An Ontogenetic Switch Drives the Positive and Negative Selection of B Cells
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(12) Patent Application Publication (10) Pub. No.: US 2012/0070450 A1 Ishikawa Et Al
US 20120070450A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2012/0070450 A1 Ishikawa et al. (43) Pub. Date: Mar. 22, 2012 (54) LEUKEMA STEM CELLMARKERS Publication Classification (51) Int. Cl. A 6LX 39/395 (2006.01) (75) Inventors: Fumihiko Ishikawa, Kanagawa CI2O I/68 (2006.01) (JP): Osamu Ohara, Kanagawa GOIN 2L/64 (2006.01) (JP); Yoriko Saito, Kanagawa (JP); A6IP35/02 (2006.01) Hiroshi Kitamura, Kanagawa (JP); C40B 30/04 (2006.01) Atsushi Hijikata, Kanagawa (JP); A63L/7088 (2006.01) Hidetoshi Ozawa, Kanagawa (JP); C07K 6/8 (2006.01) Leonard D. Shultz, Bar Harbor, C7H 2L/00 (2006.01) A6II 35/12 (2006.01) ME (US) CI2N 5/078 (2010.01) (52) U.S. Cl. .................. 424/173.1; 424/178.1; 424/93.7: (73) Assignee: RIKEN, Wako-shi (JP) 435/6.14; 435/723; 435/375; 506/9: 514/44 A: 530/389.6; 530/391.7:536/24.5 (57) ABSTRACT (21) Appl. No.: 13/258,993 The invention provides a test method for predicting the initial onset or a recurrence of acute myeloid leukemia (AML) com PCT Fled: prising (1) measuring the expression level of human leukemic (22) Mar. 24, 2010 stem cell (LSC) marker genes in a biological sample collected from a Subject for a transcription product or translation prod uct of the gene as an analyte and (2) comparing the expression (86) PCT NO.: PCT/UP2010/0551.31 level with a reference value; an LSC-targeting therapeutic agent for AML capable of Suppressing the expression of a S371 (c)(1), gene selected from among LSC marker genes or a Substance (2), (4) Date: Dec. -
Functional Analysis of the Homeobox Gene Tur-2 During Mouse Embryogenesis
Functional Analysis of The Homeobox Gene Tur-2 During Mouse Embryogenesis Shao Jun Tang A thesis submitted in conformity with the requirements for the Degree of Doctor of Philosophy Graduate Department of Molecular and Medical Genetics University of Toronto March, 1998 Copyright by Shao Jun Tang (1998) National Library Bibriothèque nationale du Canada Acquisitions and Acquisitions et Bibiiographic Services seMces bibliographiques 395 Wellington Street 395, rue Weifington OtbawaON K1AW OttawaON KYAON4 Canada Canada The author has granted a non- L'auteur a accordé une licence non exclusive licence alIowing the exclusive permettant à la National Library of Canada to Bibliothèque nationale du Canada de reproduce, loan, distri%uteor sell reproduire, prêter' distribuer ou copies of this thesis in microform, vendre des copies de cette thèse sous paper or electronic formats. la forme de microfiche/nlm, de reproduction sur papier ou sur format électronique. The author retains ownership of the L'auteur conserve la propriété du copyright in this thesis. Neither the droit d'auteur qui protège cette thèse. thesis nor substantial extracts fkom it Ni la thèse ni des extraits substantiels may be printed or otherwise de celle-ci ne doivent être imprimés reproduced without the author's ou autrement reproduits sans son permission. autorisation. Functional Analysis of The Homeobox Gene TLr-2 During Mouse Embryogenesis Doctor of Philosophy (1998) Shao Jun Tang Graduate Department of Moiecular and Medicd Genetics University of Toronto Abstract This thesis describes the clonhg of the TLx-2 homeobox gene, the determination of its developmental expression, the characterization of its fiuiction in mouse mesodem and penpheral nervous system (PNS) developrnent, the regulation of nx-2 expression in the early mouse embryo by BMP signalling, and the modulation of the function of nX-2 protein by the 14-3-3 signalling protein during neural development. -
Human Stem Cells from Single Blastomeres Reveal Pathways of Embryonic Or Trophoblast Fate Specification Tamara Zdravkovic1,2,3,4,5,‡, Kristopher L
© 2015. Published by The Company of Biologists Ltd | Development (2015) 142, 4010-4025 doi:10.1242/dev.122846 STEM CELLS AND REGENERATION RESEARCH ARTICLE Human stem cells from single blastomeres reveal pathways of embryonic or trophoblast fate specification Tamara Zdravkovic1,2,3,4,5,‡, Kristopher L. Nazor6,‡, Nicholas Larocque1,2,3,4,5, Matthew Gormley1,2,3,4,5, Matthew Donne1,2,3,7, Nathan Hunkapillar1,2,3,4,5, Gnanaratnam Giritharan8, Harold S. Bernstein4,9, Grace Wei4,10, Matthias Hebrok10, Xianmin Zeng11, Olga Genbacev1,2,3,4,5, Aras Mattis4,12, Michael T. McMaster4,5,13, Ana Krtolica8,*, Diana Valbuena14, Carlos Simón14, Louise C. Laurent6,15, Jeanne F. Loring6 and Susan J. Fisher1,2,3,4,5,7,§ ABSTRACT INTRODUCTION For many reasons, relatively little is known about human Mechanisms of initial cell fate decisions differ among species. To gain preimplantation development. The small number of cells makes insights into lineage allocation in humans, we derived ten human embryos of any species difficult to study. In humans, the technical embryonic stem cell lines (designated UCSFB1-10) from single difficulties are compounded by other challenges. Genetic variation blastomeres of four 8-cell embryos and one 12-cell embryo from a among individuals could contribute to developmental differences, a single couple. Compared with numerous conventional lines from well-appreciated phenomenon in the mouse (Dackor et al., 2009), blastocysts, they had unique gene expression and DNA methylation which is difficult to assess in humans owing to the limited patterns that were, in part, indicative of trophoblast competence. At a availability of embryos that are donated for research. -
NANOG and LIN28 Dramatically Improve Human Cell Reprogramming
© 2019. Published by The Company of Biologists Ltd | Biology Open (2019) 8, bio047225. doi:10.1242/bio.047225 RESEARCH ARTICLE NANOG and LIN28 dramatically improve human cell reprogramming by modulating LIN41 and canonical WNT activities Ling Wang, Yue Su, Chang Huang, Yexuan Yin, Alexander Chu, Alec Knupp and Young Tang* ABSTRACT (Hussein et al., 2014). The first transcriptional change occurs at the Human cell reprogramming remains extremely inefficient and the early reprogramming stage, with cells undergoing mesenchymal-to- underlying mechanisms by different reprogramming factors are epithelial transition (MET) for iPSC colony formation (Hussein elusive. We found that NANOG and LIN28 (NL) synergize to improve et al., 2014; Li et al., 2010; Samavarchi-Tehrani et al., 2010). This OCT4, SOX2, KLF4 and MYC (OSKM)-mediated reprogramming by stage is followed by the second wave that occurs during maturation ∼76-fold and shorten reprogramming latency by at least 1 week. This and stabilization, when the pluripotency regulatory network is synergy is inhibited by GLIS1 but reinforced by an inhibitor of the activated and stabilized in reprogrammed cells (Buganim et al., 2012; histone methyltransferase DOT1L (iDOT1L) to a ∼127-fold increase in Golipour et al., 2012; Hussein et al., 2014; Polo et al., 2012; TRA-1-60-positive (+) iPSC colonies. Mechanistically, NL serve as the Samavarchi-Tehrani et al., 2010). In human cells, the early-to-middle main drivers of reprogramming in cell epithelialization, the expression reprogramming stages are characterized by multiple waves of lineage- of Let-7 miRNA target LIN41, and the activation of canonical WNT/β- related gene activation in the order of developmental reversal, with CATENIN signaling, which can be further enhanced by iDOT1L MET occurring at the middle-to-late-reprogramming stage along with treatment. -
High-Mobility Group A1 Proteins May Be Involved in Estrogen Receptor Status of Breast Cancer
3786 Editorial Commentary High-mobility group A1 proteins may be involved in estrogen receptor status of breast cancer Yoshihiro Harada, Kenji Ohe Department of Pharmacotherapeutics, Faculty of Pharmaceutical Sciences, Fukuoka University, Jonan-ku, Fukuoka, Japan Correspondence to: Kenji Ohe. Department of Pharmacotherapeutics, Faculty of Pharmaceutical Sciences, Fukuoka University, Building 17, 8-19-1 Nanakuma, Jonan-ku, Fukuoka 814-180, Japan. Email: [email protected]. Provenance and Peer Review: This article was commissioned by the editorial office, Translational Cancer Research. The article did not undergo external peer review. Comment on: Gorbounov M, Carleton NM, Asch-Kendrick RJ, et al. High mobility group A1 (HMGA1) protein and gene expression correlate with ER-negativity and poor outcomes in breast cancer. Breast Cancer Res Treat 2020;179:25-35. Submitted Apr 27, 2020. Accepted for publication May 13, 2020. doi: 10.21037/tcr-20-1921 View this article at: http://dx.doi.org/10.21037/tcr-20-1921 The three types of breast cancer HMGA1 proteins: old and new proteins in breast cancer Breast cancer is one of the most common of cancers in woman. About 316,700 new cases were diagnosed as breast HMGA1 (previously called HMGI/Y) is a member of the cancer in US woman in 2019 and 41,760 were predicted to high-mobility group (HMG) proteins that were found from die from it (1). Breast cancer has a characteristic of therapy- their high mobility characteristics during polyacrylamide targeting receptors: hormone receptors (HR) that are electrophoresis of non-histone chromatin-associated estrogen receptor [ER: human ERα protein (NCBI protein proteins (3). -
A Lncrna/Lin28/Mirlet7 Axis Coupled to DNA Methylation Fine Tunes the Dynamics of a Cell State Transition
bioRxiv preprint doi: https://doi.org/10.1101/131110; this version posted April 26, 2017. 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. Li, M.A. et al A lncRNA/Lin28/Mirlet7 axis coupled to DNA methylation fine tunes the dynamics of a cell state transition Meng Amy Li1*,2,#, Paulo P. Amaral3, Priscilla Cheung2, Jan H. Bergmann4,9, Masaki Kinoshita1, Tüzer Kalkan1, Meryem Ralser1, Sam Robson3, Ferdinand von Meyenn5, Maike Paramor1, Fengtang Yang6, Caifu Chen7, Jennifer Nichols1, David L. Spector4, Tony Kouzarides3, Lin He2,#, Austin Smith1,8,# 1. Wellcome Trust - Medical Research Council Stem Cell Institute, Tennis Court Road, University of Cambridge, Cambridge, CB2 1QR, UK 2. Division of Cellular and Developmental Biology, Department of Molecular and Cellular Biology, University of California Berkeley, Berkeley, California 94705, USA 3. The Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QN, UK 4. Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA 5. Babraham Institute, Babraham, Cambridge, CB22 3AT 6. Wellcome Trust Sanger Institute, Genome Campus, Hinxton, CB10 1SA, UK 7. Integrated DNA Technologies, 200 Chesapeake Drive, Redwood City, CA 94063, USA. 8. Department of Biochemistry, University of Cambridge, CB2 1QW, UK 9. Current address: Agenus inc., Hochbergerstrasse 60C, 4057 Basel, Switzerland *. Current address. # . Correspondence: [email protected], [email protected] and [email protected] Lead contact: Austin Smith Summary Execution of pluripotency requires progression from the naïve status represented by mouse embryonic stem cells (ESCs) to a condition poised for lineage specification. -
Contribution of IL9, IL2RA and IL2RB Genetic Polymorphisms in Coronary Heart Disease in Chinese Han Population
Contribution of IL9, IL2RA and IL2RB genetic polymorphisms in coronary heart disease in Chinese Han population Xianghong Chen The Second Aliated Hospital of Hainan Medical University Xingfan Wang The Second Aliated Hospital of Hainan Medical University Zaozhang q Zhang The second Aliated Hospital of Hainan Medical University Yuewu Chen The Second Aliated Hospital of Hainan Medical University Chao Wang ( [email protected] ) The Second Aliated Hospital of Hainan Medical Universiy https://orcid.org/0000-0001-5632-9778 Research article Keywords: Posted Date: December 9th, 2019 DOI: https://doi.org/10.21203/rs.2.18401/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/11 Abstract Background: Coronary heart disease (CHD) is one of the leading causes of disability and death worldwide. In the pathogenesis of CHD, inammatory cytokines take an essential part. This study was designed to detect the potential association between IL-9, IL-2RA and IL-2RB variants and CHD in Chinese Han population. Methods: This case-control study conducted 499 CHD patients and 496 healthy controls. Seven selected SNPs were genotyped to investigate the possible association between the polymorphisms and the CHD risk. The interaction of SNP-SNP in the CHD risk was analyzed by Multifactor dimensionality reduction (MDR). Results: We observed an association between IL-9 rs55692658 (OR = 1.72, p = 0.003) and the increased CHD risk. The stratication analysis by age indicated that no matter participants who were older or younger than 61 years, IL-9 rs55692658 and IL-2RB rs1573673 contributed to the CHD susceptibility signicantly (p < 0.05, respectively). -
B Cell Checkpoints in Autoimmune Rheumatic Diseases
REVIEWS B cell checkpoints in autoimmune rheumatic diseases Samuel J. S. Rubin1,2,3, Michelle S. Bloom1,2,3 and William H. Robinson1,2,3* Abstract | B cells have important functions in the pathogenesis of autoimmune diseases, including autoimmune rheumatic diseases. In addition to producing autoantibodies, B cells contribute to autoimmunity by serving as professional antigen- presenting cells (APCs), producing cytokines, and through additional mechanisms. B cell activation and effector functions are regulated by immune checkpoints, including both activating and inhibitory checkpoint receptors that contribute to the regulation of B cell tolerance, activation, antigen presentation, T cell help, class switching, antibody production and cytokine production. The various activating checkpoint receptors include B cell activating receptors that engage with cognate receptors on T cells or other cells, as well as Toll-like receptors that can provide dual stimulation to B cells via co- engagement with the B cell receptor. Furthermore, various inhibitory checkpoint receptors, including B cell inhibitory receptors, have important functions in regulating B cell development, activation and effector functions. Therapeutically targeting B cell checkpoints represents a promising strategy for the treatment of a variety of autoimmune rheumatic diseases. Antibody- dependent B cells are multifunctional lymphocytes that contribute that serve as precursors to and thereby give rise to acti- cell- mediated cytotoxicity to the pathogenesis of autoimmune diseases -
METTL1 Promotes Let-7 Microrna Processing Via M7g Methylation
Article METTL1 Promotes let-7 MicroRNA Processing via m7G Methylation Graphical Abstract Authors Luca Pandolfini, Isaia Barbieri, Andrew J. Bannister, ..., Mara d’Onofrio, Shankar Balasubramanian, Tony Kouzarides Correspondence [email protected] In Brief Pandolfini, Barbieri, et al. show that a subgroup of tumor suppressor microRNAs, including let-7e, contain 7-methylguanosine (m7G). Methyltransferase METTL1 is required for m7G modification of miRNAs, their efficient processing, and the inhibition of lung cancer cell migration. Structurally, m7G in miRNA precursors antagonizes RNA secondary structures that would otherwise inhibit their maturation. Highlights Data Resource d Internal m7G is identified in miRNAs by two independent GSE112182 sequencing techniques GSE112180 GSE112181 d Methyltransferase METTL1 mediates m7G modification of GSE120454 specific miRNAs GSE120455 d METTL1 promotes miRNA maturation and suppresses lung cancer cell migration d m7G promotes processing by antagonizing G-quadruplex structures in miRNA precursors Pandolfini et al., 2019, Molecular Cell 74, 1278–1290 June 20, 2019 ª 2019 The Author(s). Published by Elsevier Inc. https://doi.org/10.1016/j.molcel.2019.03.040 Molecular Cell Article METTL1 Promotes let-7 MicroRNA Processing via m7G Methylation Luca Pandolfini,1,9 Isaia Barbieri,1,2,9 Andrew J. Bannister,1 Alan Hendrick,3 Byron Andrews,3 Natalie Webster,3 Pierre Murat,4,7 Pia Mach,1 Rossella Brandi,5 Samuel C. Robson,1,8 Valentina Migliori,1 Andrej Alendar,1 Mara d’Onofrio,5,6 Shankar Balasubramanian,4 -
CD Markers Are Routinely Used for the Immunophenotyping of Cells
ptglab.com 1 CD MARKER ANTIBODIES www.ptglab.com Introduction The cluster of differentiation (abbreviated as CD) is a protocol used for the identification and investigation of cell surface molecules. So-called CD markers are routinely used for the immunophenotyping of cells. Despite this use, they are not limited to roles in the immune system and perform a variety of roles in cell differentiation, adhesion, migration, blood clotting, gamete fertilization, amino acid transport and apoptosis, among many others. As such, Proteintech’s mini catalog featuring its antibodies targeting CD markers is applicable to a wide range of research disciplines. PRODUCT FOCUS PECAM1 Platelet endothelial cell adhesion of blood vessels – making up a large portion molecule-1 (PECAM1), also known as cluster of its intracellular junctions. PECAM-1 is also CD Number of differentiation 31 (CD31), is a member of present on the surface of hematopoietic the immunoglobulin gene superfamily of cell cells and immune cells including platelets, CD31 adhesion molecules. It is highly expressed monocytes, neutrophils, natural killer cells, on the surface of the endothelium – the thin megakaryocytes and some types of T-cell. Catalog Number layer of endothelial cells lining the interior 11256-1-AP Type Rabbit Polyclonal Applications ELISA, FC, IF, IHC, IP, WB 16 Publications Immunohistochemical of paraffin-embedded Figure 1: Immunofluorescence staining human hepatocirrhosis using PECAM1, CD31 of PECAM1 (11256-1-AP), Alexa 488 goat antibody (11265-1-AP) at a dilution of 1:50 anti-rabbit (green), and smooth muscle KD/KO Validated (40x objective). alpha-actin (red), courtesy of Nicola Smart. PECAM1: Customer Testimonial Nicola Smart, a cardiovascular researcher “As you can see [the immunostaining] is and a group leader at the University of extremely clean and specific [and] displays Oxford, has said of the PECAM1 antibody strong intercellular junction expression, (11265-1-AP) that it “worked beautifully as expected for a cell adhesion molecule.” on every occasion I’ve tried it.” Proteintech thanks Dr. -
The LIN28B-IMP1 Post-Transcriptional Regulon Has Opposing Effects On
Washington University School of Medicine Digital Commons@Becker Open Access Publications 2018 The IN28BL -IMP1 post-transcriptional regulon has opposing effects on oncogenic signaling in the intestine Blair B. Madison et al Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Downloaded from genesdev.cshlp.org on August 7, 2018 - Published by Cold Spring Harbor Laboratory Press The LIN28B–IMP1 post-transcriptional regulon has opposing effects on oncogenic signaling in the intestine Priya Chatterji,1,2,14 Kathryn E. Hamilton,1,3,14 Shun Liang,4 Sarah F. Andres,1 H.R. Sagara Wijeratne,4 Rei Mizuno,1 Lauren A. Simon,1,3 Philip D. Hicks,1 Shawn W. Foley,5 Jason R. Pitarresi,1 Andres J. Klein-Szanto,6,7 Amanda T. Mah,8 Laurianne Van Landeghem,9 Brian D. Gregory,5 Christopher J. Lengner,10 Blair B. Madison,11 Premal Shah,4,12 and Anil K. Rustgi1,2,13 1Department of Medicine, Division of Gastroenterology, 2Department of Genetics, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania 19014, USA; 3Department of Pediatrics, Division of Gastroenterology, Children’s Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania 19014, USA; 4Department of Genetics, Rutgers University, New Brunswick, New Jersey 08901, USA; 5Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19014, USA; 6Department of Pathology, 7Cancer Biology Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA; 8Department of Medicine, Hematology Division, Stanford University, Stanford, California 94305, USA; 9Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina 27607, USA; 10Department of Biomedical Sciences, School of Veterinary Medicine, Institute for Regenerative Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA; 11Department of Medicine, Division of Gastroenterology, Washington University School of Medicine, St. -
Avian Tail Ontogeny, Pygostyle Formation, and Interpretation of Juvenile Mesozoic Specimens Received: 27 March 2018 Dana J
www.nature.com/scientificreports OPEN Avian tail ontogeny, pygostyle formation, and interpretation of juvenile Mesozoic specimens Received: 27 March 2018 Dana J. Rashid1, Kevin Surya2, Luis M. Chiappe3, Nathan Carroll3, Kimball L. Garrett4, Bino Accepted: 23 May 2018 Varghese5, Alida Bailleul6,7, Jingmai K. O’Connor 7, Susan C. Chapman 8 & John R. Horner1,9 Published: xx xx xxxx The avian tail played a critical role in the evolutionary transition from long- to short-tailed birds, yet its ontogeny in extant birds has largely been ignored. This defcit has hampered eforts to efectively identify intermediate species during the Mesozoic transition to short tails. Here we show that fusion of distal vertebrae into the pygostyle structure does not occur in extant birds until near skeletal maturity, and mineralization of vertebral processes also occurs long after hatching. Evidence for post-hatching pygostyle formation is also demonstrated in two Cretaceous specimens, a juvenile enantiornithine and a subadult basal ornithuromorph. These fndings call for reinterpretations of Zhongornis haoae, a Cretaceous bird hypothesized to be an intermediate in the long- to short-tailed bird transition, and of the recently discovered coelurosaur tail embedded in amber. Zhongornis, as a juvenile, may not yet have formed a pygostyle, and the amber-embedded tail specimen is reinterpreted as possibly avian. Analyses of relative pygostyle lengths in extant and Cretaceous birds suggests the number of vertebrae incorporated into the pygostyle has varied considerably, further complicating the interpretation of potential transitional species. In addition, this analysis of avian tail development reveals the generation and loss of intervertebral discs in the pygostyle, vertebral bodies derived from diferent kinds of cartilage, and alternative modes of caudal vertebral process morphogenesis in birds.