DOCSLIB.ORG

BCH 304 STUDY QUESTIONS & ANSWERS Biochemist

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
BCH 304 STUDY QUESTIONS & ANSWERS Biochemist BCH 304 STUDY QUESTIONS & ANSWERS Biochemist Oh!Best Q1- What is the difference between De-novo synthesis of nucleotide and nucleotide synthesis by the salvage pathways? Answer: In De-novo synthesis, the nucleotides are synthesized from simpler precursor compounds, in essence from scratch. In salvage pathways, preformed bases are recovered and attached to ribose. Q2- Identify the sources of the atoms of purines and pyrimidines ring during their De-novo synthesis. Answer: In purines: i. Glycine provides C4, C5 and N7 5 10 ii. N , N -Formyl tetrahydrofolate (THF) provides C2 and C8 iii. Glutamine provide N3 and N9 iv. CO2 provide C6 v. Aspartate provides N1 In pyrimidines: Glutamine Aspartic acid CO2 i. Glutamine provides N3 ii. Aspartic acid provides C4, C5, C6 and N1 iii. Carbon dioxide (CO2) provides C2 Q3- Create a match (a) Excessive urate___ Spina bifida (b) Lack of adenosine deaminase___ Precursor to both ATP and GTP (c) Lack of HGPRT___ Purine (d) Carbamoyl phosphate___ Deoxynucleotide synthesis (e) Inosinate___ UTP (f) Ribonucleotide reductase___ Lesch-Nyhan disease (g) Lack of folic acid___ Immunodeficiency (h) Glutamine phosphoribosyl transferase___ Pyrimidine (i) Single ring___ Gout (j) Bicyclic ring___ First step in pyrimidine synthesis (k) Precursor to CTP___ Committed step in purine synthesis Answer: (a) Excessive urate___ Gout (b) Lack of adenosine deaminase___ Immunodeficiency (c) Lack of HGPRT___ Lesch-Nyhan disease BCH 304 STUDY QUESTIONS & ANSWERS Biochemist Oh!Best (d) Carbamoyl phosphate___ First step in pyrimidine synthesis (e) Inosinate___ Precursor to both ATP and GTP (f) Ribonucleotide reductase___ Deoxynucleotide (g) Lack of folic acid___ Spina bifida (h) Glutamine phosphoribosyl transferase___ Committed step in purine synthesis (i) Single ring___ Pyrimidine (j) Bicyclic ring___ Purine (k) Precursor to CTP___ UTP Q4- Azaserine (an analog of glutamine) inhibits the enzyme amido transferase. Identify the intermediate of purine biosynthesis that would accumulate in cells treated with Azaserine. Answer: The intermediate that would be accumulated in the cells are PRPP and formyl glycinamide ribonucleotide (FGAR). Q5- Discuss the inhibitory action of sulfanilamide and related sulfa drugs in bacteria growth in relation to nucleotide biosynthesis. Answer: There is a deficiency of N10-formyltetrahydrofolate. Sulfanilamide inhibits the synthesis of folate by acting as an analog of p-aminobenzoate, one of the precursors of folate. Q6- What are the functions of Carbamoyl phosphate synthetase (CPS)- I & II Answer: CPS-I is an enzyme located in the mitochondria involved in the production of urea. CPS-I transfers an ammonia molecule from glutamine or glutamate to a molecule of bicarbonate that has been phosphorylated by a molecule of ATP. It can only be activated by N-acetylglutamate. CPS-II is an enzyme that catalyzes the reactions that produce carbamoyl phosphate in the cytosol (as opposed to type I, which functions in the mitochondria) and it involve in pyrimidine synthesis. It is activated by ATP and PRPP and it is inhibited by UMP. Q7- Give the reaction of purine biosynthesis via the salvage pathway Adenine, hypoxanthine, guanine produced during the breakdown of high energy compounds like RNA and DNA, are salvaged to produce AMP, IMP, GMP. Adenine phosphoribosyl transferase catalyzes the formation of AMP from adenine. Hypoxanthine-guanine phosphoribosyl transferase (HGPRT) catalyzes the formation of IMP and GMP from hypoxanthine and guanine respectively. BCH 304 STUDY QUESTIONS & ANSWERS Biochemist Oh!Best Phosphoribosyl pyrophosphate (PRPP) is the donor of ribose 5-phosphate in the salvage pathway. Q8- Briefly explain the biochemistry of Lesch-Nyhan’s syndrome Lesch Nyhan syndrome is an inherited X-linked recessive disorder that affects only males mostly. It is caused by a complete deficiency of HGPRTase [an enzyme involves in purine salvage pathway] and purine (hypoxanthine and guanine) will accumulate. The HGPRTase enzyme catalyzes the following two interconversions: hypoxanthine + PRPP ↔ IMP + PPi guanine + PRPP ↔ GMP + PPi The symptoms are: urinary tract stones, mental retardation or neurological symptoms, self-mutilation (biting of fingers), excessive uric acid production. It can be treated as follows; i. Use of allopurinol: - It will only reduce uric acid formation, but does not alleviate the neurologic symptoms ii. Alkalanization of urine should be avoided. iii. High fluid intake. Q9- Name one nucleotide that acts in each of the following: (a) Second messenger (b) Phosphoryl-group transfer (c) Activation of carbohydrates (d) Activation of acetyl groups (e) Transfer of electrons (f) DNA sequencing (g) Chemotherapy (h) Allosteric effector Answer: (a) cAMP (b) ATP (c) UDP-glucose (d) acetyl CoA (e) NAD+, FAD (f) dideoxynucleotides (g) fluorouracil; (h) CTP inhibits ATCase. BCH 304 STUDY QUESTIONS & ANSWERS Biochemist Oh!Best Q10a- Discuss the De-novo synthesis of UMP UMP which is pyrimidine nucleotide is formed via the De-novo biosynthesis DHO dehydrogenase + CO2 Carbamoyl phosphate Synthetase II [CPS-II] Orotate Orotate Phosphoribosyl transferase Carbamoyl phosphate [CAP] Aspartate transcarbamylase [ATCase] Orotidine-5-monophosphate [OMP] Carbamoyl aspartate [CAA] OMP decarboxylase Dihydroorotase Dihydroorotate [DHO] Uridine-5-monophosphate [UMP] Q10b- How is this pathway regulated? The first two enzymes; carbamoyl phosphate synthetase II [CPS-II] and aspartate transcarbamoylase [ATCase] are allosteric enzymes and are regulated allosterically. Q11- If man did not lose his urate oxidase, gout would have been an unknown disease. Discuss? Gout is a clinical disorder caused by deposition of urate crystals in a joint leading to acute inflammatory response with acute pain. Most cases of gout present with the sudden onset of severe acute arthritis in a peripheral joint in the leg. Urate oxidase is a peroxisomal liver enzyme that catalyzes the enzymatic oxidation of uric acid into the more water-soluble allantoin. Urate oxidase is an endogenous enzyme found in most mammals but not in humans, which was actually caused by two (2) independent nonsense or frameshift mutations. BCH 304 STUDY QUESTIONS & ANSWERS Biochemist Oh!Best Allopurinol blocks the conversion of xanthine to uric acid, while the urate oxidase catalyzes the oxidation of uric acid to allantoin, a highly water-soluble metabolite readily excreted by the kidney. Although urate oxidase is not found in humans, but urate oxidase is used in humans for the control of increased serum uric acid in patients with acute tumour lysis syndrome after receiving chemotherapy. Q12a-Highlight the reactions of purine nucleotide cycle The purine nucleotide cycle is a metabolic pathway in which ammonia and fumarate are generated from aspartate and inosine monophosphate (IMP) in order to regulate the levels of adenine nucleotides. The cycle is composed of three enzyme-catalyzed reactions. The first stage is the deamination of the purine nucleotide Adenosine monophosphate (AMP) to form inosine monophosphate (IMP), catalyzed by the enzyme AMP deaminase: + AMP + H2O → IMP + NH4 The second stage is the formation of adenylosuccinate from IMP and the amino acid aspartate, which is coupled to the energetically favourable hydrolysis of GTP, and catalysed by the enzyme adenylosuccinate synthetase: Aspartate + IMP + GTP → Adenylosuccinate + GDP + Pi Finally, Adenylosuccinate is cleaved by the enzyme adenylosuccinate lyase to release fumarate and regenerate the starting material of AMP: Adenylosuccinate → AMP + Fumarate Q12b- How is the above pathway relevant to muscle contraction? + This cycle has the net effect of converting aspartate to fumarate plus NH4 . It plays an important role in energy metabolism in skeletal muscle, where the fumarate that it generates replenishes the levels of citric acid cycle intermediates lost in amphibolic side reactions. Skeletal muscle lacks the usual complement of anaplerotic enzymes and relies on enhanced levels of AMP deaminase, adenylosuccinate synthetase, and adenylosuccinate lyase to compensate. ATP → ADP + Pi (utilization of ATP for Muscle contraction) Purine nucleotide cycle occurs during strenuous exercise, fasting or starvation when ATP reservoirs run low. Enjoy a Stressless Exam… BCH 304 STUDY QUESTIONS & ANSWERS Biochemist Oh!Best .
Load more

Recommended publications
  • 35 Disorders of Purine and Pyrimidine Metabolism
    35 Disorders of Purine and Pyrimidine Metabolism Georges van den Berghe, M.- Françoise Vincent, Sandrine Marie 35.1 Inborn Errors of Purine Metabolism – 435 35.1.1 Phosphoribosyl Pyrophosphate Synthetase Superactivity – 435 35.1.2 Adenylosuccinase Deficiency – 436 35.1.3 AICA-Ribosiduria – 437 35.1.4 Muscle AMP Deaminase Deficiency – 437 35.1.5 Adenosine Deaminase Deficiency – 438 35.1.6 Adenosine Deaminase Superactivity – 439 35.1.7 Purine Nucleoside Phosphorylase Deficiency – 440 35.1.8 Xanthine Oxidase Deficiency – 440 35.1.9 Hypoxanthine-Guanine Phosphoribosyltransferase Deficiency – 441 35.1.10 Adenine Phosphoribosyltransferase Deficiency – 442 35.1.11 Deoxyguanosine Kinase Deficiency – 442 35.2 Inborn Errors of Pyrimidine Metabolism – 445 35.2.1 UMP Synthase Deficiency (Hereditary Orotic Aciduria) – 445 35.2.2 Dihydropyrimidine Dehydrogenase Deficiency – 445 35.2.3 Dihydropyrimidinase Deficiency – 446 35.2.4 Ureidopropionase Deficiency – 446 35.2.5 Pyrimidine 5’-Nucleotidase Deficiency – 446 35.2.6 Cytosolic 5’-Nucleotidase Superactivity – 447 35.2.7 Thymidine Phosphorylase Deficiency – 447 35.2.8 Thymidine Kinase Deficiency – 447 References – 447 434 Chapter 35 · Disorders of Purine and Pyrimidine Metabolism Purine Metabolism Purine nucleotides are essential cellular constituents 4 The catabolic pathway starts from GMP, IMP and which intervene in energy transfer, metabolic regula- AMP, and produces uric acid, a poorly soluble tion, and synthesis of DNA and RNA. Purine metabo- compound, which tends to crystallize once its lism can be divided into three pathways: plasma concentration surpasses 6.5–7 mg/dl (0.38– 4 The biosynthetic pathway, often termed de novo, 0.47 mmol/l). starts with the formation of phosphoribosyl pyro- 4 The salvage pathway utilizes the purine bases, gua- phosphate (PRPP) and leads to the synthesis of nine, hypoxanthine and adenine, which are pro- inosine monophosphate (IMP).
    [Show full text]
  • The Regulation of Carbamoyl Phosphate Synthetase-Aspartate Transcarbamoylase-Dihydroorotase (Cad) by Phosphorylation and Protein-Protein Interactions
    THE REGULATION OF CARBAMOYL PHOSPHATE SYNTHETASE-ASPARTATE TRANSCARBAMOYLASE-DIHYDROOROTASE (CAD) BY PHOSPHORYLATION AND PROTEIN-PROTEIN INTERACTIONS Eric M. Wauson A dissertation submitted to the faculty of the University of North Carolina at Chapel Hill in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Pharmacology. Chapel Hill 2007 Approved by: Lee M. Graves, Ph.D. T. Kendall Harden, Ph.D. Gary L. Johnson, Ph.D. Aziz Sancar M.D., Ph.D. Beverly S. Mitchell, M.D. 2007 Eric M. Wauson ALL RIGHTS RESERVED ii ABSTRACT Eric M. Wauson: The Regulation of Carbamoyl Phosphate Synthetase-Aspartate Transcarbamoylase-Dihydroorotase (CAD) by Phosphorylation and Protein-Protein Interactions (Under the direction of Lee M. Graves, Ph.D.) Pyrimidines have many important roles in cellular physiology, as they are used in the formation of DNA, RNA, phospholipids, and pyrimidine sugars. The first rate- limiting step in the de novo pyrimidine synthesis pathway is catalyzed by the carbamoyl phosphate synthetase II (CPSase II) part of the multienzymatic complex Carbamoyl phosphate synthetase, Aspartate transcarbamoylase, Dihydroorotase (CAD). CAD gene induction is highly correlated to cell proliferation. Additionally, CAD is allosterically inhibited or activated by uridine triphosphate (UTP) or phosphoribosyl pyrophosphate (PRPP), respectively. The phosphorylation of CAD by PKA and ERK has been reported to modulate the response of CAD to allosteric modulators. While there has been much speculation on the identity of CAD phosphorylation sites, no definitive identification of in vivo CAD phosphorylation sites has been performed. Therefore, we sought to determine the specific CAD residues phosphorylated by ERK and PKA in intact cells.
    [Show full text]
  • Developmental Outcomes with Early Orthotopic Liver Transplantation For
    Developmental Outcomes With Early Orthotopic Liver Transplantation for Infants With Neonatal-Onset Urea Cycle Defects and a Female Patient With Late-Onset Ornithine Transcarbamylase Deficiency Kim L. McBride, MD*; Geoffrey Miller, MD‡; Susan Carter, BSN*࿣; Saul Karpen, MD, PhD‡; John Goss, MD§; and Brendan Lee, MD, PhD*࿣ ABSTRACT. Urea cycle defects (UCDs) typically nherited disorders of the urea cycle are character- present with hyperammonemia, the duration and peak ized by high ammonia levels and altered amino levels of which are directly related to the neurologic acid metabolism. There are 6 well-characterized outcome. Liver transplantation can cure the underlying I urea cycle defects (UCDs), ie, N-acetylyglutamate defect for some conditions, but the preexisting neuro- synthase, carbamoyl phosphate synthase (CPS), X- logic status is a major factor in the final outcome. Mul- linked ornithine transcarbamylase (OTC), arginosuc- ticenter data indicate that most of the children who re- cinate synthase, arginosuccinate lyase, and arginase ceive transplants remain significantly neurologically deficiencies. Arginase deficiency is not typical of the impaired. We wanted to determine whether aggressive other UCDs, because it presents not with hyperam- metabolic management of ammonia levels after early monemia but with spastic diplegia. Presentation of referral/transfer to a metabolism center and early liver transplantation would result in better neurologic out- the other UCDs can be quite variable, from cata- comes. We report on 5 children with UCDs, ie, 2 male strophic neonatal illness and acute episodic enceph- patients with X-linked ornithine transcarbamylase defi- alopathy in childhood or adulthood to chronic neu- 1 ciency and 2 male patients with carbamoyl phosphate rologic disorders.
    [Show full text]
  • Carbamoyl Phosphate Synthetase I Deficiency
    Carbamoyl phosphate synthetase I deficiency Description Carbamoyl phosphate synthetase I deficiency is an inherited disorder that causes ammonia to accumulate in the blood (hyperammonemia). Ammonia, which is formed when proteins are broken down in the body, is toxic if the levels become too high. The brain is especially sensitive to the effects of excess ammonia. In the first few days of life, infants with carbamoyl phosphate synthetase I deficiency typically exhibit the effects of hyperammonemia, which may include unusual sleepiness, poorly regulated breathing rate or body temperature, unwillingness to feed, vomiting after feeding, unusual body movements, seizures, or coma. Affected individuals who survive the newborn period may experience recurrence of these symptoms if diet is not carefully managed or if they experience infections or other stressors. They may also have delayed development and intellectual disability. In some people with carbamoyl phosphate synthetase I deficiency, signs and symptoms may be less severe and appear later in life. Frequency Carbamoyl phosphate synthetase I deficiency is a rare disorder; its overall incidence is unknown. Researchers in Japan have estimated that it occurs in 1 in 800,000 newborns in that country. Causes Mutations in the CPS1 gene cause carbamoyl phosphate synthetase I deficiency. The CPS1 gene provides instructions for making the enzyme carbamoyl phosphate synthetase I. This enzyme participates in the urea cycle, which is a sequence of biochemical reactions that occurs in liver cells. The urea cycle processes excess nitrogen, generated when protein is broken down by the body, to make a compound called urea that is excreted by the kidneys. The specific role of the carbamoyl phosphate synthetase I enzyme is to control the first step of the urea cycle, a reaction in which excess nitrogen compounds are incorporated into the cycle to be processed.
    [Show full text]
  • Table S1. List of Genes Up- Or Down-Regulated in H99 When Bound by 18B7
    Table S1. List of genes up- or down-regulated in H99 when bound by 18B7. Up-regulated Genes Classification CNF03470: Formate dehydrogenase Metabolism CNC03960: Phosphate transporter, putative Metabolism CND00530: Putative urea transporter Secretion CNA02250: Ammonium transporter MEP1 Secretion CNC06440: Inositol 1-phosphate synthase Metabolism CND03490: Chitin deacetylase-like mannoprotein MP98 Cell wall CNA04560: Hypothetical protein Hypothetical CNF02180: Acetyl-CoA carboxylase, putative Metabolism CNJ00690: Uracil permease, putative Secretion CNF02510: Alcohol dehydrogenase, putative Metabolism CNE04360: Fatty acid synthase, alpha subunit-related Metabolism CNM00180: Cyclohydrolase, putative Metabolism CNL03740: AF540951 catalase isozyme P Stress CNE04370: Fatty acid synthase, beta subunit Metabolism CNA01790: Expressed protein Hypothetical CNA05700: Expressed protein Hypothetical CND03840: Vacuole fusion, non-autophagic-related protein, putative Cell wall CNM00980: Hypothetical protein Hypothetical CNI02420: Uricase (Urate oxidase), putative Metabolism CNJ01090: Xylitol dehydrogenase-related Cell wall CNC03430: Alpha-1,6-mannosyltransferase, putative Cell wall CNF04120: Expressed protein Hypothetical CNB01810: Short chain dehydrogenase, putative Metabolism CNJ01200: Hypothetical protein Hypothetical CNA01160: LSDR putative Metabolism CNH03430: Hypothetical protein Hypothetical CNM02410: Putative proteine disulfate isomerase Housekeeping CNG04200: Alpha-amylase, putative Cell wall CNC00920: NADP-dependent glutamate dehydrogenase Metabolism
    [Show full text]
  • Decreased Concentration of Xanthine Dehydrogenase (EC 1.1.1.204) in Rat Hepatomas1
    [CANCER RESEARCH 46, 3838-3841, August 1986] Decreased Concentration of Xanthine Dehydrogenase (EC 1.1.1.204) in Rat Hepatomas1 Tadashi Ikegami, Yutaka Natsumeda, and George Weber2 Laboratory for Experimental Oncology, Indiana University School of Medicine, Indianapolis, Indiana 46223 ABSTRACT Immunodiffusion disc was from Miles Laboratories, Inc., Naperville, IL. All other chemicals were also of analytical grade. Xanthine dehydrogenase (EC 1.1.1.204), the rate-limiting enzyme of Tissues. Chemically induced transplantable hepatomas were main purine degradation, was purified 642-fold to homogeneity from liver of tained as described previously (9). Hepatoma 20 was transplanted in male Wistar rats. Antibody was generated to the purified enzyme in white male Buffalo strain rats, and hepatoma 3924A was carried in male rabbits and was partially purified. For the immunotitration a radioassay ACI/N rats. Livers from Buffalo and ACI/N rats were used as controls. of high sensitivity was developed to determine low enzyme activities. Hepatoma 3924A was homogenized with 3.3 volumes and hepatoma Titration curves with the antibody showed that the xanthine dehydrogen 20 and the livers were homogenized with 5 volumes of SOHIMpotassium ase enzyme protein amounts in slowly growing hepatoma 20 and rapidly phosphate buffer, pH 7.4, containing 0.25 M sucrose and 0.3 mM growing hepatoma 3924A were 34 and 4% of those of normal liver, which EDTA, respectively. The homogenates were centrifuged at 100,000 x was in good agreement with the decrease in the activity of the enzyme to g for 30 min, and the clear supernatants were used for the enzyme 33 and 2%, respectively.
    [Show full text]
  • Nucleotide Metabolism 22
    Nucleotide Metabolism 22 For additional ancillary materials related to this chapter, please visit thePoint. I. OVERVIEW Ribonucleoside and deoxyribonucleoside phosphates (nucleotides) are essential for all cells. Without them, neither ribonucleic acid (RNA) nor deoxyribonucleic acid (DNA) can be produced, and, therefore, proteins cannot be synthesized or cells proliferate. Nucleotides also serve as carriers of activated intermediates in the synthesis of some carbohydrates, lipids, and conjugated proteins (for example, uridine diphosphate [UDP]-glucose and cytidine diphosphate [CDP]- choline) and are structural components of several essential coenzymes, such as coenzyme A, flavin adenine dinucleotide (FAD[H2]), nicotinamide adenine dinucleotide (NAD[H]), and nicotinamide adenine dinucleotide phosphate (NADP[H]). Nucleotides, such as cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), serve as second messengers in signal transduction pathways. In addition, nucleotides play an important role as energy sources in the cell. Finally, nucleotides are important regulatory compounds for many of the pathways of intermediary metabolism, inhibiting or activating key enzymes. The purine and pyrimidine bases found in nucleotides can be synthesized de novo or can be obtained through salvage pathways that allow the reuse of the preformed bases resulting from normal cell turnover. [Note: Little of the purines and pyrimidines supplied by diet is utilized and is degraded instead.] II. STRUCTURE Nucleotides are composed of a nitrogenous base; a pentose monosaccharide; and one, two, or three phosphate groups. The nitrogen-containing bases belong to two families of compounds: the purines and the pyrimidines. A. Purine and pyrimidine bases Both DNA and RNA contain the same purine bases: adenine (A) and guanine (G).
    [Show full text]
  • Cell and Gene Therapy for Carbamoyl Phosphate Synthetase 1 Deficiency
    Journal of Pediatrics and Neonatal Care Cell and Gene Therapy for Carbamoyl Phosphate Synthetase 1 Deficiency Abstract Review Article Volume 7 Issue 1 - 2017 Carbamoyl phosphate synthetase 1 (CPS1) is the first and rate-limiting enzyme in the urea cycle. CPS1 deficiency is a devastating condition, which is clinically characterized by periodic episodes of life-threatening hyperammonemia. Currently, 1Associate at Department of Genetic Medicine, Children’s there is no cure for CPS1 deficiency except for liver transplantation, which is limited Research Institute, Children’s National Health System, USA on the progress to date, cell-based therapies—including hepatocyte or stem cell 2 by a severe shortage of donors and significant risk of mortality and morbidity. Based Washington Institute for Health Sciences, Department of transplantation—and new approaches for gene therapy have become the promising Biochemistry and Molecular & Cellular Biology, Georgetown University Medical Center, USA curative treatments for CPS1 deficiency. This review outlines the current progress and *Corresponding author: Bin Li, MD, Washington Institute Keywords:challenges of cell and gene therapies for CPS1 deficiency. for Health Sciences, 4601 N Fairfax Drive, Arlington, VA therapy; Gene therapy 22203; Georgetown University Medical Center, 4000 Urea cycle defects; Carbamoyl phosphate synthetase 1 deficiency; Cell Reservoir Road, N.W., Washington D.C. 20057, United States. Tel: 202-687-6484, Fax: (202) 687-1800, Email: Abbreviations: AAVs: Adeno-Associated Viruses;
    [Show full text]
  • SUPPY Liglucosexlmtdh
    US 20100314248A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2010/0314248 A1 Worden et al. (43) Pub. Date: Dec. 16, 2010 (54) RENEWABLE BOELECTRONIC INTERFACE Publication Classification FOR ELECTROBOCATALYTC REACTOR (51) Int. Cl. (76) Inventors: Robert M. Worden, Holt, MI (US); C25B II/06 (2006.01) Brian L. Hassler, Lake Orion, MI C25B II/2 (2006.01) (US); Lawrence T. Drzal, Okemos, GOIN 27/327 (2006.01) MI (US); Ilsoon Lee, Okemo s, MI BSD L/04 (2006.01) (US) C25B 9/00 (2006.01) (52) U.S. Cl. ............... 204/403.14; 204/290.11; 204/400; Correspondence Address: 204/290.07; 427/458; 204/252: 977/734; PRICE HENEVELD COOPER DEWITT & LIT 977/742 TON, LLP 695 KENMOOR, S.E., PO BOX 2567 (57) ABSTRACT GRAND RAPIDS, MI 495.01 (US) An inexpensive, easily renewable bioelectronic device useful for bioreactors, biosensors, and biofuel cells includes an elec (21) Appl. No.: 12/766,169 trically conductive carbon electrode and a bioelectronic inter face bonded to a surface of the electrically conductive carbon (22) Filed: Apr. 23, 2010 electrode, wherein the bioelectronic interface includes cata lytically active material that is electrostatically bound directly Related U.S. Application Data or indirectly to the electrically conductive carbon electrode to (60) Provisional application No. 61/172,337, filed on Apr. facilitate easy removal upon a change in pH, thereby allowing 24, 2009. easy regeneration of the bioelectronic interface. 7\ POWER 1 - SUPPY|- LIGLUCOSEXLMtDH?till pi 6.0 - esses&aaaas-exx-xx-xx-xx-xxxxixax-e- Patent Application Publication Dec. 16, 2010 Sheet 1 of 18 US 2010/0314248 A1 Potential (nV) Patent Application Publication Dec.
    [Show full text]
  • Monitoring the Redox Status in Multiple Sclerosis
    Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted: 31 July 2020 doi:10.20944/preprints202007.0737.v1 Review Monitoring the Redox Status in Multiple Sclerosis Masaru Tanaka 1,2 and László Vécsei 1,2,* 1 MTA-SZTE, Neuroscience Research Group, Semmelweis u. 6, Szeged, H-6725 Hungary; [email protected] 2 Department of Neurology, Interdisciplinary Excellence Centre, Faculty of Medicine, University of Szeged, Semmelweis u. 6, H-6725 Szeged, Hungary * Correspondence: [email protected]; Tel.: +36-62-545-351 Received: date; Accepted: date; Published: date Abstract: Worldwide, over 2.2 million people are suffered from multiple sclerosis (MS), a multifactorial demyelinating disease of the central nervous system, characterized by multifocal inflammatory or demyelinating attacks associated with neuroinflammation and neurodegeneration. The blood, cerebrospinal fluid, and postmortem brain samples of MS patients evidenced the presence of reduction-oxidation (redox) homeostasis disturbance such as the alternations of oxidative and antioxidative enzyme activities and the presence of degradation products. This review article discussed the components of redox homeostasis including reactive chemical species, oxidative enzymes, antioxidative enzymes, and degradation products. The reactive chemical species covered frequently discussed reactive oxygen/nitrogen species, rarely featured reactive chemicals such as sulfur, carbonyls, halogens, selenium, and nucleophilic species that potentially act as reductive as well as pro-oxidative stressors. The antioxidative enzyme systems covered the nuclear factor erythroid-2-related factor 2 (NRF2)-Kelch-like ECH-associated protein 1 (KEAP1) signaling pathway, a possible biomarker sensitive to the initial phase of oxidative stress. Altered components of the redox homeostasis in MS were discussed, some of which turned to be MS subtype- or treatment-specific and thus potentially become diagnostic, prognostic, predictive, and/or therapeutic biomarkers.
    [Show full text]
  • 1 T CELL ACTIVATION TRIGGERS REVERSIBLE INOSINE-5'-MONOPHOSPHATE DEHYDROGENASE ASSEMBLY Krisna C. Duong-Ly 1, Yin-Ming Kuo 2
    bioRxiv preprint doi: https://doi.org/10.1101/315929; this version posted May 7, 2018. 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-NC-ND 4.0 International license. T CELL ACTIVATION TRIGGERS REVERSIBLE INOSINE-5’-MONOPHOSPHATE DEHYDROGENASE ASSEMBLY Krisna C. Duong-Ly1, Yin-Ming Kuo2, Matthew C. Johnson3, Justin M. Kollman3, Jonathan Soboloff4, Glenn F. Rall5, Andrew J. Andrews2, and Jeffrey R. Peterson1 1Cancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA 2Cancer Epigenetics Program, Fox Chase Cancer Center, Philadelphia, PA 3Department of Biochemistry, University of Washington, Seattle, WA 4Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA 5Blood Cell Development and Function Program, Fox Chase Cancer Center, Philadelphia, PA Correspondence to Jeffrey R. Peterson: [email protected], Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111, ORCID: 0000-0002-0604-718X; Yin-Ming Kuo’s present address is Department of Radiology, University of Pennsylvania School of Medicine, Philadelphia, PA Short running title: IMPDH FILAMENT ASSEMBLY IN T CELLS Abbreviations used: IMP: inosine-5’-monophosphate IMPDH: inosine-5’-monophosphate dehydrogenase 1 bioRxiv preprint doi: https://doi.org/10.1101/315929; this version posted May 7, 2018. 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-NC-ND 4.0 International license.
    [Show full text]
  • Nucleotide Metabolism II
    Nucleotide Metabolism II • Biosynthesis of deoxynucleotides • Salvage Pathway • Catabolism: Purines • Catabolism: Pyrimidines • Feedback inhibition in purine nucleotide biosynthesis CPS II • Cytosolic CPS II uses glutamine as the nitrogen donor to carbamoyl phosphate Regulation of pyrimidine synthesis •CPSII is allosterically regulated: PRPP and IMP are activators Several pyrimidines are inhibitors • Aspartate transcarbamoylase (ATCase) Important regulatory point in prokaryotes Catalyzes the first committed pathway step Allosteric regulators: CTP (-), CTP + UTP (-), ATP (+) • Regulation of pyrimidine nucleotide synthesis in E. coli Biosynthesis of deoxynucleotides • Uses diphosphates (ribo) • Ribonucleotide reducatase • 2 sub-units • R1- reduces, active and two allosteric sites (activity and specificity site) • R2- tyrosine radical carries electrons • removes 2' OH to H Ribonucleotide reductase reaction • removes 2' OH to H • Thioredoxin and NADPH used to regenerate sulfhydryl groups Thymidylate synthesis • UDP ------> dUMP • dUMP --------> dTMP • required THF • methylates uracil Regulation THF • Mammals cannot conjugate rings or synthesize PABA. • So must get in diet. • Sulfonamides effective in bacteria due to competitive inhibition of the incorporation of PABA Cancer Drugs • fluorouracil-- suicide inhibitor of Thy synthase • aminopterin • Methotrexate -- inhibits DHF reductase Salvage of Purines and Pyrimidines • During cellular metabolism or digestion, nucleic acids are degraded to heterocyclic bases • These bases can be salvaged
    [Show full text]