Cardiovascular Disease Products

Total Page:16

File Type:pdf, Size:1020Kb

Cardiovascular Disease Products Cardiovascular Disease Products For more information, visit: www.bosterbio.com Cardiovascular Disease Research Cardiovascular disease is the leading cause of death in developed nations. Boster Bio aims to supply researchers with high-quality antibodies and ELISA kits so they can make new discoveries and help save lives. In this catalogue you will find a comprehensive list of high-affinity Boster antibodies and high sensitivity Boster ELISA kits targeted at proteins associated with cardiovascular disease. Boster: The Fastest Growing About Bosterbio Antibody Company In 2015 Boster is an antibody manufacturer founded in 1993 by histologist Steven Xia. Over the past two decades, Boster and its products have been cited in over 20,000 publications and counting. The firm specializes in developing antibodies and ELISA kits that feature high affinity, Boster Bio received the CitaAb award for high specificity at affordable the greatest increase in number of prices. citations during 2015 than any other antibody manufacturer. Table of Contents Boster Cardiovascular Disease Related Antibodies…………..………..... 2 Boster Cardiovascular Disease Related ELISA Kits……………………..…. 9 1 High Affinity Boster Antibodies Boster supplies only the highest quality antibodies. Our high-affinity polyclonal and monoclonal antibodies are thoroughly validated by Western Blotting, Immunohistochemistry and ELISA. This is our comprehensive catalog of our antibody products related to cardiovascular disease, sorted in alphabetical order by target gene name. Catalog No Product Name Gene Name Applications Reactivity PB9242 Anti-Fetuin A AHSG WB Mouse PB9123 Anti-AAMP AAMP IHC-P Human PA1723 Anti-ABCB6 ABCB6 IHC-P Human PA1871 Anti-ABCG5 ABCG5 WB Human PB9415 Anti-ABCG5 ABCG5 WB Human PA2196-1 Anti-ACE ACE IHC-P Human PB9124 Anti-ACE ACE IHC-P Human PA2196-2 Anti-ACE ACE WB Human PA2071 Anti-ADAMTS1 ADAMTS1 WB Mouse PA1461 Anti-ADAMTS2 ADAMTS2 IHC-P Human PB9001 Anti-Adiponectin ADIPOQ IHC-P Human PB9011 Anti-Adiponectin ADIPOQ IHC-P Mouse PA2014 Anti-Adiponectin ADIPOQ WB Human PB9418 Anti-ADIPOR1 ADIPOR1 WB Human MA1001 Anti-AFP AFP IHC-P Human PB9090 Anti-AFP AFP IHC-P Human PA1421 Anti-Fetuin A AHSG WB Human PA1485 Anti-12 Lipoxygenase ALOX12 IHC-P Human PA1485-1 Anti-12 Lipoxygenase ALOX12 WB Human PB9125 Anti-Angiopoietin-1 ANGPT1 WB Human RP1037 Anti-Angiopoietin-2 ANGPT2 IHC-P Human PA1005 Anti-Angiopoietin-2 ANGPT2 WB Human PA1487 Anti-ANGPTL1 ANGPTL1 WB Human PA2075 Anti-ANGPTL3 ANGPTL3 WB Human PA1435 Anti-ANGPTL4 ANGPTL4 WB Human PA1007-1 Anti-Annexin IV ANXA4 IHC-P Human PA1007 Anti-Annexin IV ANXA4 IHC-P Human PA1500 Anti-Annexin VIII ANXA8 WB Human PB9844 Anti-APOA1 APOA1 IHC-P Mouse PB9845 Anti-APOA1 APOA1 IHC-P Rat PA1247 Anti-APOA1 APOA1 WB Human PA1439 Anti-Carbonic Anhydrase III CA3 IHC-P Human PB9371 Anti-CD36/SR-B3 CD36 IHC-P Human 3 Antibodies: A-Z by Target Gene Name This Page: AAM-CD6 Catalog No Product Name Gene Name Applications Reactivity PB9930 Anti-CD9 CD9 IHC-P Mouse PA1459 Anti-CEBP Alpha CEBPA IHC-P Human PA2019 Anti-CETP CETP WB Human PA1521 Anti-Collagen IV COL4A2 IHC-P Human PB9998 Anti-TAFI/CPB2 CPB2 WB Mouse PA1905 Anti-CSF1R/M-CSFR CSF1R WB Human PB9541 Anti-CTGF CTGF IHC-P Human PB9856 Anti-Cathepsin K CTSK IHC-P Human PA2021 Anti-CXCR5 CXCR5 WB Human PA1118 Anti-Cytochrome C CYCS IHC-P Human PB9334 Anti-Cytochrome C CYCS IHC-P Human PA1657 Anti-Cytoglobin CYGB WB Human PA1698 Anti-CYP11A1 CYP11A1 IHC-P Human PA1698-1 Anti-CYP11A1 CYP11A1 WB Mouse PB9942 Anti-CYP11A1 CYP11A1 WB Human PA1699 Anti-CYP11B1 CYP11B1 WB Human PA1489 Anti-Aromatase CYP19A1 IHC-P Human PA2107 Anti-Aromatase CYP19A1 IHC-P Rat PB9544 Anti-CYP1A1 CYP1A1 IHC-P Human PA1907 Anti-Cytochrome P450 1A2 CYP1A2 IHC-P Human PB9545 Anti-CYP1A2 CYP1A2 IHC-P Human PB9546 Anti-CYP1B1 CYP1B1 IHC-P Human PB9547 Anti-CYP24A1 CYP24A1 IHC-P Human PA1397 Anti-Cytochrome P450 2D6 CYP2D6 IHC-P Mouse PA1909 Anti-Cytochrome P450 2E1 CYP2E1 IHC-P Mouse PA1116 Anti-Cytochrome P450 20 CYP2E1 IHC-P Human PB9190 Anti-CYP2E1 CYP2E1 IHC-P Human PA1908 Anti-Cytochrome P450 2E1 CYP2E1 WB Human PA2022 Anti-CYP2U1 CYP2U1 IHC-P Human PA1940 Anti-CYP7A1 CYP7A1 IHC-P Human RP1079 Anti-CYP7A1 CYP7A1 WB Human PB9549 Anti-CYR61/CCN1 CYR61 WB Human PA1129-1 Anti-HIF-2-Alpha EPAS1 IHC-P Rat PA1129-2 Anti-HIF-2-Alpha EPAS1 WB Human PA1744 Anti-Eph Receptor A2 EPHA2 IHC-P Human PA1568 Anti-Eph Receptor A3 EPHA3 IHC-P Human PB9583 Anti-Eph Receptor A5 EPHA5 WB Human PB9584 Anti-Eph Receptor B1 EPHB1 IHC-P Human PA1569 Anti-Eph Receptor B3 EPHB3 IHC-P Human PB9701 Anti-Tissue factor/F3 F3 WB Human PB9702 Anti-Tissue factor/F3 F3 WB Mouse PA2061 Anti-Factor VIII F8 WB Human 4 Antibodies: A-Z by Target Gene Name This Page: CD9-F9 Catalog No Product Name Gene Name Applications Reactivity PA1336 Anti-Cardiac FABP FABP3 IHC-P Human PB9759 Anti-Cardiac FABP FABP3 IHC-P Human RP1085 Anti-FABP4 FABP4 IHC-P Human PA1209 Anti-FABP4 FABP4 WB Human PA1475 Anti-Fatty Acid Binding Protein 5 FABP5 IHC-P Human PA1853 Anti-Fatty Acid Binding Protein 5 FABP5 IHC-P Mouse PB9865 Anti-FASN FASN IHC-P Human PA1311 Anti-FGF1 FGF1 WB Human PB9241 Anti-FGF1 FGF1 WB Human PA1454 Anti-FGF10 FGF10 WB Human PA1032 Anti-FGF2 FGF2 IHC-P Human PB9587 Anti-FGF2 FGF2 WB Human PA1673 Anti-FGF21 FGF21 WB Human PA1033 Anti-FGF4 FGF4 WB Human PA1216 Anti-FGF8 FGF8 IHC-P Human PA1216-1 Anti-FGF8 FGF8 IHC-P Human PA1453 Anti-FGF9 FGF9 IHC-P Human PA1477 Anti-FGFR1 FGFR1 IHC-P Human PA1241 Anti-FGFR2 FGFR2 IHC-P Human PA1241-1 Anti-FGFR2 FGFR2 WB Human PA2143 Anti-FGFR3 FGFR3 IHC-P Human PB9193 Anti-FGFR4 FGFR4 IHC-P Human PA1332 Anti-VEGFD FIGF IHC-P Human PB9869 Anti-VEGFD FIGF WB Human PA1399 Anti-sVEGFR1/sFLT1 FLT1 WB Human PA1966-1 Anti-sVEGFR1/sFLT1 FLT1 WB Rat PA1966-2 Anti-sVEGFR1/sFLT1 FLT1 WB Mouse PA1966 Anti-sVEGFR1/sFLT1 FLT1 WB Rat PA1914 Anti-Flt-3ligand FLT3LG WB Human PB9588 Anti-Flt-3ligand FLT3LG WB Human PB9707 Anti-GNAQ GNAQ IHC-P Human PA1590 Anti-GST3/GST Pi GSTP1 IHC-P Human PB9184 Anti-GST3/GST Pi GSTP1 IHC-P Human PA1040 Anti-GST3/GST Pi GSTP1 WB Human PA2145 Anti-HIF3 HIF3A WB Human PB9277 Anti-HSPG2 HSPG2 IHC-P Human PA1353 Anti-IL-8 IL8 IHC-P Human PB10003 Anti-Alpha Internexin INA IHC-P Human PA1750 Anti-INPPL1 INPPL1 IHC-P Human PB9647 Anti-ITGA2B ITGA2B IHC-P Human PA2226 Anti-ITGA7 ITGA7 WB Human PA1405 Anti-Integrin Alpha V ITGAV IHC-P Human 5 Antibodies: A-Z by Target Gene Name This Page: FAB-ITG Catalog No Product Name Gene Name Applications Reactivity PB10004 Anti-ITLN1 ITLN1 IHC-P Human PB9651 Anti-KCNA5 KCNA5 WB Human PA2272 Anti-CSEN KCNIP3 WB Human MA1040 Anti-VEGFR2/KDR KDR IHC-F Human PA1989 Anti-VEGFR2/KDR KDR IHC-P Human PB9429 Anti-VEGFR2/KDR KDR WB Human PA1888 Anti-KLF3 KLF3 WB Human PA1625 Anti-KLK1 KLK1 IHC-P Human PA1633 Anti-KLK1 KLK1 IHC-P Rat PA1709 Anti-KLK1 KLK1 IHC-P Mouse PA2038 Anti-KLK1 KLK1 IHC-P Mouse PB9655 Anti-Kininogen-1/KNG1 KNG1 IHC-P Mouse PB9278 Anti-Kininogen-1/KNG1 KNG1 WB Human MA1054 Anti-Laminin LAMA1 IHC-P Feline PA1581 Anti-Laminin Gamma 1 LAMC1 IHC-P Human PB9142 Anti-Laminin LAMC1 IHC-P Human PA1967 Anti-LCAT LCAT WB Human PB9657 Anti-LCAT LCAT WB Human PA1304 Anti-LipoProtein Lipase LPL WB Bovine PA2273 Anti-LRP5 LRP5 WB Human PA2083 Anti-MADCAM-1 MADCAM1 IHC-P Human PB9058 Anti-CD10/Neprilysin MME IHC-P Human PB9725 Anti-MMP-1 MMP1 WB Human PA1380 Anti-MMP10 MMP10 WB Human PB9670 Anti-MMP10 MMP10 WB Human PA2146 Anti-MMP-12 MMP12 WB Human PA2147 Anti-MMP-14 MMP14 IHC-P Human PA1115 Anti-MMP-14 MMP14 IHC-P Human PB9283 Anti-MMP-14 MMP14 WB Human PA1123 Anti-MMP16 MMP16 IHC-P Human PA1122-2 Anti-MMP-2 MMP2 IHC-P Human PB9267 Anti-MMP-3 MMP3 WB Human PA1471 Anti-MMP-7 MMP7 IHC-P Mouse PA1207 Anti-MMP-8 MMP8 IHC-P Human PB10008 Anti-MMP-9 MMP9 IHC-P Mouse PA1357 Anti-MMP-9 MMP9 WB Human PA1929 Anti-NADPH Oxidase 4 NOX4 IHC-P Human PA1930 Anti-NOXA1 NOXA1 WB Human PB9295 Anti-ANP NPPA WB Human PA1246 Anti-LXR Alpha NR1H3 WB Human PA1246-1 Anti-LXR Alpha NR1H3 WB Human PB9729 Anti-NR2F2 NR2F2 WB Human 6 Antibodies: A-Z by Target Gene Name This Page: ITL-NR2 Catalog No Product Name Gene Name Applications Reactivity PB9300 Anti-Neuropilin-1 NRP1 IHC-P Human PA1752 Anti-Neuropilin-1 NRP1 WB Human PA1832 Anti-LOX-1/OLR1 OLR1 WB Human PA1833 Anti-LOX-1/OLR1 OLR1 WB Human PA1949 Anti-OSBP1 OSBP WB Human PB9311 Anti-PDGF-BB PDGFB WB Human PA1678 Anti-PDGF Receptor Alpha PDGFRA IHC-P Human PB9771 Anti-PDGFRA PDGFRA IHC-P Human PA1411 Anti-Podoplanin/gp36 PDPN WB Human PA1674 Anti-Podoplanin/gp36 PDPN WB Human PA1675 Anti-Podoplanin/gp36 PDPN WB Mouse PA2045 Anti-PGK1 PGK1 IHC-P Human PB9774 Anti-PGK1 PGK1 WB Human PB9775 Anti-PGRMC1 PGRMC1 IHC-P Human PA2278 Anti-Plakophilin 2 PKP2 WB Human PA1344 Anti-uPAR PLAUR IHC-P Human PB9380 Anti-PLD1 PLD1 WB Human PA2228 Anti-PLTP PLTP IHC-P Human PA1211 Anti-COX2/Cyclooxygenase 2 PTGS2 IHC-P Human PA1725 Anti-COX2/Cyclooxygenase 2 PTGS2 IHC-P Human PB9138 Anti-COX2/Cyclooxygenase 2 PTGS2 WB Human PA1574 Anti-FAK PTK2 WB Human PB9674 Anti-FAK PTK2 WB Human PB9885 Anti-RNH1 RNH1 WB Human PA1896 Anti-Syndecan 2 SDC2 IHC-P Human PA1359 Anti-sL-Selectin SELL WB Mouse PA1715 Anti-P-Selectin SELP IHC-P Human PA1638 Anti-Kallistatin/Serpina4 SERPINA4 IHC-P Human PA2218 Anti-Serpin C1/Antithrombin-III SERPINC1 WB Human PA1933 Anti-Prosurfactant Protein C SFTPC WB Human PA2169 Anti-NKCC1 SLC12A2 IHC-P Human PA1431 Anti-OPN SPP1 IHC-P Human PA1432 Anti-OPN SPP1 IHC-P Mouse MA1090 Anti-Spectrin(Alpha And Beta) (Monoclonal,SPTA1 SB-SP1) WB Human PA1777 Anti-SPTLC1 SPTLC1 IHC-P Human PB9894 Anti-SPTLC1 SPTLC1 IHC-P Human PB9822 Anti-SULT2B1 SULT2B1
Recommended publications
  • Epha4/Tie2 Crosstalk Regulates Leptomeningeal Collateral Remodeling Following Ischemic Stroke
    EphA4/Tie2 crosstalk regulates leptomeningeal collateral remodeling following ischemic stroke Benjamin Okyere, … , John B. Matson, Michelle H. Theus J Clin Invest. 2019. https://doi.org/10.1172/JCI131493. Research In-Press Preview Neuroscience Vascular biology Leptomeningeal anastomoses or pial collateral vessels play a critical role in cerebral blood flow (CBF) restoration following ischemic stroke. The magnitude of this adaptive response is postulated to be controlled by the endothelium, although the underlying molecular mechanisms remain under investigation. Here we demonstrated that endothelial genetic deletion, using EphA4f/f/Tie2-Cre and EphA4f/f/VeCahderin-CreERT2 mice and vessel painting strategies, implicated EphA4 receptor tyrosine kinase as a major suppressor of pial collateral remodeling, CBF and functional recovery following permanent middle cerebral artery occlusion. Pial collateral remodeling is limited by the cross talk between EphA4-Tie2 signaling in vascular endothelial cells, which is mediated through p-Akt regulation. Furthermore, peptide inhibition of EphA4 resulted in acceleration of the pial arteriogenic response. Our findings demonstrate EphA4 is a negative regulator of Tie2 receptor signaling which limits pial collateral arteriogenesis following cerebrovascular occlusion. Therapeutic targeting of EphA4 and/or Tie2 represents an attractive new strategy for improving collateral function, neural tissue health and functional recovery following ischemic stroke. Find the latest version: https://jci.me/131493/pdf 1 EphA4/Tie2
    [Show full text]
  • PLATFORM ABSTRACTS Abstract Abstract Numbers Numbers Tuesday, November 6 41
    American Society of Human Genetics 62nd Annual Meeting November 6–10, 2012 San Francisco, California PLATFORM ABSTRACTS Abstract Abstract Numbers Numbers Tuesday, November 6 41. Genes Underlying Neurological Disease Room 134 #196–#204 2. 4:30–6:30pm: Plenary Abstract 42. Cancer Genetics III: Common Presentations Hall D #1–#6 Variants Ballroom 104 #205–#213 43. Genetics of Craniofacial and Wednesday, November 7 Musculoskeletal Disorders Room 124 #214–#222 10:30am–12:45 pm: Concurrent Platform Session A (11–19): 44. Tools for Phenotype Analysis Room 132 #223–#231 11. Genetics of Autism Spectrum 45. Therapy of Genetic Disorders Room 130 #232–#240 Disorders Hall D #7–#15 46. Pharmacogenetics: From Discovery 12. New Methods for Big Data Ballroom 103 #16–#24 to Implementation Room 123 #241–#249 13. Cancer Genetics I: Rare Variants Room 135 #25–#33 14. Quantitation and Measurement of Friday, November 9 Regulatory Oversight by the Cell Room 134 #34–#42 8:00am–10:15am: Concurrent Platform Session D (47–55): 15. New Loci for Obesity, Diabetes, and 47. Structural and Regulatory Genomic Related Traits Ballroom 104 #43–#51 Variation Hall D #250–#258 16. Neuromuscular Disease and 48. Neuropsychiatric Disorders Ballroom 103 #259–#267 Deafness Room 124 #52–#60 49. Common Variants, Rare Variants, 17. Chromosomes and Disease Room 132 #61–#69 and Everything in-Between Room 135 #268–#276 18. Prenatal and Perinatal Genetics Room 130 #70–#78 50. Population Genetics Genome-Wide Room 134 #277–#285 19. Vascular and Congenital Heart 51. Endless Forms Most Beautiful: Disease Room 123 #79–#87 Variant Discovery in Genomic Data Ballroom 104 #286–#294 52.
    [Show full text]
  • Harnessing Low-Density Lipoprotein Receptor Protein 6 (LRP6) Genetic Variation and Wnt Signaling for Innovative Diagnostics in Complex Diseases
    OPEN The Pharmacogenomics Journal (2018) 18, 351–358 www.nature.com/tpj REVIEW Harnessing low-density lipoprotein receptor protein 6 (LRP6) genetic variation and Wnt signaling for innovative diagnostics in complex diseases Z-M Wang1,2, J-Q Luo1,2, L-Y Xu3, H-H Zhou1,2 and W Zhang1,2 Wnt signaling regulates a broad variety of processes in both embryonic development and various diseases. Recent studies indicated that some genetic variants in Wnt signaling pathway may serve as predictors of diseases. Low-density lipoprotein receptor protein 6 (LRP6) is a Wnt co-receptor with essential functions in the Wnt/β-catenin pathway, and mutations in LRP6 gene are linked to many complex human diseases, including metabolic syndrome, cancer, Alzheimer’s disease and osteoporosis. Therefore, we focus on the role of LRP6 genetic polymorphisms and Wnt signaling in complex diseases, and the mechanisms from mouse models and cell lines. It is also highly anticipated that LRP6 variants will be applied clinically in the future. The brief review provided here could be a useful resource for future research and may contribute to a more accurate diagnosis in complex diseases. The Pharmacogenomics Journal (2018) 18, 351–358; doi:10.1038/tpj.2017.28; published online 11 July 2017 INTRODUCTION signaling pathways and expressed in various target organs.1 LDLR- The Wnt1 gene was identified in 1982. Ensuing studies in related proteins 5/6 (LRP5/6) belong to this large family and Drosophila and Xenopus unveiled a highly conserved Wnt/ function as co-receptors of the Wnt/β-catenin pathway. These β-catenin pathway, namely, canonical Wnt signaling.
    [Show full text]
  • LRP5 Promotes Adipose Progenitor Cell Fitness and Adipocyte Insulin Sensitivity
    bioRxiv preprint doi: https://doi.org/10.1101/2020.03.04.976647; this version posted March 5, 2020. 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. LRP5 promotes adipose progenitor cell fitness and adipocyte insulin sensitivity Short title: LRP5 and adipose tissue biology Authors: Nellie Y. Loh1, Senthil K. Vasan1, Manu Verma1, Agata Wesolowska-Andersen2, Matt J. Neville1,3, Clive Osmond4, Celia L. Gregson5, Fredrik Karpe1,3 and Constantinos Christodoulides1. Affiliations: 1 Oxford Centre for Diabetes, Endocrinology and Metabolism, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 7LE, UK 2 Wellcome Trust Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford, Oxford OX3 7BN, UK 3 NIHR Oxford Biomedical Research Centre, OUH Foundation Trust, Oxford OX3 7LE, UK 4 MRC Lifecourse Epidemiology Unit, Southampton General Hospital, University of Southampton, Tremona Road, Southampton SO17 1BJ, UK 5 Musculoskeletal Research Unit, Translational Health Sciences, University of Bristol, Southmead Hospital, Bristol BS10 5NB, UK Address for correspondence to: Dr Constantinos Christodoulides Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford OX3 7LE, UK E-mail: [email protected] Phone: +44-1865-857111 Keywords: LRP5, adipose, adipogenesis, fat distribution, WNT, human. Word count: 3964 words, 4 figures, 2 tables 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.03.04.976647; this version posted March 5, 2020. 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.
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • Single-Cell RNA Sequencing Demonstrates the Molecular and Cellular Reprogramming of Metastatic Lung Adenocarcinoma
    ARTICLE https://doi.org/10.1038/s41467-020-16164-1 OPEN Single-cell RNA sequencing demonstrates the molecular and cellular reprogramming of metastatic lung adenocarcinoma Nayoung Kim 1,2,3,13, Hong Kwan Kim4,13, Kyungjong Lee 5,13, Yourae Hong 1,6, Jong Ho Cho4, Jung Won Choi7, Jung-Il Lee7, Yeon-Lim Suh8,BoMiKu9, Hye Hyeon Eum 1,2,3, Soyean Choi 1, Yoon-La Choi6,10,11, Je-Gun Joung1, Woong-Yang Park 1,2,6, Hyun Ae Jung12, Jong-Mu Sun12, Se-Hoon Lee12, ✉ ✉ Jin Seok Ahn12, Keunchil Park12, Myung-Ju Ahn 12 & Hae-Ock Lee 1,2,3,6 1234567890():,; Advanced metastatic cancer poses utmost clinical challenges and may present molecular and cellular features distinct from an early-stage cancer. Herein, we present single-cell tran- scriptome profiling of metastatic lung adenocarcinoma, the most prevalent histological lung cancer type diagnosed at stage IV in over 40% of all cases. From 208,506 cells populating the normal tissues or early to metastatic stage cancer in 44 patients, we identify a cancer cell subtype deviating from the normal differentiation trajectory and dominating the metastatic stage. In all stages, the stromal and immune cell dynamics reveal ontological and functional changes that create a pro-tumoral and immunosuppressive microenvironment. Normal resident myeloid cell populations are gradually replaced with monocyte-derived macrophages and dendritic cells, along with T-cell exhaustion. This extensive single-cell analysis enhances our understanding of molecular and cellular dynamics in metastatic lung cancer and reveals potential diagnostic and therapeutic targets in cancer-microenvironment interactions. 1 Samsung Genome Institute, Samsung Medical Center, Seoul 06351, Korea.
    [Show full text]
  • (LRP5) Is Essential for Normal Cholesterol Metabolism and Glucose-Induced Insulin Secretion
    Low-density lipoprotein receptor-related protein 5 (LRP5) is essential for normal cholesterol metabolism and glucose-induced insulin secretion Takahiro Fujinoa,b, Hiroshi Asabab,c, Man-Jong Kangb,d, Yukio Ikedaa,b,c, Hideyuki Sonea,b, Shinji Takadae,f,g, Dong-Ho Kima, Ryoichi X. Iokaa, Masao Onoh, Hiroko Tomoyorii, Minoru Okuboj, Toshio Murasej, Akihisa Kamatakia, Joji Yamamotoa,c, Kenta Magooria, Sadao Takahashik, Yoshiharu Miyamotoh, Hisashi Oishih, Masato Noseh, Mitsuyo Okazakil, Shinichi Usuil, Katsumi Imaizumii, Masashi Yanagisawac,m, Juro Sakaia,c,n, and Tokuo T. Yamamotoa aGene Research Center and Division of Nephrology, Endocrinology, and Vascular Medicine, Department of Medicine, Tohoku University, Sendai 980-8574, Japan; cYanagisawa Orphan Receptor Project, Exploratory Research for Advanced Technology, Japan Science and Technology Corporation, Tokyo 135-0064, Japan; dDepartment of Animal Science, College of Agriculture, Chonnam National University, Kwangju 500-600, Korea; eGraduate School of Science, Kyoto University, Kyoto 606-8502, Japan; fKondoh Differentiation Signaling Project, Exploratory Research for Advanced Technology, Japan Science and Technology Corporation, Kyoto 606-8305, Japan; gCenter for Integrative Bioscience, Okazaki, Aichi 444-8585, Japan; hDepartments of Pathology and Orthopedics, Ehime University School of Medicine, Ehime 791-0295, Japan; iLaboratory of Nutritional Chemistry, Graduate School of Agriculture, Kyusyu University, Fukuoka 812-8581, Japan; jDepartment of Endocrinology and Metabolism, Toranomon Hospital, Tokyo 105-8470, Japan; kThird Department of Internal Medicine, Fukui Medical University, Fukui 910-1193, Japan; lLaboratory of Chemistry, College of Liberal Arts and Sciences, Tokyo Medical and Dental University, Chiba 282-0827, Japan; and mHoward Hughes Medical Institute, Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75235-9050 Edited by Michael S.
    [Show full text]
  • Associations of Apolipoprotein E and Low‐Density Lipoprotein
    J Periodont Res 2015; 50: 509–518 © 2014 John Wiley & Sons A/S. All rights reserved Published by John Wiley & Sons Ltd JOURNAL OF PERIODONTAL RESEARCH doi:10.1111/jre.12237 H. Gao*, Y. Tian*, H. Meng, J. Hou, Associations of L. Xu, L. Zhang, D. Shi, R. Lu, X. Feng, X. Wang, Z. Chen Department of Periodontology, Peking apolipoprotein E and University School and Hospital of Stomatology, Beijing, China low-density lipoprotein receptor-related protein 5 polymorphisms with dyslipidemia and generalized aggressive periodontitis in a Chinese population Gao H, Tian Y, Meng H, Hou J, Xu L, Zhang L, Shi D, Lu R, Feng X, Wang X, Chen Z. Associations of apolipoprotein E and low-density lipoprotein receptor- related protein 5 polymorphisms with dyslipidemia and generalized aggressive periodontitis in a Chinese population. J Periodont Res 2015; 50: 509–518. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd Background and Objective: Dyslipidemia is associated with aggressive periodonti- tis, a condition characterized by the rapid destruction of the periodontium. Apo- lipoprotein E (APOE) and low-density lipoprotein receptor-related protein 5 (LRP5) are involved in immunomodulation and inflammatory activity. We eval- uated the association of LRP5 and APOE polymorphisms with serum lipid con- centrations and generalized aggressive periodontitis within a Chinese population. Material and Methods: Mean serum lipid concentrations were compared across LRP5 and APOE polymorphisms, among cases (n = 185) and controls (n = 138). Multivariable logistic regression was used to evaluate the independent and combined associations of LRP5 and APOE polymorphisms with generalized Huanxin Meng, BDS, MS, PhD, Peking aggressive periodontitis.
    [Show full text]
  • 4 Transcription and Secretion Novel Regulator of Angiopoietin-Like Protein A
    Acute-Phase Protein α1-Antitrypsin−−A Novel Regulator of Angiopoietin-like Protein 4 Transcription and Secretion This information is current as Eileen Frenzel, Sabine Wrenger, Stephan Immenschuh, of September 28, 2021. Rembert Koczulla, Ravi Mahadeva, H. Joachim Deeg, Charles A. Dinarello, Tobias Welte, A. Mario Q. Marcondes and Sabina Janciauskiene J Immunol 2014; 192:5354-5362; Prepublished online 23 April 2014; Downloaded from doi: 10.4049/jimmunol.1400378 http://www.jimmunol.org/content/192/11/5354 Supplementary http://www.jimmunol.org/content/suppl/2014/04/23/jimmunol.140037 http://www.jimmunol.org/ Material 8.DCSupplemental References This article cites 56 articles, 25 of which you can access for free at: http://www.jimmunol.org/content/192/11/5354.full#ref-list-1 Why The JI? Submit online. by guest on September 28, 2021 • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2014 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Acute-Phase Protein a1-Antitrypsin—A Novel Regulator of Angiopoietin-like Protein 4 Transcription and Secretion Eileen Frenzel,* Sabine Wrenger,* Stephan Immenschuh,† Rembert Koczulla,‡ Ravi Mahadeva,x H.
    [Show full text]
  • Angiocrine Endothelium: from Physiology to Cancer Jennifer Pasquier1,2*, Pegah Ghiabi2, Lotf Chouchane3,4,5, Kais Razzouk1, Shahin Rafi3 and Arash Rafi1,2,3
    Pasquier et al. J Transl Med (2020) 18:52 https://doi.org/10.1186/s12967-020-02244-9 Journal of Translational Medicine REVIEW Open Access Angiocrine endothelium: from physiology to cancer Jennifer Pasquier1,2*, Pegah Ghiabi2, Lotf Chouchane3,4,5, Kais Razzouk1, Shahin Rafi3 and Arash Rafi1,2,3 Abstract The concept of cancer as a cell-autonomous disease has been challenged by the wealth of knowledge gathered in the past decades on the importance of tumor microenvironment (TM) in cancer progression and metastasis. The sig- nifcance of endothelial cells (ECs) in this scenario was initially attributed to their role in vasculogenesis and angiogen- esis that is critical for tumor initiation and growth. Nevertheless, the identifcation of endothelial-derived angiocrine factors illustrated an alternative non-angiogenic function of ECs contributing to both physiological and pathological tissue development. Gene expression profling studies have demonstrated distinctive expression patterns in tumor- associated endothelial cells that imply a bilateral crosstalk between tumor and its endothelium. Recently, some of the molecular determinants of this reciprocal interaction have been identifed which are considered as potential targets for developing novel anti-angiocrine therapeutic strategies. Keywords: Angiocrine, Endothelium, Cancer, Cancer microenvironment, Angiogenesis Introduction of blood vessels in initiation of tumor growth and stated Metastatic disease accounts for about 90% of patient that in the absence of such angiogenesis, tumors can- mortality. Te difculty in controlling and eradicating not expand their mass or display a metastatic phenotype metastasis might be related to the heterotypic interaction [7]. Based on this theory, many investigators assumed of tumor and its microenvironment [1].
    [Show full text]
  • Stromal Cell Interactions Mediated by Hypoxia-Inducible Factors Promote Angiogenesis, Lymphangiogenesis, and Metastasis
    Oncogene (2013) 32, 4057–4063 & 2013 Macmillan Publishers Limited All rights reserved 0950-9232/13 www.nature.com/onc REVIEW Cancer–stromal cell interactions mediated by hypoxia-inducible factors promote angiogenesis, lymphangiogenesis, and metastasis GL Semenza Interactions between cancer cells and stromal cells, including blood vessel endothelial cells (BECs), lymphatic vessel endothelial cells (LECs), bone marrow-derived angiogenic cells (BMDACs) and other bone marrow-derived cells (BMDCs) play important roles in cancer progression. Intratumoral hypoxia, which affects both cancer and stromal cells, is associated with a significantly increased risk of metastasis and mortality in many human cancers. Recent studies have begun to delineate the molecular mechanisms underlying the effect of intratumoral hypoxia on cancer progression. Reduced O2 availability induces the activity of hypoxia- inducible factors (HIFs), which activate the transcription of target genes encoding proteins that play important roles in many critical aspects of cancer biology. Included among these are secreted factors, including angiopoietin 2, angiopoietin-like 4, placental growth factor, platelet-derived growth factor B, stem cell factor (kit ligand), stromal-derived factor 1, and vascular endothelial growth factor. These factors are produced by hypoxic cancer cells and directly mediate functional interactions with BECs, LECs, BMDACs and other BMDCs that promote angiogenesis, lymphangiogenesis, and metastasis. In addition, lysyl oxidase (LOX) and LOX-like proteins,
    [Show full text]
  • Coexpression of ATP-Binding Cassette Proteins ABCG5 and ABCG8 Permits Their Transport to the Apical Surface
    Coexpression of ATP-binding cassette proteins ABCG5 and ABCG8 permits their transport to the apical surface Gregory A. Graf, … , Jonathan C. Cohen, Helen H. Hobbs J Clin Invest. 2002;110(5):659-669. https://doi.org/10.1172/JCI16000. Article Cardiology Mutations in either ATP-binding cassette (ABC) G5 or ABCG8 cause sitosterolemia, an autosomal recessive disorder of sterol trafficking. To determine the site of action of ABCG5 and ABCG8, we expressed recombinant, epitope-tagged mouse ABCG5 and ABCG8 in cultured cells. Both ABCG5 and ABCG8 underwent N-linked glycosylation. When either protein was expressed individually in cells, the N-linked sugars remained sensitive to Endoglycosidase H (Endo H). When ABCG5 and ABCG8 were coexpressed, the attached sugars were Endo H–resistant and neuraminidase-sensitive, indicating that the proteins were transported to the trans-Golgi complex. The mature, glycosylated forms of ABCG5 and ABCG8 coimmunoprecipitated, consistent with heterodimerization of these two proteins. The Endo H–sensitive forms of ABCG5 and ABCG8 were confined to the endoplasmic reticulum (ER), whereas the mature forms were present in non-ER fractions in cultured hepatocytes. Immunoelectron microscopy revealed ABCG5 and ABCG8 on the plasma membrane of these cells. In polarized WIF-B cells, recombinant ABCG5 localized to the apical (canalicular) membrane when coexpressed with ABCG8, but not when expressed alone. To our knowledge this is the first direct demonstration that trafficking of an ABC half-transporter to the cell surface requires the presence of its dimerization partner. Find the latest version: https://jci.me/16000/pdf Coexpression of ATP-binding cassette See the related Commentary beginning on page 605.
    [Show full text]