Akinori Miyashita2, Ryozo Kuwano2,3, Takeshi Ikeuchi2 and Akihiro Nakaya1* Abstract Background: Genome-wide association studies (GWASs) have identified single-nucleotide polymorphisms (SNPs) that may be genetic factors underlying Alzheimer’s disease (AD). However, how these AD-associated SNPs (AD SNPs) contribute to the pathogenesis of this disease is poorly understood because most of them are located in non-coding regions, such as introns and intergenic regions. Previous studies reported that some disease-associated SNPs affect regulatory elements including enhancers. We hypothesized that non-coding AD SNPs are located in enhancers and affect gene expression levels via chromatin loops. Methods: To characterize AD SNPs within non-coding regions, we extracted 406 AD SNPs with GWAS p-values of less than 1.00 × 10− 6 from the GWAS catalog database. Of these, we selected 392 SNPs within non-coding regions. Next, we checked whether those non-coding AD SNPs were located in enhancers that typically regulate gene expression levels using publicly available data for enhancers that were predicted in 127 human tissues or cell types. We sought expression quantitative trait locus (eQTL) genes affected by non-coding AD SNPs within enhancers because enhancers are regulatory elements that influence the gene expression levels. To elucidate how the non- coding AD SNPs within enhancers affect the gene expression levels, we identified chromatin-chromatin interactions by Hi-C experiments.
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