A Bioinformatics Model of Human Diseases on the Basis Of
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FGF19 Protects Hepatocellular Carcinoma Cells Against Endoplasmic Reticulum Stress Via Activation of FGFR4-Gsk3β-Nrf2 Signaling
Author Manuscript Published OnlineFirst on September 26, 2017; DOI: 10.1158/0008-5472.CAN-17-2039 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. FGF19 protects hepatocellular carcinoma cells against endoplasmic reticulum stress via activation of FGFR4-GSK3β-Nrf2 signaling Yong Teng1,2#*, Huakan Zhao3,4#, Lixia Gao1, Wenfa Zhang3, Austin Y Shull5, Chloe Shay6 1. Department of Oral Biology, Augusta University, Augusta, GA, USA 2. Georgia Cancer Center, Augusta University, Augusta, GA, USA 3. School of Life Sciences, Chongqing University, Chongqing, China 4. Institute of Cancer, Xinqiao Hospital, Third Military Medical University, Chongqing, China 5. Department of Biology, Presbyterian College, Clinton, SC, USA 6. Emory Children’s Center, Emory University, Atlanta, GA, USA # These authors contributed equally to this work Running Title: Role of FGF19 in ER stress Key Words: FGF19, FGFR4, Nrf2, HCC, ER stress, anticancer Abbreviations list: AARE: amino-acid-response element; ANOVA: analysis of variance; ARE: antioxidant response elements; ATF4: activating transcription factor 4; ChIP-qPCR: chromatin immunoprecipitation quantitative-PCR; CV: cyclic voltammetry; DMSO: dimethyl sulfoxide; EMT: epithelial-mesenchymal transition; ER: endoplasmic reticulum; FGF19: fibroblast growth factor 19; FGFR4: FGF receptor 4; GSK3β: glycogen synthase kinase •− 3β; HCC: hepatocellular carcinoma; Nrf2: nuclear factor E2-related factor 2; O2 : superoxide; PBS: phosphate-buffered saline; ROS: reactive free -
Release Β ATP-Induced IL-1 and Canonical Nicotinic Agonists Inhibit Phosphocholine-Modified Macromolecules
Phosphocholine-Modified Macromolecules and Canonical Nicotinic Agonists Inhibit ATP-Induced IL-1β Release This information is current as Andreas Hecker, Mira Küllmar, Sigrid Wilker, Katrin of September 24, 2021. Richter, Anna Zakrzewicz, Srebrena Atanasova, Verena Mathes, Thomas Timm, Sabrina Lerner, Jochen Klein, Andreas Kaufmann, Stefan Bauer, Winfried Padberg, Wolfgang Kummer, Sabina Janciauskiene, Martin Fronius, Elke K. H. Schweda, Günter Lochnit and Veronika Grau Downloaded from J Immunol 2015; 195:2325-2334; Prepublished online 22 July 2015; doi: 10.4049/jimmunol.1400974 http://www.jimmunol.org/content/195/5/2325 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2015/07/22/jimmunol.140097 Material 4.DCSupplemental References This article cites 42 articles, 11 of which you can access for free at: http://www.jimmunol.org/content/195/5/2325.full#ref-list-1 by guest on September 24, 2021 Why The JI? Submit online. • 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 © 2015 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. -
Rabbit Anti-CHRNA10/FITC Conjugated Antibody-SL12111R-FITC
SunLong Biotech Co.,LTD Tel: 0086-571- 56623320 Fax:0086-571- 56623318 E-mail:[email protected] www.sunlongbiotech.com Rabbit Anti-CHRNA10/FITC Conjugated antibody SL12111R-FITC Product Name: Anti-CHRNA10/FITC Chinese Name: FITC标记的烟碱型乙酰胆碱受体α10/AChRα10抗体 Acetylcholine receptor, neuronal nicotinic, alpha-10 subunit; ACH10_HUMAN; Alpha 10 nAChR; Cholinergic receptor nicotinic alpha 10; Cholinergic receptor, neuronal nicotinic, alpha polypeptide 10; Cholinergic receptor, nicotinic, alpha polypeptide 10; Alias: CHRNA 10; CHRNA10; NACHR alpha 10; NACHR alpha-10; NACHRA10; Neuronal acetylcholine receptor protein subunit alpha 10; Neuronal acetylcholine receptor subunit alpha-10; Nicotinic acetylcholine receptor subunit alpha 10; Nicotinic acetylcholine receptor subunit alpha-10. Organism Species: Rabbit Clonality: Polyclonal React Species: Human,Mouse,Rat,Dog,Pig,Cow,Horse,Rabbit,Sheep, ICC=1:50-200IF=1:50-200 Applications: not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. Molecular weight: 47kDa Cellular localization: The cell membrane Form: Lyophilizedwww.sunlongbiotech.com or Liquid Concentration: 1mg/ml immunogen: KLH conjugated synthetic peptide derived from human CHRNA10 Lsotype: IgG Purification: affinity purified by Protein A Storage Buffer: 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year Storage: when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. background: Product Detail: Members of the ligand-gated ion channel receptor family are characterized by their fast transmitting response to neurotransmitters. -
ARTICLES Fibroblast Growth Factors 1, 2, 17, and 19 Are The
0031-3998/07/6103-0267 PEDIATRIC RESEARCH Vol. 61, No. 3, 2007 Copyright © 2007 International Pediatric Research Foundation, Inc. Printed in U.S.A. ARTICLES Fibroblast Growth Factors 1, 2, 17, and 19 Are the Predominant FGF Ligands Expressed in Human Fetal Growth Plate Cartilage PAVEL KREJCI, DEBORAH KRAKOW, PERTCHOUI B. MEKIKIAN, AND WILLIAM R. WILCOX Medical Genetics Institute [P.K., D.K., P.B.M., W.R.W.], Cedars-Sinai Medical Center, Los Angeles, California 90048; Department of Obstetrics and Gynecology [D.K.] and Department of Pediatrics [W.R.W.], UCLA School of Medicine, Los Angeles, California 90095 ABSTRACT: Fibroblast growth factors (FGF) regulate bone growth, (G380R) or TD (K650E) mutations (4–6). When expressed at but their expression in human cartilage is unclear. Here, we deter- physiologic levels, FGFR3-G380R required, like its wild-type mined the expression of entire FGF family in human fetal growth counterpart, ligand for activation (7). Similarly, in vitro cul- plate cartilage. Using reverse transcriptase PCR, the transcripts for tivated human TD chondrocytes as well as chondrocytes FGF1, 2, 5, 8–14, 16–19, and 21 were found. However, only FGF1, isolated from Fgfr3-K644M mice had an identical time course 2, 17, and 19 were detectable at the protein level. By immunohisto- of Fgfr3 activation compared with wild-type chondrocytes and chemistry, FGF17 and 19 were uniformly expressed within the showed no receptor activation in the absence of ligand (8,9). growth plate. In contrast, FGF1 was found only in proliferating and hypertrophic chondrocytes whereas FGF2 localized predominantly to Despite the importance of the FGF ligand for activation of the resting and proliferating cartilage. -
Gene Expression Analysis Identifies Potential Biomarkers of Neurofibromatosis Type 1 Including Adrenomedullin
Published OnlineFirst August 25, 2010; DOI: 10.1158/1078-0432.CCR-10-0613 Clinical Imaging, Diagnosis, Prognosis Cancer Research Gene Expression Analysis Identifies Potential Biomarkers of Neurofibromatosis Type 1 Including Adrenomedullin Trent R. Hummel1, Walter J. Jessen1, Shyra J. Miller1, Lan Kluwe4, Victor F. Mautner4, Margaret R. Wallace5, Conxi Lázaro6, Grier P. Page7, Paul F. Worley8, Bruce J. Aronow2, Elizabeth K. Schorry3, and Nancy Ratner1 Abstract Purpose: Plexiform neurofibromas (pNF) are Schwann cell tumors found in a third of individuals with neurofibromatosis type 1 (NF1). pNF can undergo transformation to malignant peripheral nerve sheath tumors (MPNST). There are no identified serum biomarkers of pNF tumor burden or transformation to MPNST. Serum biomarkers would be useful to verify NF1 diagnosis, monitor tumor burden, and/or detect transformation. Experimental Design: We used microarray gene expression analysis to define 92 genes that encode putative secreted proteins in neurofibroma Schwann cells, neurofibromas, and MPNST. We validated dif- ferential expression by quantitative reverse transcription-PCR, Western blotting, and ELISA assays in cell conditioned medium and control and NF1 patient sera. Results: Of 13 candidate genes evaluated, only adrenomedullin (ADM) was confirmed as differentially expressed and elevated in serum of NF1 patients. ADM protein concentrati on was further elevated in serum of a small sampling of NF1 patients with MPNST. MPNST cell conditioned medium, containing ADM and hepatocyte growth factor, stimulated MPNST migration and endothelial cell proliferation. Conclusions: Thus, microarray analysis identifies potential serum biomarkers for disease, and ADM is a serum biomarker of NF1. ADM serum levels do not seem to correlate with the presence of pNFs but may be a biomarker of transformation to MPNST. -
GABA Receptors
D Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews Review No.7 / 1-2011 GABA receptors Wolfgang Froestl , CNS & Chemistry Expert, AC Immune SA, PSE Building B - EPFL, CH-1015 Lausanne, Phone: +41 21 693 91 43, FAX: +41 21 693 91 20, E-mail: [email protected] GABA Activation of the GABA A receptor leads to an influx of chloride GABA ( -aminobutyric acid; Figure 1) is the most important and ions and to a hyperpolarization of the membrane. 16 subunits with γ most abundant inhibitory neurotransmitter in the mammalian molecular weights between 50 and 65 kD have been identified brain 1,2 , where it was first discovered in 1950 3-5 . It is a small achiral so far, 6 subunits, 3 subunits, 3 subunits, and the , , α β γ δ ε θ molecule with molecular weight of 103 g/mol and high water solu - and subunits 8,9 . π bility. At 25°C one gram of water can dissolve 1.3 grams of GABA. 2 Such a hydrophilic molecule (log P = -2.13, PSA = 63.3 Å ) cannot In the meantime all GABA A receptor binding sites have been eluci - cross the blood brain barrier. It is produced in the brain by decarb- dated in great detail. The GABA site is located at the interface oxylation of L-glutamic acid by the enzyme glutamic acid decarb- between and subunits. Benzodiazepines interact with subunit α β oxylase (GAD, EC 4.1.1.15). It is a neutral amino acid with pK = combinations ( ) ( ) , which is the most abundant combi - 1 α1 2 β2 2 γ2 4.23 and pK = 10.43. -
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. -
Transcriptomic Analysis of Native Versus Cultured Human and Mouse Dorsal Root Ganglia Focused on Pharmacological Targets Short
bioRxiv preprint doi: https://doi.org/10.1101/766865; this version posted September 12, 2019. 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-ND 4.0 International license. Transcriptomic analysis of native versus cultured human and mouse dorsal root ganglia focused on pharmacological targets Short title: Comparative transcriptomics of acutely dissected versus cultured DRGs Andi Wangzhou1, Lisa A. McIlvried2, Candler Paige1, Paulino Barragan-Iglesias1, Carolyn A. Guzman1, Gregory Dussor1, Pradipta R. Ray1,#, Robert W. Gereau IV2, # and Theodore J. Price1, # 1The University of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, 800 W Campbell Rd. Richardson, TX, 75080, USA 2Washington University Pain Center and Department of Anesthesiology, Washington University School of Medicine # corresponding authors [email protected], [email protected] and [email protected] Funding: NIH grants T32DA007261 (LM); NS065926 and NS102161 (TJP); NS106953 and NS042595 (RWG). The authors declare no conflicts of interest Author Contributions Conceived of the Project: PRR, RWG IV and TJP Performed Experiments: AW, LAM, CP, PB-I Supervised Experiments: GD, RWG IV, TJP Analyzed Data: AW, LAM, CP, CAG, PRR Supervised Bioinformatics Analysis: PRR Drew Figures: AW, PRR Wrote and Edited Manuscript: AW, LAM, CP, GD, PRR, RWG IV, TJP All authors approved the final version of the manuscript. 1 bioRxiv preprint doi: https://doi.org/10.1101/766865; this version posted September 12, 2019. 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. -
Molecular Mediators of Acute and Chronic Itch in Mouse and Human Sensory Neurons Manouela Valtcheva Washington University in St
Washington University in St. Louis Washington University Open Scholarship Arts & Sciences Electronic Theses and Dissertations Arts & Sciences Spring 5-15-2018 Molecular Mediators of Acute and Chronic Itch in Mouse and Human Sensory Neurons Manouela Valtcheva Washington University in St. Louis Follow this and additional works at: https://openscholarship.wustl.edu/art_sci_etds Part of the Neuroscience and Neurobiology Commons Recommended Citation Valtcheva, Manouela, "Molecular Mediators of Acute and Chronic Itch in Mouse and Human Sensory Neurons" (2018). Arts & Sciences Electronic Theses and Dissertations. 1596. https://openscholarship.wustl.edu/art_sci_etds/1596 This Dissertation is brought to you for free and open access by the Arts & Sciences at Washington University Open Scholarship. It has been accepted for inclusion in Arts & Sciences Electronic Theses and Dissertations by an authorized administrator of Washington University Open Scholarship. For more information, please contact [email protected]. WASHINGTON UNIVERSITY IN ST. LOUIS Division of Biology and Biomedical Sciences Neurosciences Dissertation Examination Committee: Robert W. Gereau, IV, Chair Yu-Qing Cao Sanjay Jain Qin Liu Durga Mohapatra Molecular Mediators of Acute and Chronic Itch in Mouse and Human Sensory Neurons by Manouela Vesselinova Valtcheva A dissertation presented to The Graduate School of Washington University in partial fulfillment of the requirements for the degree of Doctor of Philosophy May 2018 St. Louis, Missouri © 2018, Manouela V. Valtcheva Table -
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]. -
Research Article Microarray-Based Comparisons of Ion Channel Expression Patterns: Human Keratinocytes to Reprogrammed Hipscs To
Hindawi Publishing Corporation Stem Cells International Volume 2013, Article ID 784629, 25 pages http://dx.doi.org/10.1155/2013/784629 Research Article Microarray-Based Comparisons of Ion Channel Expression Patterns: Human Keratinocytes to Reprogrammed hiPSCs to Differentiated Neuronal and Cardiac Progeny Leonhard Linta,1 Marianne Stockmann,1 Qiong Lin,2 André Lechel,3 Christian Proepper,1 Tobias M. Boeckers,1 Alexander Kleger,3 and Stefan Liebau1 1 InstituteforAnatomyCellBiology,UlmUniversity,Albert-EinsteinAllee11,89081Ulm,Germany 2 Institute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen, Pauwelstrasse 30, 52074 Aachen, Germany 3 Department of Internal Medicine I, Ulm University, Albert-Einstein Allee 11, 89081 Ulm, Germany Correspondence should be addressed to Alexander Kleger; [email protected] and Stefan Liebau; [email protected] Received 31 January 2013; Accepted 6 March 2013 Academic Editor: Michael Levin Copyright © 2013 Leonhard Linta et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Ion channels are involved in a large variety of cellular processes including stem cell differentiation. Numerous families of ion channels are present in the organism which can be distinguished by means of, for example, ion selectivity, gating mechanism, composition, or cell biological function. To characterize the distinct expression of this group of ion channels we have compared the mRNA expression levels of ion channel genes between human keratinocyte-derived induced pluripotent stem cells (hiPSCs) and their somatic cell source, keratinocytes from plucked human hair. This comparison revealed that 26% of the analyzed probes showed an upregulation of ion channels in hiPSCs while just 6% were downregulated. -
Artemin, a Novel Member of the GDNF Ligand Family, Supports Peripheral and Central Neurons and Signals Through the GFR␣3–RET Receptor Complex
CORE Metadata, citation and similar papers at core.ac.uk Provided by Elsevier - Publisher Connector Neuron, Vol. 21, 1291±1302, December, 1998, Copyright 1998 by Cell Press Artemin, a Novel Member of the GDNF Ligand Family, Supports Peripheral and Central Neurons and Signals through the GFRa3±RET Receptor Complex Robert H. Baloh,* Malu G. Tansey,² et al., 1998; Milbrandt et al., 1998; reviewed by Grondin Patricia A. Lampe,² Timothy J. Fahrner,* and Gash, 1998). However, the GDNF ligands also influ- Hideki Enomoto,* Kelli S. Simburger,* ence a broad spectrum of other neuronal populations Melanie L. Leitner,² Toshiyuki Araki,* in both the CNS and PNS. GDNF and NTN both support Eugene M. Johnson, Jr.,² the survival of many peripheral neurons in culture, in- and Jeffrey Milbrandt*³ cluding sympathetic, parasympathetic, sensory, and en- *Department of Pathology and teric neurons (Buj-Bello et al., 1995; Ebendal et al., 1995; Department of Internal Medicine Trupp et al., 1995; Kotzbauer et al., 1996; Heuckeroth ² Department of Neurology and et al., 1998). In contrast, PSP does not share any of Department of Molecular Biology these peripheral activities but does support the survival and Pharmacology of dopaminergic midbrain neurons and motor neurons Washington University (Milbrandt et al., 1998). Despite the fact that GDNF acts School of Medicine on many cell populations in vitro, analysis of GDNF St. Louis, Missouri 63110 knockout mice revealed that the major developmental importance of GDNF is in the enteric nervous system and in kidney organogenesis, both of which are lost in Summary GDNF null mice (Moore et al., 1996; Pichel et al., 1996; Sanchez et al., 1996).