BD Stem Cell Resource Markers of Self-Renewal and Differentiation
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The Prevalence of MADH4 and BMPR1A Mutations in Juvenile Polyposis and Absence of BMPR2, BMPR1B, and ACVR1 Mutations
484 ORIGINAL ARTICLE J Med Genet: first published as 10.1136/jmg.2004.018598 on 2 July 2004. Downloaded from The prevalence of MADH4 and BMPR1A mutations in juvenile polyposis and absence of BMPR2, BMPR1B, and ACVR1 mutations J R Howe, M G Sayed, A F Ahmed, J Ringold, J Larsen-Haidle, A Merg, F A Mitros, C A Vaccaro, G M Petersen, F M Giardiello, S T Tinley, L A Aaltonen, H T Lynch ............................................................................................................................... J Med Genet 2004;41:484–491. doi: 10.1136/jmg.2004.018598 Background: Juvenile polyposis (JP) is an autosomal dominant syndrome predisposing to colorectal and gastric cancer. We have identified mutations in two genes causing JP, MADH4 and bone morphogenetic protein receptor 1A (BMPR1A): both are involved in bone morphogenetic protein (BMP) mediated signalling and are members of the TGF-b superfamily. This study determined the prevalence of mutations See end of article for in MADH4 and BMPR1A, as well as three other BMP/activin pathway candidate genes in a large number authors’ affiliations ....................... of JP patients. Methods: DNA was extracted from the blood of JP patients and used for PCR amplification of each exon of Correspondence to: these five genes, using primers flanking each intron–exon boundary. Mutations were determined by Dr J R Howe, Department of Surgery, 4644 JCP, comparison to wild type sequences using sequence analysis software. A total of 77 JP cases were University of Iowa College sequenced for mutations in the MADH4, BMPR1A, BMPR1B, BMPR2, and/or ACVR1 (activin A receptor) of Medicine, 200 Hawkins genes. The latter three genes were analysed when MADH4 and BMPR1A sequencing found no mutations. -
Early B-Cell Factors Are Required for Specifying Multiple Retinal Cell Types and Subtypes from Postmitotic Precursors
11902 • The Journal of Neuroscience, September 8, 2010 • 30(36):11902–11916 Development/Plasticity/Repair Early B-Cell Factors Are Required for Specifying Multiple Retinal Cell Types and Subtypes from Postmitotic Precursors Kangxin Jin,1,2 Haisong Jiang,1,2 Zeqian Mo,3 and Mengqing Xiang1,2 1Center for Advanced Biotechnology and Medicine and Department of Pediatrics, 2Graduate Program in Molecular Genetics, Microbiology and Immunology, and 3Department of Cell Biology and Neuroscience, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854 The establishment of functional retinal circuits in the mammalian retina depends critically on the proper generation and assembly of six classes of neurons, five of which consist of two or more subtypes that differ in morphologies, physiological properties, and/or sublaminar positions. How these diverse neuronal types and subtypes arise during retinogenesis still remains largely to be defined at the molecular level. Here we show that all four family members of the early B-cell factor (Ebf) helix-loop-helix transcription factors are similarly expressedduringmouseretinogenesisinseveralneuronaltypesandsubtypesincludingganglion,amacrine,bipolar,andhorizontalcells, and that their expression in ganglion cells depends on the ganglion cell specification factor Brn3b. Misexpressed Ebfs bias retinal precursors toward the fates of non-AII glycinergic amacrine, type 2 OFF-cone bipolar and horizontal cells, whereas a dominant-negative Ebf suppresses the differentiation of these cells as well as ganglion cells. Reducing Ebf1 expression by RNA interference (RNAi) leads to an inhibitory effect similar to that of the dominant-negative Ebf, effectively neutralizes the promotive effect of wild-type Ebf1, but has no impact on the promotive effect of an RNAi-resistant Ebf1. -
Human Endoglin/CD105 Quantikine
Quantikine® ELISA Human Endoglin/CD105 Immunoassay Catalog Number DNDG00 For the quantitative determination of human Endoglin concentrations in cell culture supernates, serum, and plasma. This package insert must be read in its entirety before using this product. For research use only. Not for use in diagnostic procedures. TABLE OF CONTENTS SECTION PAGE INTRODUCTION .....................................................................................................................................................................1 PRINCIPLE OF THE ASSAY ...................................................................................................................................................2 LIMITATIONS OF THE PROCEDURE .................................................................................................................................2 TECHNICAL HINTS .................................................................................................................................................................2 MATERIALS PROVIDED & STORAGE CONDITIONS ...................................................................................................3 OTHER SUPPLIES REQUIRED .............................................................................................................................................3 PRECAUTIONS .........................................................................................................................................................................4 SAMPLE COLLECTION & STORAGE -
Synergetic Effect of Recoverin and Calmodulin on Regulation of Rhodopsin Kinase
Thomas Jefferson University Jefferson Digital Commons Department of Biochemistry and Molecular Department of Biochemistry and Molecular Biology Faculty Papers Biology 1-1-2012 Synergetic effect of recoverin and calmodulin on regulation of rhodopsin kinase. Ilya I Grigoriev Lomonosov Moscow State University Ivan I Senin Lomonosov Moscow State University Natalya K Tikhomirova Lomonosov Moscow State University Konstantin E Komolov Lomonosov Moscow State University; University of Oldenburg, Oldenburg, Germany; Department of FBiochemistrollow this andy and additional Molecular works Biology at: ,https:/ Thomas/jdc.jeff Jeffersonerson.edu/bmpfp University Ser geiPar tE of P theermy Medicalakov Biochemistry Commons, and the Medical Molecular Biology Commons LetInstitute us for knowBiological Instrumentationhow access of the tRussiano this Academy document of Sciences benefits ouy RecommendedSee next page for Citation additional authors Grigoriev, Ilya I; Senin, Ivan I; Tikhomirova, Natalya K; Komolov, Konstantin E; Permyakov, Sergei E; Zernii, Evgeni Yu; Koch, Karl-Wilhelm; and Philippov, Pavel P, "Synergetic effect of recoverin and calmodulin on regulation of rhodopsin kinase." (2012). Department of Biochemistry and Molecular Biology Faculty Papers. Paper 36. https://jdc.jefferson.edu/bmpfp/36 This Article is brought to you for free and open access by the Jefferson Digital Commons. The Jefferson Digital Commons is a service of Thomas Jefferson University's Center for Teaching and Learning (CTL). The Commons is a showcase for Jefferson books and journals, peer-reviewed scholarly publications, unique historical collections from the University archives, and teaching tools. The Jefferson Digital Commons allows researchers and interested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. This article has been accepted for inclusion in Department of Biochemistry and Molecular Biology Faculty Papers by an authorized administrator of the Jefferson Digital Commons. -
The Role of the TGF- Co-Receptor Endoglin in Cancer
1 The role of the TGF- co-receptor endoglin in cancer Eduardo Pérez-Gómez1,†, Gaelle del Castillo1, Juan Francisco Santibáñez2, Jose Miguel López-Novoa3, Carmelo Bernabéu4 and 1,* Miguel Quintanilla . 1Instituto de Investigaciones Biomédicas Alberto Sols, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad Autónoma de Madrid, 28029-Madrid, Spain; 2Institute for Medical Research, University of Belgrado, Belgrado, Serbia; 3Instituto Reina Sofía de Investigación Nefrológica, Departamento de Fisiología y Farmacología, Universidad de Salamanca, Salamanca, Spain; 4Centro de Investigaciones Biológicas, CSIC, and CIBER de Enfermedades Raras (CIBERER), Madrid, Spain. E-mails: [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected] † Current address: Departamento de Bioquímica y Biología Molecular I, Facultad de Biología, Universidad Complutense de Madrid, Madrid, Spain *Corresponding author 2 ABSTRACT Endoglin (CD105) is an auxiliary membrane receptor of transforming growth factor- (TGF-) that interacts with type I and type II TGF- receptors and modulates TGF- signalling. Mutations in endoglin are involved in Hereditary Hemorrhagic Telangiectasia type I, a disorder characterized by cutaneous telangiectasias, epistaxis (nosebleeds) and major arteriovenous shunts, mainly in liver and lung. Endoglin is overexpressed in the tumor-associated vascular endothelium where it modulates angiogenesis. This feature makes endoglin a promising target for antiangiogenic cancer therapy. Recent studies on human and experimental models of carcinogenesis point to an important tumor cell-autonomous role of endoglin by regulating proliferation, migration, invasion and metastasis. These studies suggest that endoglin behaves as a suppressor of malignancy in experimental and human carcinogenesis. In this review, we evaluate the implication of endoglin in tumor development underlying studies developed in our laboratories in recent years. -
Absence of S100A4 in the Mouse Lens Induces an Aberrant Retina-Specific Differentiation Program and Cataract
www.nature.com/scientificreports OPEN Absence of S100A4 in the mouse lens induces an aberrant retina‑specifc diferentiation program and cataract Rupalatha Maddala1*, Junyuan Gao2, Richard T. Mathias2, Tylor R. Lewis1, Vadim Y. Arshavsky1,3, Adriana Levine4, Jonathan M. Backer4,5, Anne R. Bresnick4 & Ponugoti V. Rao1,3* S100A4, a member of the S100 family of multifunctional calcium‑binding proteins, participates in several physiological and pathological processes. In this study, we demonstrate that S100A4 expression is robustly induced in diferentiating fber cells of the ocular lens and that S100A4 (−/−) knockout mice develop late‑onset cortical cataracts. Transcriptome profling of lenses from S100A4 (−/−) mice revealed a robust increase in the expression of multiple photoreceptor‑ and Müller glia‑specifc genes, as well as the olfactory sensory neuron‑specifc gene, S100A5. This aberrant transcriptional profle is characterized by corresponding increases in the levels of proteins encoded by the aberrantly upregulated genes. Ingenuity pathway network and curated pathway analyses of diferentially expressed genes in S100A4 (−/−) lenses identifed Crx and Nrl transcription factors as the most signifcant upstream regulators, and revealed that many of the upregulated genes possess promoters containing a high‑density of CpG islands bearing trimethylation marks at histone H3K27 and/or H3K4, respectively. In support of this fnding, we further documented that S100A4 (−/−) knockout lenses have altered levels of trimethylated H3K27 and H3K4. Taken together, -
Molecular Classification of Patients with Unexplained Hamartomatous and Hyperplastic Polyposis
ORIGINAL CONTRIBUTION Molecular Classification of Patients With Unexplained Hamartomatous and Hyperplastic Polyposis Kevin Sweet, MS, CGC Context Significant proportions of patients with hamartomatous polyposis or with Joseph Willis, MD hyperplastic/mixed polyposis remain without specific clinical and molecular diagnosis Xiao-Ping Zhou, MD, PhD or present atypically. Assigning a syndromic diagnosis is important because it guides management, especially surveillance and prophylactic surgery. Carol Gallione, PhD Objective To systematically classify patients with unexplained hamartomatous or hy- Takeshi Sawada, MD, PhD perplastic/mixed polyposis by extensive molecular analysis in the context of central Pia Alhopuro, MD rereview of histopathology results. Sok Kean Khoo, PhD Design, Setting, and Patients Prospective, referral-based study of 49 unrelated patients from outside institutions (n=28) and at a comprehensive cancer center (n=21), Attila Patocs, MD, PhD conducted from May 2, 2002, until December 15, 2004. Germline analysis of PTEN, Cossette Martin, PhD BMPR1A, STK11 (sequence, deletion), SMAD4, and ENG (sequence), specific exon screen- Scott Bridgeman, BSc ing of BRAF, MYH, and BHD, and rereview of polyp histology results were performed. John Heinz, PhD Main Outcome Measures Molecular, clinical, and histopathological findings in pa- tients with unexplained polyposis. Robert Pilarski, MS, CGC Results Of the 49 patients, 11 (22%) had germline mutations. Of 14 patients with Rainer Lehtonen, BSc juvenile polyposis, 2 with early-onset disease had mutations in ENG, encoding endo- Thomas W. Prior, PhD glin, previously only associated with hereditary hemorrhagic telangiectasia; 1 had hemi- zygous deletion encompassing PTEN and BMPR1A; and 1 had an SMAD4 mutation. Thierry Frebourg, MD, PhD One individual previously classified with Peutz-Jeghers syndrome had a PTEN dele- Bin Tean Teh, MD, PhD tion. -
Miami University – the Graduate School
MIAMI UNIVERSITY – THE GRADUATE SCHOOL CERTIFICATE FOR APPROVING THE DISSERTATION We hereby approve the Dissertation Of Elvis K. Tiburu Candidate for the Degree: Doctor of Philosophy Dr. Gary A. Lorigan, Director Dr. Christopher A. Makaroff, Reader Dr. Robert E. Minto, Reader Dr. Richard T. Taylor, Reader Dr. David G. Pennock Graduate School Representative ABSTRACT DEVELOPMENT OF NEW METHODS FOR THE ALIGNMENT OF LONGER CHAIN PHOSPHOLIPIDS IN BICELLES AND SOLID-STATE NMR STUDIES OF PHOSPHOLAMBAN by Elvis K. Tiburu Magnetically aligned phospholipid bilayers or bicelles are model systems that mimic biological membranes for magnetic resonance studies. A long chain phospholipid bilayer system that spontaneously aligns in a static magnetic field was characterized utilizing solid-state NMR spectroscopy. The oriented membrane system was composed of a mixture of the bilayer-forming phospholipid palmitoylstearoylphosphatidylcholine (PSPC) and the short-chain phospholipid dihexanoylphosphatidylcholine (DHPC) that breaks up the extended bilayers into bilayered micelles or bicelles that are highly hydrated. Traditionally, the shorter 14-carbon chain phospholipid dimyristoyl- phosphatidylcholine (DMPC) has been utilized as the bilayer-forming phospholipid in bicelle studies. The effect of cholesterol in bicelles containing chain perdeuterated 2 DMPC, a partially deuterated (a-[2,2,3,4,4,6- H6]) cholesterol, and stearic acid-d35 has been reported as a function of temperature using 2H solid-state NMR spectroscopy. The order parameters of the labeled probes were calculated and compared with values obtained from unoriented samples in the literature. In addition, 2H solid-state NMR spectroscopy was used to investigate the orientation and side chain dynamics of specific- labeled methyl groups of leucines in PLB in unoriented as well as in magnetically and mechanically aligned phospholipids bilayers. -
Biochemical Journal
www.biochemj.org Biochem. J. (2007) 405, 199–221 (Printed in Great Britain) doi:10.1042/BJ20070255 199 REVIEW ARTICLE Structures and metal-ion-binding properties of the Ca2+-binding helix–loop–helix EF-hand motifs Jessica L. GIFFORD*, Michael P. WALSH† and Hans J. VOGEL*1 *Structural Biology Research Group, Department of Biological Sciences, University of Calgary, Calgary, Alberta, Canada T2N 1N4, and †Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1 The ‘EF-hand’ Ca2+-binding motif plays an essential role in interaction site or structure formation from a molten-globule eukaryotic cellular signalling, and the proteins containing this apo state. EF-hand proteins exhibit various sensitivities to Ca2+, motif constitute a large and functionally diverse family. The EF- reflecting the intrinsic binding ability of the EF-hand as well as hand is defined by its helix–loop–helix secondary structure as the degree of co-operativity in Ca2+ binding to paired EF-hands. well as the ligands presented by the loop to bind the Ca2+ ion. The Two additional factors can influence the ability of an EF-hand identity of these ligands is semi-conserved in the most common to bind Ca2+: selectivity over Mg2+ (a cation with very similar (the ‘canonical’) EF-hand; however, several non-canonical EF- chemical properties to Ca2+ and with a cytoplasmic concentration hands exist that bind Ca2+ by a different co-ordination mechanism. several orders of magnitude higher) and interaction with a protein EF-hands tend to occur in pairs, which form a discrete domain so target. -
Dimerization of Neuronal Calcium Sensor Proteins
UC Davis UC Davis Previously Published Works Title Dimerization of Neuronal Calcium Sensor Proteins. Permalink https://escholarship.org/uc/item/8426s2jv Author Ames, James B Publication Date 2018 DOI 10.3389/fnmol.2018.00397 Peer reviewed eScholarship.org Powered by the California Digital Library University of California REVIEW published: 02 November 2018 doi: 10.3389/fnmol.2018.00397 Dimerization of Neuronal Calcium Sensor Proteins James B. Ames* Department of Chemistry, University of California, Davis, Davis, CA, United States 2 Neuronal calcium sensor (NCS) proteins are EF-hand containing Ca C binding proteins that regulate sensory signal transduction. Many NCS proteins (recoverin, GCAPs, neurocalcin and visinin-like protein 1 (VILIP1)) form functional dimers under physiological conditions. The dimeric NCS proteins have similar amino acid sequences (50% homology) but each bind to and regulate very different physiological targets. Retinal 2 recoverin binds to rhodopsin kinase and promotes Ca C-dependent desensitization of light-excited rhodopsin during visual phototransduction. The guanylyl cyclase activating proteins (GCAP1–5) each bind and activate retinal guanylyl cyclases (RetGCs) in light- adapted photoreceptors. VILIP1 binds to membrane targets that modulate neuronal secretion. Here, I review atomic-level structures of dimeric forms of recoverin, GCAPs and VILIP1. The distinct dimeric structures in each case suggest that NCS dimerization may play a role in modulating specific target recognition. The dimerization of recoverin 2 2 and VILIP1 is Ca C-dependent and enhances their membrane-targeting Ca C-myristoyl switch function. The dimerization of GCAP1 and GCAP2 facilitate their binding to dimeric 2 RetGCs and may allosterically control the Ca C-dependent activation of RetGCs. -
Differential Expression of Endoglin in Human Melanoma Cells Expressing the V3 Isoform of Versican by Microarray Analysis
MOLECULAR MEDICINE REPORTS 3: 1035-1039, 2010 Differential expression of endoglin in human melanoma cells expressing the V3 isoform of versican by microarray analysis LAIA MIQUEL-SERRA, DANIEL HERNÁNDEZ, MARÍA-JOSÉ DOCAMPO and ANNA BASSOLS Departament de Bioquímica i Biologia Molecular, Universitat Autònoma de Barcelona, 08193 Cerdanyola del Vallès, Spain Received May 28, 2010; Accepted August 13, 2010 DOI: 10.3892/mmr.2010.357 Abstract. Versican is a large chondroitin sulfate proteoglycan overexpression reduced tumor growth rate in mice, but favored produced by several tumor types, including malignant mela- the appearance of secondary tumors (12). noma, which exists as four different splice variants. The large Endoglin (ENG, CD105) is a cell surface component of the isoforms V0 and V1 promote melanoma cell proliferation. transforming growth factor (TGF)-β receptor complex (13), We previously described that overexpression of the short V3 which is highly expressed in the tumor-associated vascular isoform in MeWo human melanoma cells markedly reduced endothelium (14) and in tumor cells. The expression of tumor cell growth in vitro and in vivo, but favored the appear- endoglin appears to play an important role in cancer progres- ance of secondary tumors. This study aimed to elucidate the sion, influencing cell proliferation, motility, invasiveness and mechanisms of V3 by identifying differentially expressed tumorigenicity (15). genes between parental and V3-expressing MeWo melanoma In the present study, we used a high-throughput approach cells using microarray analysis. V3 expression significantly to gain further insight into the mechanism by which the V3 reduced the expression of endoglin, a transforming growth isoform exerts its effects on tumor progression. -
Paraneoplastic Neurological and Muscular Syndromes
Paraneoplastic neurological and muscular syndromes Short compendium Version 4.5, April 2016 By Finn E. Somnier, M.D., D.Sc. (Med.), copyright ® Department of Autoimmunology and Biomarkers, Statens Serum Institut, Copenhagen, Denmark 30/01/2016, Copyright, Finn E. Somnier, MD., D.S. (Med.) Table of contents PARANEOPLASTIC NEUROLOGICAL SYNDROMES .................................................... 4 DEFINITION, SPECIAL FEATURES, IMMUNE MECHANISMS ................................................................ 4 SHORT INTRODUCTION TO THE IMMUNE SYSTEM .................................................. 7 DIAGNOSTIC STRATEGY ..................................................................................................... 12 THERAPEUTIC CONSIDERATIONS .................................................................................. 18 SYNDROMES OF THE CENTRAL NERVOUS SYSTEM ................................................ 22 MORVAN’S FIBRILLARY CHOREA ................................................................................................ 22 PARANEOPLASTIC CEREBELLAR DEGENERATION (PCD) ...................................................... 24 Anti-Hu syndrome .................................................................................................................. 25 Anti-Yo syndrome ................................................................................................................... 26 Anti-CV2 / CRMP5 syndrome ............................................................................................