Biochemistry Steady State
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Biochemistrystanford00kornrich.Pdf
University of California Berkeley Regional Oral History Office University of California The Bancroft Library Berkeley, California Program in the History of the Biosciences and Biotechnology Arthur Kornberg, M.D. BIOCHEMISTRY AT STANFORD, BIOTECHNOLOGY AT DNAX With an Introduction by Joshua Lederberg Interviews Conducted by Sally Smith Hughes, Ph.D. in 1997 Copyright 1998 by The Regents of the University of California Since 1954 the Regional Oral History Office has been interviewing leading participants in or well-placed witnesses to major events in the development of Northern California, the West, and the Nation. Oral history is a method of collecting historical information through tape-recorded interviews between a narrator with firsthand knowledge of historically significant events and a well- informed interviewer, with the goal of preserving substantive additions to the historical record. The tape recording is transcribed, lightly edited for continuity and clarity, and reviewed by the interviewee. The corrected manuscript is indexed, bound with photographs and illustrative materials, and placed in The Bancroft Library at the University of California, Berkeley, and in other research collections for scholarly use. Because it is primary material, oral history is not intended to present the final, verified, or complete narrative of events. It is a spoken account, offered by the interviewee in response to questioning, and as such it is reflective, partisan, deeply involved, and irreplaceable. ************************************ All uses of this manuscript are covered by a legal agreement between The Regents of the University of California and Arthur Kornberg, M.D., dated June 18, 1997. The manuscript is thereby made available for research purposes. All literary rights in the manuscript, including the right to publish, are reserved to The Bancroft Library of the University of California, Berkeley. -
Biochemical and Comparative Transcriptome Analyses Reveal
biomolecules Article Biochemical and Comparative Transcriptome Analyses Reveal Key Genes Involved in Major Metabolic Regulation Related to Colored Leaf Formation in Osmanthus fragrans ‘Yinbi Shuanghui’ during Development Xuan Chen 1,2, Xiulian Yang 1,3, Jun Xie 2, Wenjie Ding 1,3, Yuli Li 1,3, Yuanzheng Yue 1,3,* and Lianggui Wang 1,3,* 1 Key Laboratory of Landscape Architecture, Jiangsu Province, College of Landscape Architecture, Nanjing Forestry University, No. 159 Longpan Road, Nanjing 210037, China; [email protected] (X.C.); [email protected] (X.Y.); [email protected] (W.D.); [email protected] (Y.L.) 2 College of Fine Arts, Nanjing Normal University of Special Education, No.1 Shennong Road, Nanjing 210038, China; [email protected] 3 Co-Innovation Center for Sustainable Forestry in Southern China, Nanjing Forestry University, Nanjing 210037, China * Correspondence: [email protected] (Y.Y.); [email protected] (L.W.); Tel.: +86-138-0900-7625 (L.W.) Received: 25 February 2020; Accepted: 1 April 2020; Published: 4 April 2020 Abstract: Osmanthus fragrans ‘Yinbi Shuanghui’ not only has a beautiful shape and fresh floral fragrance, but also rich leaf colors that change, making the tree useful for landscaping. In order to study the mechanisms of color formation in O. fragrans ‘Yinbi Shuanghui’ leaves, we analyzed the colored and green leaves at different developmental stages in terms of leaf pigment content, cell structure, and transcriptome data. We found that the chlorophyll content in the colored leaves was lower than that of green leaves throughout development. By analyzing the structure of chloroplasts, the colored leaves demonstrated more stromal lamellae and low numbers of granum thylakoid. -
Effects in Reversible Exothermic Reactions
Effects in reversible exothermic reactions. Effect of Temperature on Equilibrium A temperature change occurs when temperature is increased or decreased by the flow of heat. This shifts chemical equilibria toward the products or reactants, which can be determined by studying the reaction and deciding whether it is endothermic or exothermic. Introduction Le Châtelier's principle states that a change in temperature, pressure, or concentration of reactants in an equilibrated system will stimulate a response that partially off-sets the change to establish a new equilibrium. In the case of changing temperature, adding or removing of heat shifts the equilibrium. However, reactions invariably involve changes in enthalpy, with energy (typically in the form of heat, but can involve light) either being absorbed or released during the reaction. Some chemical reactions -- like burning wood or exploding TNT -- release heat to their surroundings. Chemists call these exothermic reactions. Increasing the temperature affects an exothermic reaction in two different ways: by changing the rate of the reaction and by changing the balance between products and reactants at the end of the reaction. Generally speaking, your reaction will speed up because a higher temperature means more heat and energy in your system. However, in some cases, raising the temperature might shift equilibrium and prevent some of your reaction from occurring Reaction Rates Nearly all reactions go faster as the temperature increases -- exothermic reactions included. The reaction between oxygen in the air and the chemicals in the tip of a match, for example, is so slow at room temperature that nothing seems to happen. When you heat up the tip of the match by striking it against the striker strip on the box, however, the temperature increases and with it the rate of the reaction until it burns with a hot flame. -
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Published OnlineFirst February 12, 2018; DOI: 10.1158/0008-5472.CAN-17-2215 Cancer Metabolism and Chemical Biology Research RSK Regulates PFK-2 Activity to Promote Metabolic Rewiring in Melanoma Thibault Houles1, Simon-Pierre Gravel2,Genevieve Lavoie1, Sejeong Shin3, Mathilde Savall1, Antoine Meant 1, Benoit Grondin1, Louis Gaboury1,4, Sang-Oh Yoon3, Julie St-Pierre2, and Philippe P. Roux1,4 Abstract Metabolic reprogramming is a hallmark of cancer that includes glycolytic flux in melanoma cells, suggesting an important role for increased glucose uptake and accelerated aerobic glycolysis. This RSK in BRAF-mediated metabolic rewiring. Consistent with this, phenotypeisrequiredtofulfill anabolic demands associated with expression of a phosphorylation-deficient mutant of PFKFB2 aberrant cell proliferation and is often mediated by oncogenic decreased aerobic glycolysis and reduced the growth of melanoma drivers such as activated BRAF. In this study, we show that the in mice. Together, these results indicate that RSK-mediated phos- MAPK-activated p90 ribosomal S6 kinase (RSK) is necessary to phorylation of PFKFB2 plays a key role in the metabolism and maintain glycolytic metabolism in BRAF-mutated melanoma growth of BRAF-mutated melanomas. cells. RSK directly phosphorylated the regulatory domain of Significance: RSK promotes glycolytic metabolism and the 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 2 (PFKFB2), growth of BRAF-mutated melanoma by driving phosphory- an enzyme that catalyzes the synthesis of fructose-2,6-bisphosphate lation of an important glycolytic enzyme. Cancer Res; 78(9); during glycolysis. Inhibition of RSK reduced PFKFB2 activity and 2191–204. Ó2018 AACR. Introduction but recently developed therapies that target components of the MAPK pathway have demonstrated survival advantage in pati- Melanoma is the most aggressive form of skin cancer and arises ents with BRAF-mutated tumors (7). -
Crucible of Science: the Story of the Cori Laboratory
Crucible of Science This page intentionally left blank Crucible of Science THE STORY OF THE CORI LABORATORY JOHN H. EXTON 3 3 Oxford University Press is a department of the University of Oxford. It furthers the University’s objective of excellence in research, scholarship, and education by publishing worldwide. Oxford New York Auckland Cape Town Dar es Salaam Hong Kong Karachi Kuala Lumpur Madrid Melbourne Mexico City Nairobi New Delhi Shanghai Taipei Toronto With offi ces in Argentina Austria Brazil Chile Czech Republic France Greece Guatemala Hungary Italy Japan Poland Portugal Singapore South Korea Switzerland Th ailand Turkey Ukraine Vietnam Oxford is a registered trademark of Oxford University Press in the UK and certain other countries. Published in the United States of America by Oxford University Press 198 Madison Avenue, New York, NY 10016 © Oxford University Press 2013 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitt ed, in any form or by any means, without the prior permission in writing of Oxford University Press, or as expressly permitt ed by law, by license, or under terms agreed with the appropriate reproduction rights organization. Inquiries concerning reproduction outside the scope of the above should be sent to the Rights Department, Oxford University Press, at the address above. You must not circulate this work in any other form and you must impose this same condition on any acquirer. CIP data is on fi le at the Library of Congress ISBN 978–0–19–986107–1 9 8 7 6 5 4 3 2 1 Printed in the United States of America on acid-free paper Dedicated to Charles Rawlinson (Rollo) Park This page intentionally left blank Contents Acknowledgments ix I n t r o d u c t i o n xi 1. -
Allosteric Regulation
Hanjia’s Biochemistry Lecture Hanjia’s Biochemistry Lecture Chapter 15 Essential Questions • Before this class, ask your self the following questions: Reginald H. Garrett – What are the properties of regulatory enzymes? Enzyygme Regulation Charles M. Grisham • How do you know this enzyme is a regulatory enzyme? – How do regulatory enzymes sense the momentary needfll?ds of cells? ?Դৣ • How signal is delivered ᑣ٫݅ ፐำᆛઠ – Wha t mo lecu lar mec han isms are used to regu la te enzyme activity? http://lms. ls. ntou. edu. tw/course/106 [email protected] 2 Hanjia’s Biochemistry Lecture Hanjia’s Biochemistry Lecture Outline 15. 1 – What Factors Influence Enzymatic Activity? • Part 1 Factors that influence enzymatic activity 1. The availability of substrates and cofactors! – Zymogen, isozyme and covalent modification! 2. Product accu m ul ates b the rate will dec r ease! • Part 2: The general features of allosteric 3. The amount of enzyme present at any moment – Genetic regulation of enzyme synthesis and decay regulation 4. Regulation of Enzyme activity – The mechanisms of allosteric regulation – Zymogens, isozymes , and modulator proteins may play – Example of a enzyme controlled by both a role allosteric regulation and covalent modification – Enzyme activity can be regulated through covalent modification • Part 3: Special focus on hemoglobin and – Allosteric Regulation myoglbilobin 3 4 Hanjia’s Biochemistry Lecture Hanjia’s Biochemistry Lecture Regulation 1: Zymogen … The proteolytic activation of chymotrypsinogen • Zymogens are inactive -
Genetic Mutations and Non-Coding RNA-Based Epigenetic Alterations Mediating the Warburg Effect in Colorectal Carcinogenesis
biology Review Genetic Mutations and Non-Coding RNA-Based Epigenetic Alterations Mediating the Warburg Effect in Colorectal Carcinogenesis Batoul Abi Zamer 1,2 , Wafaa Abumustafa 1,2, Mawieh Hamad 2,3 , Azzam A. Maghazachi 2,4 and Jibran Sualeh Muhammad 1,2,* 1 Department of Basic Medical Sciences, College of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates; [email protected] (B.A.Z.); [email protected] (W.A.) 2 Sharjah Institute for Medical Research, University of Sharjah, Sharjah 27272, United Arab Emirates; [email protected] (M.H.); [email protected] (A.A.M.) 3 Department of Medical Laboratory Sciences, College of Health Sciences, University of Sharjah, Sharjah 27272, United Arab Emirates 4 Department of Clinical Sciences, College of Medicine, University of Sharjah, Sharjah 27272, United Arab Emirates * Correspondence: [email protected]; Tel.: +971-6-5057293 Simple Summary: Colorectal cancer is one of the most leading causes of death worldwide. The Hallmark of colorectal cancer is the increase of glucose uptake and lactate production even in the presence of oxygen, a phenomenon known as the “Warburg effect”. This review summarizes the genetic mutations and epigenetic alterations, focusing on non-coding RNA associated with the oncogenes, tumor suppresser genes, and enzymes involved in the “Warburg effect”, in addition to Citation: Abi Zamer, B.; Abumustafa, their clinical impacts on colorectal cancer. This knowledge may open the door for novel therapeutic W.; Hamad, M.; Maghazachi, A.A.; approaches to target colorectal cancer. Muhammad, J.S. Genetic Mutations and Non-Coding RNA-Based Abstract: Colorectal cancer (CRC) development is a gradual process defined by the accumulation of Epigenetic Alterations Mediating the numerous genetic mutations and epigenetic alterations leading to the adenoma-carcinoma sequence. -
Glucokinase Regulatory Network in Pancreatic -Cells and Liver
Glucokinase Regulatory Network in Pancreatic -Cells and Liver Simone Baltrusch1 and Markus Tiedge2 The low-affinity glucose-phosphorylating enzyme glucokinase GLUCOKINASE AND ITS EXCEPTIONAL ROLE IN THE (GK) is the flux-limiting glucose sensor in liver and -cells of HEXOKINASE GENE FAMILY the pancreas. Furthermore, GK is also expressed in various The glucose-phosphorylating enzyme glucokinase (GK) neuroendocrine cell types. This review describes the complex (hexokinase type IV) has unique characteristics compared network of GK regulation, which shows fundamental differ- ences in liver and pancreatic -cells. Tissue-specific GK pro- with the ubiquitously expressed hexokinase isoforms type moters determine a higher gene expression level and glucose I–III. The smaller 50-kDa size of the GK protein distin- phosphorylation capacity in liver than in pancreatic -cells. guishes it from the 100-kDa hexokinase isoforms (1). From The second hallmark of tissue-specific GK regulation is based a historical point of view, several kinetic preferences on posttranslational mechanisms in which the high-affinity allowed this enzyme to act as a metabolic glucose sensor: regulatory protein in the liver undergoes glucose- and 1) its low affinity for glucose, in the physiological concen- fructose-dependent shuttling between cytoplasm and nu- tration range between 5 and 7 mmol/l, 2) a cooperative cleus. In -cells, GK resides outside the nucleus but has behavior for glucose with a Hill coefficient (nHill) between been reported to interact with insulin secretory gran- 1.5 and 1.7, and 3) a lack of feedback inhibition by ules. The unbound diffusible GK fraction likely deter- mines the glucose sensor activity of insulin-producing glucose-6-phosphate within the physiological concentra- cells. -
Review Of: General Comments
January 15, 2013 Review of: Quantifying drivers of chemical disequilibrium in the Earth’s atmosphere E. Simoncini, N. Virgo , and A. Kleidon Earth Syst. Dynam. Discuss., 3, 1287–1320, 2012 Reviewer: Elbert Branscomb General Comments This paper addresses questions of significant general interest, namely how to es- timate the power needed to maintain atmospheric chemical disequilibria, what the magnitude of that power is in the important case of the CH4=O2 disequilib- rium found in the earth’s atmosphere, and the issue of whether the result, and in particular the general approach, might aid in detecting life on other planets. The thermodynamic approach taken to estimating the power is presented as the paper’s main contribution. The manuscript seems clearly within the scope of ESD. However, in my judgment the manuscript does not rise above the threshold sufficient to justify publication either with regard to significance or original contribution. At the same time, I do not view the shortfall as being so great, or beyond reasonable dispute, that I would object to being overridden on this judgment by other reviewers or editors. In summary, my reasons for this negative decision come down to two points. First, to my mind the case is not made that power calculations of the type considered could in any practical case assist in deciding whether some distant planet was ‘metabolizing‘. The analysis presented in effect argues against this idea - as the authors themselves essentially acknowledge with commendable candor; the powers predicted are too small and, more importantly, no practical strategy seems to exist for determining, for a distant planet, either the needed production fluxes (required to estimate the power by the proposed method) or what fraction of the power involved could not be explainable as due to abiotic processes. -
An Introduction to Metabolism
CAMPBELL BIOLOGY IN FOCUS URRY • CAIN • WASSERMAN • MINORSKY • REECE 6 An Introduction to Metabolism Lecture Presentations by Kathleen Fitzpatrick and Nicole Tunbridge, Simon Fraser University © 2016 Pearson Education, Inc. SECOND EDITION The Energy of Life . The living cell is a miniature chemical factory where thousands of reactions occur . The cell extracts energy and applies energy to perform work . Some organisms even convert energy to light, as in bioluminescence © 2016 Pearson Education, Inc. Figure 6.1 © 2016 Pearson Education, Inc. Concept 6.1: An organism’s metabolism transforms matter and energy . Metabolism is the totality of an organism’s chemical reactions . Metabolism is an emergent property of life that arises from interactions between molecules within the cell © 2016 Pearson Education, Inc. Metabolic Pathways . A metabolic pathway begins with a specific molecule and ends with a product . Each step is catalyzed by a specific enzyme © 2016 Pearson Education, Inc. Figure 6.UN01 Enzyme 1 Enzyme 2 Enzyme 3 A B C D Reaction 1 Reaction 2 Reaction 3 Starting Product molecule © 2016 Pearson Education, Inc. Catabolic pathways release energy by breaking down complex molecules into simpler compounds . One example of catabolism is cellular respiration, the breakdown of glucose and other organic fuels to carbon dioxide and water © 2016 Pearson Education, Inc. Anabolic pathways consume energy to build complex molecules from simpler ones . The synthesis of proteins from amino acids is an example of anabolism . Bioenergetics is the study of how energy flows through living organisms © 2016 Pearson Education, Inc. Forms of Energy . Energy is the capacity to cause change . Energy exists in various forms, some of which can perform work © 2016 Pearson Education, Inc. -
CH4103 Organic and Biological Chemistry LCM Lectures 1-8
CH4103 Organic and Biological Chemistry LCM Lectures 1-8 Dr Louis C. Morrill School of Chemistry, Cardiff University Main Building, Rm 1.47B [email protected] Autumn Semester For further information see Learning Central: CH4103/Learning Materials/LCM 1 Unit 1: Recap In Unit 1 with Dr Elliott you have learnt some key fundamentals in O-Chem: • Drawing and naming organic compounds (Lecture 1) • Molecular shape and hybridisation - sp3, sp2 and sp (Lecture 2) • Constitutional and stereoisomers (Lectures 3-7) • Conformations of acyclic and cyclic organic structures (Lectures 4 and 5) • Conjugation and resonance (Lecture 8) • Reactive intermediates – carbocations, carbanions and radicals (Lectures 8 and 9) • Acids and bases – pH and pKa (Lecture 9) These are the first tools in your synthetic toolbox and are essential knowledge – please revise these topics diligently. Further supporting learning materials can be found on Learning Central and within Organic Chemistry 2nd Ed. (J. Clayden, N. Greeves and S. Warren) – Chapters 1-8. For further information see Learning Central: CH4103/Learning Materials/LCM 2 Unit 2: Lecture Synopsis • Lecture 1: Describing an Organic Reaction. Homolytic vs heterolytic bond breaking, bond dissociation energy (BDE), enthalpy and ΔH°, entropy and ΔS°, Gibbs free energy and ΔG°, equilibria. • Lecture 2: Reaction Kinetics and the Hammond Postulate. Differentiating thermodynamics and kinetics, rate laws, activation energy (Ea), the Arrhenius equation, free energy diagrams, intermediates and transition states, the Hammond postulate. • Lecture 3: Curly Arrows for Electron Movement. How molecules interact, nucleophiles and electrophiles, use of curly arrows to represent electron movement, curly arrows for nucleophilic attack / substitution, loss of a leaving group / elimination, proton transfers and carbocation rearrangements. -
5. Bioenergetics
Life Sciences - LS (Molecules and their interaction relevant to Biology) 5. BIOENERGETICS Oxidative Phosphorylation Oxidative phosphorylation (or OXPHOS in short) is the metabolic pathway in which the mitochondria in cells use their structure, enzymes, and energy released by the oxidation of nutrients to reform ATP. Although the many forms of life on earth use a range of different nutrients, ATP is the molecule that supplies energy to metabolism. Almost all aerobic organisms carry out oxidative phosphorylation. Oxidative phosphorylation began with the report in 1906 by Arthur Harden of a vital role for phosphate in cellular fermentation, but initially only sugar phosphates were known to be involved. 1940s, Herman Kalckar work on this between the oxidation of sugars and the generation of ATP was firmly established, confirming the central role of ATP in energy transfer that had been proposed by Fritz Albert Lipmann in 1941. Later, in 1949, Morris Friedkin and Albert L. Lehninger proved that the coenzyme NADH linked metabolic pathways such as the citric acid cycle and the synthesis of ATP. This pathway is probably so pervasive because it is a highly efficient way of releasing energy, compared to alternative fermentation processes such as anaerobic glycolysis. 5.1 Electron Transport Chain The electron transport chain (aka ETC) is a process in which the NADH and [FADH ] produced 2 during glycolysis, -oxidation, and other catabolic processes are oxidized thus releasing energy in the form of ATP. The mechanism by which ATP is formed in the ETC is called chemiosmotic phosphorylation. Fig. : Electron Transport Chain Overview The electron transport chain is present in multiple copies in the inner mitochondrial membrane of eukaryotes and the plasma membrane of prokaryotes.