DOCSLIB.ORG

A Unique Estrogen Receptor-Regulated Gene That Is Activated by Antiestrogens (Electrophile Response Element͞tamoxifen͞antioxidant͞breast Cancer)

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
A Unique Estrogen Receptor-Regulated Gene That Is Activated by Antiestrogens (Electrophile Response Element͞tamoxifen͞antioxidant͞breast Cancer) Proc. Natl. Acad. Sci. USA Vol. 94, pp. 2581–2586, March 1997 Medical Sciences The quinone reductase gene: A unique estrogen receptor-regulated gene that is activated by antiestrogens (electrophile response elementytamoxifenyantioxidantybreast cancer) MONICA M. MONTANO* AND BENITA S. KATZENELLENBOGEN*†‡ *Departments of Molecular and Integrative Physiology and †Cell and Structural Biology, University of Illinois and College of Medicine, Urbana, IL 61801-3704 Communicated by Jack Gorski, University of Wisconsin, Madison, WI, December 30, 1996 (received for review October 4, 1996) ABSTRACT Antiestrogens are thought to exert most of 10 and 11). These widely distributed enzymes detoxify elec- their beneficial effects in breast cancer by antagonizing the trophiles, thereby protecting cells against the toxic and neo- actions of estrogen. We report here that antiestrogens also plastic effects of carcinogens. stimulate the expression of quinone reductase (QR) [NAD- Using the technique of RNA differential display (12), we (P)H:quinone oxidoreductase, EC 1.6.99.2], which may pro- have identified in this report QR mRNA as a species that is vide protective effects against the toxicity and mutagenicity expressed at much higher levels in an MCF-7 breast cancer cell caused by quinones. QR is up-regulated by low concentrations subline that has been grown long term in the presence of the of antiestrogens (trans-hydroxytamoxifen, tamoxifen, and antiestrogen trans-hydroxytamoxifen (TOT) (13). We there- ICI182,780) in estrogen receptor (ER)-containing breast can- fore undertook the examination of its regulation by antiestro- cer cells, and this increase is suppressed by estrogen via an gens as a possible basis for the proposed antioxidant action of ER-dependent mechanism. Since regulation of the QR gene, as tamoxifen. The molecular mechanisms for the induction of well as other genes involved in detoxification such as the phase 2 enzymes by antiestrogen were also explored in view of glutathione S-transferase Ya subunit (GST Ya) gene, is known their importance in devising strategies for chemoprotection to be mediated by an electrophile antioxidant response ele- y against cancer. It has been reported that the induction of the ment (EpREyARE), we examined the effects of antiestrogens GST Ya subunit (GST Ya) and QR genes is mediated through on a 41-bp electrophile responsive region derived from the GST Ya gene. Transfection of this EpRE-containing region an electrophile (or antioxidant) response element (EpRE or into ER-negative breast cancer cells in the presence or absence ARE) (14, 15), although the identity of the EpREyARE of an expression vector for the human ER, as well as mu- enhancer binding protein(s) is not known. tagenesis studies, revealed that the EpRE-containing con- In our studies, we have observed that the QR gene shows struct was activated by antiestrogen to the same extent as by reversed pharmacology, being markedly up-regulated by an- tert-butylhydroquinone (TBHQ), a known activator of EpREs; tiestrogen and suppressed by estrogen in breast cancer cells. however, only the stimulation by antiestrogen, and not TBHQ, Our data indicate that there are two pathways for QR up- required ER and was repressed by estradiol, although activa- regulation, one that is antiestrogen modulated and estrogen tion by both inducers mapped to the same 10-bp EpRE receptor (ER) dependent, and a second that is stimulated by consensus sequence. Thus, there appear to be two pathways known electrophile inducers such as tert-butylhydroquinone for QR induction, one that is activated by electrophile induc- (TBHQ) and is ER independent. Transfection and mutagen- ers such as TBHQ and is ER independent, and a second that esis studies on gene constructs with the 41-bp EpRE- is antiestrogen regulated and ER dependent; both pathways containing region from the GST Ya gene indicate that anties- act through the EpRE. The anticancer action of antiestrogens trogen-mediated activation occurs at the transcriptional level may thus derive not only from the already well-known repres- via the EpRE and requires the ER. These observations have sion of estrogen-stimulated activities but also from the acti- broad implications regarding potential antiestrogen regulation vation of detoxifying enzymes, such as QR, that may contrib- of a variety of genes whose transcription is under the control ute to the beneficial antioxidant activity of antiestrogens. of EpREyAREs. Tamoxifen is an anticancer drug that is widely used in the MATERIALS AND METHODS treatment of breast cancer (1–4). It is also being assessed as a preventive agent for this disease and for other potential Chemicals and Materials. Cell culture media were pur- benefits, such as protection against cardiovascular disease and chased from GIBCO. Calf serum was from HyClone and fetal osteoporosis (5, 6). It has been proposed that tamoxifen may calf serum (FCS) from Sigma. The antiestrogens ICI182,780 function as an anticancer drug, possibly by acting as an (ICI), tamoxifen, and TOT were kindly provided by Alan antioxidant (7–9). However, the basis for the antioxidant Wakeling and Zeneca Pharmaceuticals (Macclesfield, En- capabilities of tamoxifen has not been well characterized. gland). 12-Tetradecanoate 13-acetate (TPA), NADPH, men- Phase 2 detoxification enzymes such as NAD(P)H:(qui- adione, and cytochrome c were obtained from Sigma. TBHQ none-acceptor) oxidoreductase [quinone reductase (QR)], was obtained from Aldrich. glutathione S-transferases (GSTs), epoxide hydrolase, and UDP-glucuronosyltransferases are induced in cells by electro- philic compounds and phenolic antioxidants (reviewed in refs. Abbreviations: ER, estrogen receptor; E2, estradiol; QR, quinone reductase; TBHQ, tert-butylhydroquinone; EpREyARE, electro- phileyantioxidant response element; GST Ya, glutathione S- The publication costs of this article were defrayed in part by page charge transferase Ya subunit; TOT, trans-hydroxytamoxifen; GH, growth payment. This article must therefore be hereby marked ‘‘advertisement’’ in hormone; TPA, 12-tetradecanoate 13-acetate; TRE, TPA response accordance with 18 U.S.C. §1734 solely to indicate this fact. element; b-gal, b-galactosidase; ICI, ICI182,780. ‡To whom reprint requests should be addressed at: Department of Copyright q 1997 by THE NATIONAL ACADEMY OF SCIENCES OF THE USA Molecular and Integrative Physiology, University of Illinois, 524 0027-8424y97y942581-6$2.00y0 Burrill Hall, 407 South Goodwin Avenue, Urbana, IL 61801. e-mail: PNAS is available online at http:yywww.pnas.org. [email protected]. 2581 Downloaded by guest on September 26, 2021 2582 Medical Sciences: Montano and Katzenellenbogen Proc. Natl. Acad. Sci. USA 94 (1997) Plasmids. The growth hormone (GH) reporter gene con- inhibitor (GIBCO) for 30 min at 378C. After phenoly structs p284GstYa-GH (containing the mouse GST Ya gene chloroform extraction and ethanol precipitation, three reverse minimal promoter region), p41–284GstYa-GH (containing transcription reactions were performed for each RNA sample the mouse GST Ya gene minimal promoter and the 59 using 0.2 mg of DNA-free total RNA in 13 reverse transcrip- upstream 41-bp EpRE-containing region), and pTREX2– tion buffer (25 mM TriszCl, pH 8.3y37.6 mM KCly1.5 mM 284GstYa-GH [containing the mouse GST Ya gene minimal MgCl2y5mMDTT)and20mM each of dATP, dCTP, dGTP, promoter region and two consensus TPA response element and dTTP, and 0.2 mMofHindIII restriction site-containing (TRE) sites] were kindly provided by Paul Talalay (The John one-base anchored oligo(dT) primers [either H-T11A (59- Hopkins University School of Medicine) (16). AAGCTTTTTTTTTTTA-39), H-T11C (59-AAGCTT- Five reporter constructs, each containing mutations intro- TTTTTTTTTC-39), or HT11G (59-AAGCTTTTTTT- duced sequentially into the 41-bp fragment containing the TTTTG-39)]. After the solution was heated at 658C for 5 min EpRE, were constructed by site-directed mutagenesis (17), and cooled to 378C, 100 units of Moloney murine leukemia with modification (18). The ScaIySacI fragment of p41– virus reverse transcriptase was added for 1 hr. PCRs were 284GstYa-GH was inserted into the SacIySmaI site of Blue- performed in reaction mixtures containing 0.1 vol of reverse script II SK1 (Stratagene) to make p41–284GstYa-BSK1. transcription reaction mixture, 13 PCR buffer (10 mM TriszCl, Mutagenic oligonucleotides were then annealed to single- pH 8.4y50 mM KCly1.5 mM MgCl2y0.001% gelatin), 2 mM stranded DNA generated using the f1 origin of replication in each of dATP, dCTP, dGTP, and dTTP, 0.2 mMofHindIII Bluescript II SK1. The mutagenic oligonucleotides used in restriction site-containing arbitrary 13-mer oligonucleotide five separate mutagenesis reactions were: 59-CAGTGCCA- [either H-AP1 (59-AAGCTTGATTGCC-39), H-AP2 (59- AGCTCTGCAGAAAAATGACATTGC-39,59-AGCTTA- AAGCTTCGACTGT-39), H-AP3 (59-AAGCTTTGGT- GCTTGGGTCCATGGTTGCTAATGGTG-39,59-TTGGA- CAG-39), H-AP4 (59-AAGCTTCTCAACG) or H-AP5 (59- AATGACATTGCTCTTCGTGACAAAGCA-39,59-GACA- AAGCTTAGTAGGC-39)], 0.2 mM of the corresponding Hin- TTGCTAATTTGGATCCAGCAACTTTGTC-39, and 59- dIII restriction site-containing one-base anchored oligo(dT) TAATGGTGACAAAGATCTTGTGTCGACTCTAG-39. primer, 0.1 mCi of 35S-dATP (1 Ci 5 37 GBq), and 1 unit of To make each of the five mutated p41–284GstYa-GH reporter AmpliTaq DNA polymerase (Perkin–ElmeryCetus). Light constructs (M1–M5) the NdeIySacI fragment of p41– mineral oil was overlaid and the PCR reactions were per- 284GstYa-GH was then replaced with the mutated NdeIySacI formed at 948C for 30 sec and 40 cycles of 948C for 30 sec, 408C fragment of p41–284GstYa-BSK1. for 2 min, 728C for 30 sec, followed by 728C for 5 min. Stop The expression vector for the wild-type human ER and the buffer (95% formamidey10 mM EDTA, pH 8.0y0.09% xylene mutant ER that lacks activation function-2 activity (ERS554fs) cyanoly0.09% bromophenol blue) was added to each sample has been described (19). The expression vector for the ER and heated at 808C for 2 min before loading on 6% polyacryl- DNA binding mutant, ER (missing amino acids 185– DBDmut amide sequencing gels. After electrophoresis the gels were 251), was constructed by replacing the EagI EagI fragment y exposed to Kodak XAR-5 film for 48 hr.
Load more

Recommended publications
  • MICHAEL J. WELCH, Ph.D. Personal Information
    CURRICULUM VITAE – MICHAEL J. WELCH, Ph.D. Personal Information: a. Sex: Male b. Birth date: 28 June 1939 c. Birthplace: Stoke-on-Trent, England Citizenship: USA__X__ Other____ Addresses and Telephone Numbers: Office: Division of Radiological Sciences Department of Radiology Washington University School of Medicine 510 South Kingshighway Blvd. Campus Box 8225 St. Louis, Missouri 63110 USA 314-362-8436 314-362-8399 fax Home: 312 N. Meramec #200 St. Louis, MO 63105 314-727-1550 Present Positions: Professor of Radiology Professor of Chemistry Professor of Developmental Biology Professor of Biomedical Engineering Washington University in St. Louis Education: Undergraduate: B.A. Degree in Natural Sciences – Cambridge University, England, 1961 Graduate: M.A. Degree in Natural Sciences – Cambridge University, England, 1964 Ph.D. Degree Chemistry – University of London, England, 1965 1 Academic Position/Employment: 9/62 - 8/65 Graduate Student Queen Mary College Department of Chemistry University of London London, England 9/65 - 9/67 Research Associate Brookhaven National Laboratory Upton, New York 9/67 - 7/70 Assistant Professor of Radiation Chemistry The Edward Mallinckrodt Institute of Radiology Washington University School of Medicine St. Louis, Missouri 9/69 - 1/71 Assistant Professor of Chemistry Department of Chemistry Washington University St. Louis, Missouri 7/70 - 7/74 Associate Professor of Radiation Chemistry The Edward Mallinckrodt Institute of Radiology Washington University School of Medicine St. Louis, Missouri 1/71 - 7/75 Associate Professor of Chemistry Department of Chemistry Washington University St. Louis, Missouri 7/75 - 7/78 Adjunct Professor Department of Chemistry Washington University St. Louis, Missouri 7/74 - 1991 Professor of Radiation Chemistry The Edward Mallinckrodt Institute of Radiology Washington University School of Medicine St.
    [Show full text]
  • February 18, 1999
    6/20/2020 Curriculum Vitae John A. Katzenellenbogen Contact Information: 461 Roger Adams Laboratory, Box 37 Dept. of Chemistry, Univ. of Illinois 600 South Mathews Avenue 217 333 6310 (office) Fax: 217 333 7325 Urbana, Illinois 61801 E-mail: [email protected] Biographical Background: Place of Birth: Poughkeepsie, New York Citizenship: USA Educational Background: B.A. Chemistry (Summa cum laude) Harvard College 1962-66 M.A. Chemistry Harvard University 1966-67 Ph.D. Chemistry Harvard University 1967-69 (Research Advisor: E. J. Corey) Professional Employment: University of Illinois at Champaign-Urbana Assistant Professor of Chemistry 1969–1975 Associate Professor of Chemistry 1975–1979 Professor of Chemistry 1979–present Beckman Institute Affiliate 1988–present Roger Adams Professor of Chemistry 1992–1996 Swanlund Professor of Chemistry 1996-present Professor of Bioengineering (joint appointment) 2001-present Awards, Fellowships, Honors: Award for Outstanding Achievement in Chemistry in Cancer Research, American Association for Cancer Research (2018) Medicinal Chemistry Hall of Fame, American Chemical Society (2018) The President’s Award, Society for Radiopharmaceutical Sciences (2017) Fred Conrad Koch Lifetime Achievement Award, The Endocrine Society [with Benita Katzenellenbogen] (2016) Inaugural Philip Portoghese Lectureship in Medicinal Chemistry, American Chemical Society (2010) Royal Society of Chemistry Centenary Lectureship Award (2009) Leading Edge in Basic Science Award, Society of Toxicology (2010) Gustavus John Esselen Award
    [Show full text]
  • New Compounds Block Master Regulator of Cancer Growth, Metastasis 7 January 2020, by Diana Yates
    New compounds block master regulator of cancer growth, metastasis 7 January 2020, by Diana Yates The researchers focused on FOXM1 because it is found in higher abundance in cancer cells than in healthy human cells, said Benita Katzenellenbogen, a University of Illinois professor of molecular and integrative physiology who led the study with U. of I. chemistry professor John Katzenellenbogen and life sciences research specialist Yvonne Ziegler. "FOXM1 is a key factor that makes breast cancer and many other cancers more aggressive and more difficult to treat," Benita Katzenellenbogen said. "Because it is a master regulator of cancer growth and metastasis, there has been great interest in developing compounds that would be effective in blocking it." Researchers including, from left, graduate student Valeria Sanabria Guillen, research scientist Sung Hoon So far, no successful drug agents have been Kim, researcher Kathy Carlson, chemistry professor developed to reduce the effects of FOXM1, John John Katzenellenbogen, research specialist Yvonne Katzenellenbogen said. Ziegler, and molecular and integrative physiology professor Benita Katzenellenbogen developed new drug "There are reports of other inhibitors of FOXM1, but agents to inhibit a pathway that contributes to cancer. these are generally less potent and do not work The compounds killed cancer cells and reduced the growth of breast cancer tumors in mice. Credit: L. Brian well in the body," he said. "Our compounds have Stauffer good anti-tumor activity in animal models. They behave well in vivo and have long half-lives in the blood. Some work well when given orally, which is desirable for ultimate patient use." Scientists have developed new drug compounds that thwart the pro-cancer activity of FOXM1, a The researchers developed the new drugs by transcription factor that regulates the activity of analyzing the properties of various compounds in a dozens of genes.
    [Show full text]
  • From the Editors
    CICR NEWSLETTER – June 2018 From the Editors This quarter, following the AACR Annual Meeting 2018, we have chosen to focus on “Contributions of Rational Drug Design towards Precision Medicine.” CICR Editor, Dr. Zoe Cournia, and CICR Editor-elect, Dr. Alex Waterson, along with CICR Editorial Board members, Drs. Iain Watson; Terry Moore; and Martin Swarbrick, have assembled an overview of the topic. In this newsletter, you will also find Selected Research Highlights on precision medicine and recent FDA approvals and the related Profile of the Early-career Researcher, Dr. Steve Staben, of Genentech, along with Global News, Upcoming Conferences, Funding Opportunities, and, of course, an update from Prof. Julian Blagg, CICR Working Group Chairperson, on CICR news and activities. Contributions of rational drug design towards precision medicine Rational drug design began to rise to prominence in the 1980s, superseding a model for drug discovery based more on synthetic organic chemistry and high throughput screening, fueled by significant and continual increases in computing power and advances in structural biology. The antiviral zanamivir is widely acknowledged as one of the first marketed drugs to have been identified by rational design: in what now seems a very familiar approach, X-ray crystallographic data facilitated an understanding of the structure of neuraminidase leading to the discovery and development of this transition-state analogue inhibitor. Additional drugs designed rationally in the 1990s include Saquinavir, discovered based on peptide derivatives that were transition- state mimetics of a sequence found in several retroviral substrates, and ritonavir, utilizing rational design on the structure of the C2-symmetric homodimer structure of HIV-1 PR, which has a single active site.
    [Show full text]
  • Commencement 1991-2000
    Jlfek BUMS} *_y#e Johns Hopkins University # ConfejTing of Degrees at the Close of the 1 1 1th Academic Year * A% 24, 72P5 Digitized by the Internet Archive in 2012 with funding from LYRASIS Members and Sloan Foundation http://archive.org/details/commencement1993 JOHNSUNIVERSITYHOPKINS Office of the Registrar 75 Garland Hall / 3400 N. Charles Street July ,1993 Baltimore MD 21218-2688 (410)516-8080 For those who use the Commencement Program as an official record of the awarding of degrees, please note the following changes to the 1993 Commencement Program: 1. Bachelor of Arts (Arts and Sciences) pages 22-24 Add: Chi Yung Ann Charles Neilson Curlett, Jr. Laura E. Greenwald Zubin Razzaque Khan Delete: Cholmin I. Ann Robert Wayne Jenkins Douglas Allen Besen Dennis Joseph McDonald Paul Anthony Brown Emily M. Miller Renan Carlos Castillo Michelle Nance Leon Chao Kate Byxbe Pessin James Edward Crawford Carlos Antonio Pfeiffer Robert James Dunn David Evan Ross Kelly Lynn Grey Adwoa Aya Sanderson Lover Highjr. Robert Marshall Searles Jane Jungeon Hong Catherine Hughes Tokheim Jeffrey Michael Wills 2. Bachelor of Science in Biomedical Engineering (Engineering) page 24 Add: Irian Amanat 3. Bachelor of Science in Chemical Engineering (Engineering) page 24 Delete: Robert William Apollo 4. Bachelor of Science in Electrical Engineering (Engineering) page 25 Delete: John Joseph Pollock 5. Bachelor of Science in Mathematical Science (Engineering) page 25 Delete: Matthew DeBari Junge 6. Performer's Certificates (Peabody) page 26 Add: Eddie Forest Stallings, Jr. Voice . 7. Bachelor of Music (Peabody) page 26 Add: Eddie Forest Stallings, Jr. Music Education Max Vont. Violin 8.
    [Show full text]
  • Molecular Determinants of Tissue Selectivity in Estrogen Receptor Modulators
    Proc. Natl. Acad. Sci. USA Vol. 94, pp. 14105–14110, December 1997 Pharmacology Molecular determinants of tissue selectivity in estrogen receptor modulators TIMOTHY A. GRESE*, JAMES P. SLUKA*, HENRY U. BRYANT,GEORGE J. CULLINAN,ANDREW L. GLASEBROOK, CHARLES D. JONES,KEN MATSUMOTO,ALAN D. PALKOWITZ,MASAHIKO SATO,JOHN D. TERMINE, MARK A. WINTER,NA N. YANG, AND JEFFREY A. DODGE* Endocrine Research, Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46285 Edited by Paul Talalay, The Johns Hopkins University School of Medicine, Baltimore, MD, and approved October 3, 1997 (received for review July 3, 1997) ABSTRACT Interaction of the estrogen receptoryligand molecular conformation of individual ligands (11–14). The complex with a DNA estrogen response element is known to recent characterization of a new ER isoform, ERb, adds a regulate gene transcription. In turn, specific conformations of further layer of complexity, because ligands with different the receptor-ligand complex have been postulated to influence structural characteristics may exhibit different binding profiles unique subsets of estrogen-responsive genes resulting in differ- depending on which ER isoform is being evaluated (15, 16). ential modulation and, ultimately, tissue-selective outcomes. The To date, ER ligands have been grouped into four classes on the estrogen receptor ligands raloxifene and tamoxifen have dem- basis of in vivo pharmacology, and representatives of these classes onstrated such tissue-specific estrogen agonistyantagonist ef- indeed have been shown to exhibit unique profiles with respect to fects. Both agents antagonize the effects of estrogen on mammary transcriptional activation (9). Differential effects on mammary, tissue while mimicking the actions of estrogen on bone.
    [Show full text]
  • The Androgen Derivative 5A-Androstane-3B,17B-Diol Inhibits Prostate Cancer Cell Migration Through Activation of the Estrogen Receptor B Subtype
    Research Article The Androgen Derivative 5A-Androstane-3B,17B-Diol Inhibits Prostate Cancer Cell Migration Through Activation of the Estrogen Receptor B Subtype Vittoria Guerini,1 Daniela Sau,1 Eugenia Scaccianoce,1 Paola Rusmini,1 Paolo Ciana,3 Adriana Maggi,3 Paolo G.V. Martini,4 Benita S. Katzenellenbogen,4 Luciano Martini,1 Marcella Motta,1,2 and Angelo Poletti1 1Institute of Endocrinology, 2Center for Endocrinological Oncology, and 3Department of Pharmacological Sciences, University of Milan, Italy; and 4Department of Molecular and Integrative Physiology, University of Illinois, Urbana-Champaign, Illinois Abstract androgen blockade. Most patients initially respond to androgen Prostate cancer growth depends, in its earlier stages, on ablation therapies, but relapse with hormone-refractory prostate androgens and is usually pharmacologically modulated with cancer (3), as a consequence of clonal selection of androgen- androgen blockade. However, androgen-ablation therapy may independent foci. Androgen-resistant tumors are generally charac- generate androgen-independent prostate cancer, often char- terized by an increased invasiveness. Therefore, it is important to find new approaches to control prostate cancer progression acterized by an increased invasiveness. We have found that the 5A-reduced testosterone derivative, dihydrotestosterone (the towards androgen-insensitivity. most potent natural androgen) inhibits cell migration with an In prostate cells, testosterone, is first irreversibly reduced by the a androgen receptor–independent
    [Show full text]
  • MCB Permit No
    A Magazine | The School of Molecular and Cellular Biology at the University of Illinois at Urbana-Champaign | Issue 9, 2015 University of Illinois at Urbana-Champaign School of Molecular and Cellular Biology Nonprofit org. U.S. postage 393 Morrill Hall PAID 505 South Goodwin Avenue Champaign, IL MCB Permit no. 75 Urbana, IL 61801 mcb.illinois.edu UMBRELLA OPPORTUNITIES: GRADUATE PROGRAM GIVES STUDENTS CHANCE TO EXPLORE College of Liberal Arts and Sciences LETTER FROM THE DIRECTOR TABLE OF CONTENTS 4 Umbrella Opportunities Graduate Program Gives Students Chance to Explore It was a beautiful fall in Champaign Illinois, reminiscent of what was typical before 6 Heart and Splicy Development the last couple of years of early snow. Matching the sunny weather is the warm glow The Kalsotra Lab reflected by the accomplishments of our faculty, staff, students and alumni that we 7 Targeting Cancer with T Cells are pleased to share with you in this edition of our annual magazine. David Kranz, PhD ’82, Microbiology 8 First in Class In October we celebrated the success of three alumni who were recognized by the Guy Padbury, MS ’85, PhD ’88, Biochemistry College of Liberal Arts and Sciences during their homecoming celebration. Tom 9 Gene taranis Key to Regeneration of Fruit Fly Epithelial Tissues Cycyota (B.S. ’80 Biology) received the LAS Humanitarian Award for his Smith-Bolton Lab outstanding service as President and CEO of AlloSource. His work to improve the lives of many through the use of donated human tissue is legendary. At the same 10 An Interview with Ann Carpenter PhD ’03, Cell and Developmental Biology event, an LAS Alumni Achievement Award was bestowed upon David Kranz (M.S.
    [Show full text]
  • Mastfff Chicago, Illinois PREFACE
    CONF-92QU37- DB93 010828 PROCEEDINGS OF A WORKSHOP ON MOLECULAR NUCLEAR MEDICINE Embassy Row Hotel, 2015 Massachusetts Avenue, N.W. Was! ington, D.C. January 23-24, 1992 Prepared by: U.S. Department of Energy Medical Applications and Biophysical Research Division Office of Health and Environmental Research Washington, D.C. 20585 Editor, Richard C. Reba The University of Chicago MASTfff Chicago, Illinois PREFACE Molecular Nuclear Medicine is developing into a new research area to improve the health and welfare of the public. Within the Department of Energy, the Program in Molecular Nuclear Medicine will support novel molecular approaches for diagnostic and therapeutic applications of nuclear medicine. To exploit the opportunities presented by the revolution in the biological sciences, the strategy is to integrate the scientific and technical power of molecular biology with the existing nuclear medicine program at the Department of Energy. Research in molecular biology has provided significant Insight Into the mechanisms of macromolecular Interactions underlying normal genetic, cellular and physiological processes. Any Insult (arising from diet, drug abuse, environmental exposure, Infection, etc.) that undermines these natural mechanisms can disrupt macromoiecular interactions and regulatory functions, leading to pathological states and disease. Molecular technologies, when coupled with the range of Instrumentation and techniques of nuclear medicine, have the potential to provide tools of much higher sensitivity and precision for detecting, localizing and, potentially for ameliorating, macromolecular, cellular and systemic pathologies. The Workshop represents the Department of Energy's commitment to accelerate the integration of molecular biology and biotechnology with nuclear medicine, and to develop an Innovative Molecular Nuclear Medicine Research Program.
    [Show full text]
  • DECEMBER 2015 NEWSLETTER GREETINGS from the HEAD Milan Bagchi in THIS ISSUE Welcome to the 2015 Edition of the MIP Newsletter
    DECEMBER 2015 NEWSLETTER GREETINGS FROM THE HEAD Milan Bagchi IN THIS ISSUE Welcome to the 2015 edition of the MIP newsletter. As you turn its pages, you will come across an article Greetings from the Head by Milan Bagchi 1 that describes the early history of our department. You will be impressed that physiology has a long and Progress In Women’s rich tradition at the University of Illinois. The University Reproductive Health and opened its doors in 1867 and physiology was taught as a Fertility subject starting in 1871. A long line of dedicated faculty members continued by Jeanne Bullock Goldberg 2-3 to carry the flag of physiology until the department was formally established Physiology at University of in 1949 with R.E. Johnson as Head. In 1959, the department moved to its Illinois, Urbana-Champaign: The current location in Burrill Hall. For the past 66 years, the department has First Hundred Years (1870-1970) continued to thrive as one of the oldest and most prestigious physiology by Deb Aronson 4-5 departments in the nation recognized for its cutting edge research in comparative physiology, cardiovascular physiology, biophysics, neuroscience, MIP family news 5-6 endocrinology, reproductive biology, and metabolic health. Recent Publications 7 A watershed event this year was the announcement that the University of Illinois Regional College of Medicine (COM) at Urbana-Champaign will close ABOUT THE its doors within the next few years. The Carle Illinois College of Medicine, an NEWSLETTER engineering-based medical school, will take its place. One cannot help but feel a bit nostalgic about the old COM, which was intimately associated with The Molecular and Integrative Physiology Newsletter is an annual publication of the our department and provided such stellar faculty as Benita Katzenellenbogen, Department of Molecular and Integrative Byron Kemper, Martha Gillette, David Sherwood, Phil Best, and many others.
    [Show full text]