A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (CYTOSINE; THYMINE; and URACIL) and form the basic structure of the barbiturates.
Pyrimidines with a RIBOSE and phosphate attached that can polymerize to form DNA and RNA.
Dimers found in DNA chains damaged by ULTRAVIOLET RAYS. They consist of two adjacent PYRIMIDINE NUCLEOTIDES, usually THYMINE nucleotides, in which the pyrimidine residues are covalently joined by a cyclobutane ring. These dimers block DNA REPLICATION.
Pyrimidines with a RIBOSE attached that can be phosphorylated to PYRIMIDINE NUCLEOTIDES.
An enzyme which catalyzes an endonucleolytic cleavage near PYRIMIDINE DIMERS to produce a 5'-phosphate product. The enzyme acts on the damaged DNA strand, from the 5' side of the damaged site.
Pentosyltransferases that catalyze the reaction between a pyrimidine nucleoside and orthophosphate to form a free pyrimidine and ribose-5-phosphate.
The enzyme catalyzing the formation of orotidine-5'-phosphoric acid (orotidylic acid) from orotic acid and 5-phosphoribosyl-1-pyrophosphate in the course of pyrimidine nucleotide biosynthesis. EC 2.4.2.10.
That portion of the electromagnetic spectrum immediately below the visible range and extending into the x-ray frequencies. The longer wavelengths (near-UV or biotic or vital rays) are necessary for the endogenous synthesis of vitamin D and are also called antirachitic rays; the shorter, ionizing wavelengths (far-UV or abiotic or extravital rays) are viricidal, bactericidal, mutagenic, and carcinogenic and are used as disinfectants.
A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include ADENINE and GUANINE, constituents of nucleic acids, as well as many alkaloids such as CAFFEINE and THEOPHYLLINE. Uric acid is the metabolic end product of purine metabolism.
An enzyme that, in the course of pyrimidine biosynthesis, catalyzes ring closure by removal of water from N-carbamoylaspartate to yield dihydro-orotic acid. EC 3.5.2.3.
An enzyme that catalyzes the reactivation by light of UV-irradiated DNA. It breaks two carbon-carbon bonds in PYRIMIDINE DIMERS in DNA.
An enzyme that catalyzes the conversion of carbamoyl phosphate and L-aspartate to yield orthophosphate and N-carbamoyl-L-aspartate. (From Enzyme Nomenclature, 1992) EC 2.1.3.2.
Purines attached to a RIBOSE and a phosphate that can polymerize to form DNA and RNA.
An enzyme that catalyzes the formation of carbamoyl phosphate from ATP, carbon dioxide, and glutamine. This enzyme is important in the de novo biosynthesis of pyrimidines. EC 6.3.5.5.
Orotidine-5'-phosphate carboxy-lyase. Catalyzes the decarboxylation of orotidylic acid to yield uridylic acid in the final step of the pyrimidine nucleotide biosynthesis pathway. EC 4.1.1.23.
An enzyme that catalyzes the transfer of ribose from uridine to orthophosphate, forming uracil and ribose 1-phosphate.
A pyrimidine nucleoside that is composed of the base CYTOSINE linked to the five-carbon sugar D-RIBOSE.
An enzyme that in the course of pyrimidine biosynthesis, catalyzes the oxidation of dihydro-orotic acid to orotic acid utilizing oxygen as the electron acceptor. This enzyme is a flavoprotein which contains both FLAVIN-ADENINE DINUCLEOTIDE and FLAVIN MONONUCLEOTIDE as well as iron-sulfur centers. EC 1.3.3.1.
An enzyme that catalyzes the phosphorylation of uridine and cytidine to uridine 5'-phosphate and cytidine 5'-phosphate, respectively. ATP, dUTP, dGTP, and dATP are effective phosphate donors. EC 2.7.1.48.
Enzymes of the transferase class that catalyze the transfer of a pentose group from one compound to another.
Purine or pyrimidine bases attached to a ribose or deoxyribose. (From King & Stansfield, A Dictionary of Genetics, 4th ed)
5'-Uridylic acid. A uracil nucleotide containing one phosphate group esterified to the sugar moiety in the 2', 3' or 5' position.
The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.
Purines with a RIBOSE attached that can be phosphorylated to PURINE NUCLEOTIDES.
Uridine 5'-(tetrahydrogen triphosphate). A uracil nucleotide containing three phosphate groups esterified to the sugar moiety.
A purine or pyrimidine base bonded to DEOXYRIBOSE.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
2'-Deoxyuridine. An antimetabolite that is converted to deoxyuridine triphosphate during DNA synthesis. Laboratory suppression of deoxyuridine is used to diagnose megaloblastic anemias due to vitamin B12 and folate deficiencies.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Nucleosides in which the purine or pyrimidine base is combined with ribose. (Dorland, 28th ed)
The monomeric units from which DNA or RNA polymers are constructed. They consist of a purine or pyrimidine base, a pentose sugar, and a phosphate group. (From King & Stansfield, A Dictionary of Genetics, 4th ed)
3-((4-Amino-2-methyl-5-pyrimidinyl)methyl)-5-(2- hydroxyethyl)-4-methylthiazolium chloride.
The monoanhydride of carbamic acid with PHOSPHORIC ACID. It is an important intermediate metabolite and is synthesized enzymatically by CARBAMYL-PHOSPHATE SYNTHASE (AMMONIA) and CARBAMOYL-PHOSPHATE SYNTHASE (GLUTAMINE-HYDROLYZING).
The spatial arrangement of the atoms of a nucleic acid or polynucleotide that results in its characteristic 3-dimensional shape.
A subclass of enzymes which includes all dehydrogenases acting on carbon-carbon bonds. This enzyme group includes all the enzymes that introduce double bonds into substrates by direct dehydrogenation of carbon-carbon single bonds.
A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.
A triazine nucleoside used as an antineoplastic antimetabolite. It interferes with pyrimidine biosynthesis thereby preventing formation of cellular nucleic acids. As the triacetate, it is also effective as an antipsoriatic.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
The rate dynamics in chemical or physical systems.
A pyrimidine base that is a fundamental unit of nucleic acids.
A class of enzymes involved in the hydrolysis of the N-glycosidic bond of nitrogen-linked sugars.
A group of enzymes catalyzing the endonucleolytic cleavage of DNA. They include members of EC 3.1.21.-, EC 3.1.22.-, EC 3.1.23.- (DNA RESTRICTION ENZYMES), EC 3.1.24.- (DNA RESTRICTION ENZYMES), and EC 3.1.25.-.
Cytidine 5'-(tetrahydrogen triphosphate). A cytosine nucleotide containing three phosphate groups esterified to the sugar moiety.
An oxidoreductase involved in pyrimidine base degradation. It catalyzes the catabolism of THYMINE; URACIL and the chemotherapeutic drug, 5-FLUOROURACIL.
A purine base and a fundamental unit of ADENINE NUCLEOTIDES.
A class of enzymes that catalyze the conversion of a nucleotide and water to a nucleoside and orthophosphate. EC 3.1.3.-.
The key substance in the biosynthesis of histidine, tryptophan, and purine and pyrimidine nucleotides.
A glycoprotein enzyme present in various organs and in many cells. The enzyme catalyzes the hydrolysis of a 5'-ribonucleotide to a ribonucleoside and orthophosphate in the presence of water. It is cation-dependent and exists in a membrane-bound and soluble form. EC 3.1.3.5.
Polymers made up of a few (2-20) nucleotides. In molecular genetics, they refer to a short sequence synthesized to match a region where a mutation is known to occur, and then used as a probe (OLIGONUCLEOTIDE PROBES). (Dorland, 28th ed)
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Nucleotides in which the purine or pyrimidine base is combined with ribose. (Dorland, 28th ed)
Deoxycytidine (dihydrogen phosphate). A deoxycytosine nucleotide containing one phosphate group esterified to the deoxyribose moiety in the 2'-,3'- or 5- positions.
A rare, pigmentary, and atrophic autosomal recessive disease. It is manifested as an extreme photosensitivity to ULTRAVIOLET RAYS as the result of a deficiency in the enzyme that permits excisional repair of ultraviolet-damaged DNA.
A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.
The location of the atoms, groups or ions relative to one another in a molecule, as well as the number, type and location of covalent bonds.
A simple organophosphorus compound that inhibits DNA polymerase, especially in viruses and is used as an antiviral agent.
An antineoplastic antimetabolite that is metabolized to fluorouracil when administered by rapid injection; when administered by slow, continuous, intra-arterial infusion, it is converted to floxuridine monophosphate. It has been used to treat hepatic metastases of gastrointestinal adenocarcinomas and for palliation in malignant neoplasms of the liver and gastrointestinal tract.
The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.
Inhibitors of the enzyme, dihydrofolate reductase (TETRAHYDROFOLATE DEHYDROGENASE), which converts dihydrofolate (FH2) to tetrahydrofolate (FH4). They are frequently used in cancer chemotherapy. (From AMA, Drug Evaluations Annual, 1994, p2033)
A group of deoxyribonucleotides (up to 12) in which the phosphate residues of each deoxyribonucleotide act as bridges in forming diester linkages between the deoxyribose moieties.
An enzyme that catalyzes the hydrolytic deamination of deoxycytidylic acid to deoxyuridylic acid and ammonia. It plays an important role in the regulation of the pool of deoxynucleotides in higher organisms. The enzyme also acts on some 5-substituted deoxycytidylic acids. EC 3.5.4.12.
A purine nucleoside that has guanine linked by its N9 nitrogen to the C1 carbon of ribose. It is a component of ribonucleic acid and its nucleotides play important roles in metabolism. (From Dorland, 28th ed)
A family of DNA repair enzymes that recognize damaged nucleotide bases and remove them by hydrolyzing the N-glycosidic bond that attaches them to the sugar backbone of the DNA molecule. The process called BASE EXCISION REPAIR can be completed by a DNA-(APURINIC OR APYRIMIDINIC SITE) LYASE which excises the remaining RIBOSE sugar from the DNA.
The effects of ionizing and nonionizing radiation upon living organisms, organs and tissues, and their constituents, and upon physiologic processes. It includes the effect of irradiation on food, drugs, and chemicals.
Phosphate esters of THYMIDINE in N-glycosidic linkage with ribose or deoxyribose, as occurs in nucleic acids. (From Dorland, 28th ed, p1154)
A rather large group of enzymes comprising not only those transferring phosphate but also diphosphate, nucleotidyl residues, and others. These have also been subdivided according to the acceptor group. (From Enzyme Nomenclature, 1992) EC 2.7.
5-Bromo-2,4(1H,3H)-pyrimidinedione. Brominated derivative of uracil that acts as an antimetabolite, substituting for thymine in DNA. It is used mainly as an experimental mutagen, but its deoxyriboside (BROMODEOXYURIDINE) is used to treat neoplasms.
Proteins involved in the transport of NUCLEOSIDES across cellular membranes.
An enzyme that catalyzes the formation of carbamoyl phosphate from ATP, carbon dioxide, and ammonia. This enzyme is specific for arginine biosynthesis or the urea cycle. Absence or lack of this enzyme may cause CARBAMOYL-PHOSPHATE SYNTHASE I DEFICIENCY DISEASE. EC 6.3.4.16.
4-Hydroxy-1-(beta-D-ribofuranosyl)-2-pyridinone. Analog of uridine lacking a ring-nitrogen in the 3-position. Functions as an antineoplastic agent.
Azoles with an OXYGEN and a NITROGEN next to each other at the 1,2 positions, in contrast to OXAZOLES that have nitrogens at the 1,3 positions.
5-Thymidylic acid. A thymine nucleotide containing one phosphate group esterified to the deoxyribose moiety.
Cytosine nucleotides which contain deoxyribose as the sugar moiety.
Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
A uracil nucleotide containing a pyrophosphate group esterified to C5 of the sugar moiety.
A genus of gram-positive, spherical bacteria found in soils and fresh water, and frequently on the skin of man and other animals.
Enzymes that catalyze the hydrolysis of the internal bonds and thereby the formation of polynucleotides or oligonucleotides from ribo- or deoxyribonucleotide chains. EC 3.1.-.
An enzyme of the transferase class that catalyzes the reaction 5,10-methylenetetrahydrofolate and dUMP to dihydrofolate and dTMP in the synthesis of thymidine triphosphate. (From Dorland, 27th ed) EC 2.1.1.45.
An enzyme that catalyzes reversible reactions of a nucleoside triphosphate, e.g., ATP, with a nucleoside monophosphate, e.g., UMP, to form ADP and UDP. Many nucleoside monophosphates can act as acceptor while many ribo- and deoxyribonucleoside triphosphates can act as donor. EC 2.7.4.4.
The relationship between the dose of administered radiation and the response of the organism or tissue to the radiation.
One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter.
A purine or pyrimidine base bonded to a DEOXYRIBOSE containing a bond to a phosphate group.
Pairing of purine and pyrimidine bases by HYDROGEN BONDING in double-stranded DNA or RNA.
Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (MAGNETIC RESONANCE IMAGING).
5-Bromo-2'-deoxycytidine. Can be incorporated into DNA in the presence of DNA polymerase, replacing dCTP.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Purine bases related to hypoxanthine, an intermediate product of uric acid synthesis and a breakdown product of adenine catabolism.
Proteins involved in the transport of NUCLEOTIDES across cellular membranes.
A urea cycle enzyme that catalyzes the formation of orthophosphate and L-citrulline (CITRULLINE) from CARBAMOYL PHOSPHATE and L-ornithine (ORNITHINE). Deficiency of this enzyme may be transmitted as an X-linked trait. EC 2.1.3.3.
Hydrolysate of DNA in which purine bases have been removed.
Established cell cultures that have the potential to propagate indefinitely.
The removal of an amino group (NH2) from a chemical compound.
The class of all enzymes catalyzing oxidoreduction reactions. The substrate that is oxidized is regarded as a hydrogen donor. The systematic name is based on donor:acceptor oxidoreductase. The recommended name will be dehydrogenase, wherever this is possible; as an alternative, reductase can be used. Oxidase is only used in cases where O2 is the acceptor. (Enzyme Nomenclature, 1992, p9)
A polynucleotide consisting essentially of chains with a repeating backbone of phosphate and ribose units to which nitrogenous bases are attached. RNA is unique among biological macromolecules in that it can encode genetic information, serve as an abundant structural component of cells, and also possesses catalytic activity. (Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Pyrazolopyrimidine ribonucleosides isolated from Nocardia interforma. They are antineoplastic antibiotics with cytostatic properties.
An enzyme that catalyzes the conversion of ATP and thymidine to ADP and thymidine 5'-phosphate. Deoxyuridine can also act as an acceptor and dGTP as a donor. (From Enzyme Nomenclature, 1992) EC 2.7.1.21.
The prototype species of PNEUMOCYSTIS infecting the laboratory rat, Rattus norvegicus (RATS). It was formerly called Pneumocystis carinii f. sp. carinii. Other species of Pneumocystis can also infect rats.
A low-energy attractive force between hydrogen and another element. It plays a major role in determining the properties of water, proteins, and other compounds.
An enzyme of the oxidoreductase class that catalyzes the reaction 7,8-dihyrofolate and NADPH to yield 5,6,7,8-tetrahydrofolate and NADPH+, producing reduced folate for amino acid metabolism, purine ring synthesis, and the formation of deoxythymidine monophosphate. Methotrexate and other folic acid antagonists used as chemotherapeutic drugs act by inhibiting this enzyme. (Dorland, 27th ed) EC 1.5.1.3.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
An enzyme which catalyzes the endonucleolytic cleavage of phosphodiester bonds at purinic or apyrimidinic sites (AP-sites) to produce 5'-Phosphooligonucleotide end products. The enzyme prefers single-stranded DNA (ssDNA) and was formerly classified as EC 3.1.4.30.
The interference in synthesis of an enzyme due to the elevated level of an effector substance, usually a metabolite, whose presence would cause depression of the gene responsible for enzyme synthesis.
A group of 13 or more deoxyribonucleotides in which the phosphate residues of each deoxyribonucleotide act as bridges in forming diester linkages between the deoxyribose moieties.
The process by which a DNA molecule is duplicated.
Deoxyribonucleic acid that makes up the genetic material of bacteria.
Linear furanocoumarins which are found in many PLANTS, especially UMBELLIFERAE and RUTACEAE, as well as PSORALEA from which they were originally discovered. They can intercalate DNA and, in an UV-initiated reaction of the furan portion, alkylate PYRIMIDINES, resulting in PHOTOSENSITIVITY DISORDERS.
An enzyme that catalyzes the transfer of 2-deoxy-D-ribose from THYMIDINE to orthophosphate, thereby liberating thymidine.
A subdiscipline of genetics that studies RADIATION EFFECTS on the components and processes of biological inheritance.
Uracil nucleotides which contain deoxyribose as the sugar moiety.
The relative amounts of the PURINES and PYRIMIDINES in a nucleic acid.
Derivatives of carbamic acid, H2NC(=O)OH. Included under this heading are N-substituted and O-substituted carbamic acids. In general carbamate esters are referred to as urethanes, and polymers that include repeating units of carbamate are referred to as POLYURETHANES. Note however that polyurethanes are derived from the polymerization of ISOCYANATES and the singular term URETHANE refers to the ethyl ester of carbamic acid.
A group of ribonucleotides (up to 12) in which the phosphate residues of each ribonucleotide act as bridges in forming diester linkages between the ribose moieties.
DNA-dependent DNA polymerases found in bacteria, animal and plant cells. During the replication process, these enzymes catalyze the addition of deoxyribonucleotide residues to the end of a DNA strand in the presence of DNA as template-primer. They also possess exonuclease activity and therefore function in DNA repair.
A class of enzymes that catalyze the cleavage of C-C, C-O, and C-N, and other bonds by other means than by hydrolysis or oxidation. (Enzyme Nomenclature, 1992) EC 4.
Proteins obtained from ESCHERICHIA COLI.
A purine and a reaction intermediate in the metabolism of adenosine and in the formation of nucleic acids by the salvage pathway.
An antiviral derivative of THYMIDINE used mainly in the treatment of primary keratoconjunctivitis and recurrent epithelial keratitis due to HERPES SIMPLEX virus. (From Martindale, The Extra Pharmacopoeia, 30th ed, p557)
An analog of DEOXYURIDINE that inhibits viral DNA synthesis. The drug is used as an antiviral agent.
Ribose substituted in the 1-, 3-, or 5-position by a phosphoric acid moiety.
The study of crystal structure using X-RAY DIFFRACTION techniques. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.
Transferases are enzymes transferring a group, for example, the methyl group or a glycosyl group, from one compound (generally regarded as donor) to another compound (generally regarded as acceptor). The classification is based on the scheme "donor:acceptor group transferase". (Enzyme Nomenclature, 1992) EC 2.
Sulfhydryl analog of INOSINE that inhibits nucleoside transport across erythrocyte plasma membranes, and has immunosuppressive properties. It has been used similarly to MERCAPTOPURINE in the treatment of leukemia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p503)
Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
Double-stranded nucleic acid molecules (DNA-DNA or DNA-RNA) which contain regions of nucleotide mismatches (non-complementary). In vivo, these heteroduplexes can result from mutation or genetic recombination; in vitro, they are formed by nucleic acid hybridization. Electron microscopic analysis of the resulting heteroduplexes facilitates the mapping of regions of base sequence homology of nucleic acids.
A series of 7 virulent phages which infect E. coli. The T-even phages T2, T4; (BACTERIOPHAGE T4), and T6, and the phage T5 are called "autonomously virulent" because they cause cessation of all bacterial metabolism on infection. Phages T1, T3; (BACTERIOPHAGE T3), and T7; (BACTERIOPHAGE T7) are called "dependent virulent" because they depend on continued bacterial metabolism during the lytic cycle. The T-even phages contain 5-hydroxymethylcytosine in place of ordinary cytosine in their DNA.
Enzymes which catalyze the hydrolases of ester bonds within DNA. EC 3.1.-.
Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of causes.
Extrachromosomal, usually CIRCULAR DNA molecules that are self-replicating and transferable from one organism to another. They are found in a variety of bacterial, archaeal, fungal, algal, and plant species. They are used in GENETIC ENGINEERING as CLONING VECTORS.
A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.
Determination of the spectra of ultraviolet absorption by specific molecules in gases or liquids, for example Cl2, SO2, NO2, CS2, ozone, mercury vapor, and various unsaturated compounds. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
An enzyme catalyzing the formation of AMP from adenine and phosphoribosylpyrophosphate. It can act as a salvage enzyme for recycling of adenine into nucleic acids. EC 2.4.2.7.
Adenosine molecules which can be substituted in any position, but are lacking one hydroxyl group in the ribose part of the molecule.
Systems of enzymes which function sequentially by catalyzing consecutive reactions linked by common metabolic intermediates. They may involve simply a transfer of water molecules or hydrogen atoms and may be associated with large supramolecular structures such as MITOCHONDRIA or RIBOSOMES.
A purine nucleoside that has hypoxanthine linked by the N9 nitrogen to the C1 carbon of ribose. It is an intermediate in the degradation of purines and purine nucleosides to uric acid and in pathways of purine salvage. It also occurs in the anticodon of certain transfer RNA molecules. (Dorland, 28th ed)
A DNA repair enzyme that is an N-glycosyl hydrolase with specificity for DNA-containing ring-opened N(7)-methylguanine residues.
An enzyme that catalyzes reversibly the phosphorylation of deoxycytidine with the formation of a nucleoside diphosphate and deoxycytidine monophosphate. Cytosine arabinoside can also act as an acceptor. All natural nucleoside triphosphates, except deoxycytidine triphosphate, can act as donors. The enzyme is induced by some viruses, particularly the herpes simplex virus (HERPESVIRUS HOMINIS). EC 2.7.1.74.
A pentose active in biological systems usually in its D-form.
Coronary vasodilator with some antiarrhythmic activity.
A subdiscipline of genetics which deals with the genetic mechanisms and processes of microorganisms.
A class of organic compounds containing two ring structures, one of which is made up of more than one kind of atom, usually carbon plus another atom. The heterocycle may be either aromatic or nonaromatic.
An autosomal recessive disorder affecting DIHYDROPYRIMIDINE DEHYDROGENASE and causing familial pyrimidinemia. It is characterized by thymine-uraciluria in homozygous deficient patients. Even a partial deficiency in the enzyme leaves individuals at risk for developing severe 5-FLUOROURACIL-associated toxicity.
The normality of a solution with respect to HYDROGEN ions; H+. It is related to acidity measurements in most cases by pH = log 1/2[1/(H+)], where (H+) is the hydrogen ion concentration in gram equivalents per liter of solution. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
Azoles of two nitrogens at the 1,2 positions, next to each other, in contrast with IMIDAZOLES in which they are at the 1,3 positions.
A RNA-binding protein that binds to polypyriminidine rich regions in the INTRONS of messenger RNAs. Polypyrimidine tract-binding protein may be involved in regulating the ALTERNATIVE SPLICING of mRNAs since its presence on an intronic RNA region that is upstream of an EXON inhibits the splicing of the exon into the final mRNA product.
Derivatives of formic acids. Included under this heading are a broad variety of acid forms, salts, esters, and amides that are formed with a single carbon carboxy group.
A serotype of Salmonella enterica that is a frequent agent of Salmonella gastroenteritis in humans. It also causes PARATYPHOID FEVER.
Catalyze the hydrolysis of nucleotides with the elimination of ammonia.
A DNA repair enzyme that catalyses the excision of ribose residues at apurinic and apyrimidinic DNA sites that can result from the action of DNA GLYCOSYLASES. The enzyme catalyzes a beta-elimination reaction in which the C-O-P bond 3' to the apurinic or apyrimidinic site in DNA is broken, leaving a 3'-terminal unsaturated sugar and a product with a terminal 5'-phosphate. This enzyme was previously listed under EC 3.1.25.2.
A nucleoside consisting of the base guanine and the sugar deoxyribose.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A ZINC FINGER MOTIF protein that recognizes and interacts with damaged DNA. It is a DNA-binding protein that plays an essential role in NUCLEOTIDE EXCISION REPAIR. Mutations in this protein are associated with the most severe form of XERODERMA PIGMENTOSUM.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A rigorously mathematical analysis of energy relationships (heat, work, temperature, and equilibrium). It describes systems whose states are determined by thermal parameters, such as temperature, in addition to mechanical and electromagnetic parameters. (From Hawley's Condensed Chemical Dictionary, 12th ed)
A methylated nucleotide base found in eukaryotic DNA. In ANIMALS, the DNA METHYLATION of CYTOSINE to form 5-methylcytosine is found primarily in the palindromic sequence CpG. In PLANTS, the methylated sequence is CpNpGp, where N can be any base.
The facilitation of a chemical reaction by material (catalyst) that is not consumed by the reaction.
Antimetabolites that are useful in cancer chemotherapy.
The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
Stable carbon atoms that have the same atomic number as the element carbon, but differ in atomic weight. C-13 is a stable carbon isotope.
Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly.
Organic compounds that contain phosphorus as an integral part of the molecule. Included under this heading is broad array of synthetic compounds that are used as PESTICIDES and DRUGS.
Agents that are capable of inserting themselves between the successive bases in DNA, thus kinking, uncoiling or otherwise deforming it and therefore preventing its proper functioning. They are used in the study of DNA.
The phenomenon whereby compounds whose molecules have the same number and kind of atoms and the same atomic arrangement, but differ in their spatial relationships. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)
A fractionated cell extract that maintains a biological function. A subcellular fraction isolated by ultracentrifugation or other separation techniques must first be isolated so that a process can be studied free from all of the complex side reactions that occur in a cell. The cell-free system is therefore widely used in cell biology. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p166)
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.
An enzyme that catalyzes the formation of ADP plus AMP from adenosine plus ATP. It can serve as a salvage mechanism for returning adenosine to nucleic acids. EC 2.7.1.20.
An antibiotic purine ribonucleoside that readily substitutes for adenosine in the biological system, but its incorporation into DNA and RNA has an inhibitory effect on the metabolism of these nucleic acids.
Organic compounds composed exclusively of carbon and hydrogen where no carbon atoms join to form a ring structure.
High molecular weight polymers containing a mixture of purine and pyrimidine nucleotides chained together by ribose or deoxyribose linkages.
A species of gram-positive bacteria that is a common soil and water saprophyte.
A basic science concerned with the composition, structure, and properties of matter; and the reactions that occur between substances and the associated energy exchange.
A symporter protein that couples the transport of FOLIC ACID with HYDROGEN IONS. The transporter functions most effectively under acidic conditions.
Enzymes that catalyze the endonucleolytic cleavage of single-stranded regions of DNA or RNA molecules while leaving the double-stranded regions intact. They are particularly useful in the laboratory for producing "blunt-ended" DNA molecules from DNA with single-stranded ends and for sensitive GENETIC TECHNIQUES such as NUCLEASE PROTECTION ASSAYS that involve the detection of single-stranded DNA and RNA.
Unstable isotopes of carbon that decay or disintegrate emitting radiation. C atoms with atomic weights 10, 11, and 14-16 are radioactive carbon isotopes.
A species of the genus SACCHAROMYCES, family Saccharomycetaceae, order Saccharomycetales, known as "baker's" or "brewer's" yeast. The dried form is used as a dietary supplement.
The composition, conformation, and properties of atoms and molecules, and their reaction and interaction processes.
Cytidine (dihydrogen phosphate). A cytosine nucleotide containing one phosphate group esterified to the sugar moiety in the 2', 3' or 5' position.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
A genus of ascomycetous fungi of the family Saccharomycetaceae, order SACCHAROMYCETALES.

Activation of c-Abl tyrosine kinase requires caspase activation and is not involved in JNK/SAPK activation during apoptosis of human monocytic leukemia U937 cells. (1/8131)

Genotoxic stress triggers the activation of several sensor molecules, such as p53, JNK1/SAPK and c-Abl, and occasionally promotes the cells to apoptosis. We previously reported that JNK1/SAPK regulates genotoxic stress-induced apoptosis in p53-negative U937 cells by activating caspases. c-Abl is expected to act upstream of JNK1/SAPK activation upon treatment with genotoxic stressors, but its involvement in apoptosis development is still unclear. We herein investigated the kinase activities of c-Abl and JNK1/SAPK during apoptosis elicited by genotoxic anticancer drugs and tumor necrosis factor (TNF) in U937 cells and their apoptosis-resistant variant UK711 cells. We found that the activation of JNK1/SAPK and c-Abl correlated well with apoptosis development in these cell lines. Unexpectedly, however, the JNK1/SAPK activation preceded the c-Abl activation. Moreover, the caspase inhibitor Z-Asp suppressed c-Abl activation and the onset of apoptosis but not the JNK1/SAPK activation. Interestingly, c-Abl tyrosine kinase inhibition by CGP 57148 reduced apoptosis without interfering with JNK1/SAPK activation. These results indicate that c-Abl acts not upstream of JNK1/ SAPK but downstream of caspases during the development of p53-independent apoptosis and is possibly involved in accelerating execution of the cell death pathway.  (+info)

Selection and characterization of pre-mRNA splicing enhancers: identification of novel SR protein-specific enhancer sequences. (2/8131)

Splicing enhancers are RNA sequences required for accurate splice site recognition and the control of alternative splicing. In this study, we used an in vitro selection procedure to identify and characterize novel RNA sequences capable of functioning as pre-mRNA splicing enhancers. Randomized 18-nucleotide RNA sequences were inserted downstream from a Drosophila doublesex pre-mRNA enhancer-dependent splicing substrate. Functional splicing enhancers were then selected by multiple rounds of in vitro splicing in nuclear extracts, reverse transcription, and selective PCR amplification of the spliced products. Characterization of the selected splicing enhancers revealed a highly heterogeneous population of sequences, but we identified six classes of recurring degenerate sequence motifs five to seven nucleotides in length including novel splicing enhancer sequence motifs. Analysis of selected splicing enhancer elements and other enhancers in S100 complementation assays led to the identification of individual enhancers capable of being activated by specific serine/arginine (SR)-rich splicing factors (SC35, 9G8, and SF2/ASF). In addition, a potent splicing enhancer sequence isolated in the selection specifically binds a 20-kDa SR protein. This enhancer sequence has a high level of sequence homology with a recently identified RNA-protein adduct that can be immunoprecipitated with an SRp20-specific antibody. We conclude that distinct classes of selected enhancers are activated by specific SR proteins, but there is considerable sequence degeneracy within each class. The results presented here, in conjunction with previous studies, reveal a remarkably broad spectrum of RNA sequences capable of binding specific SR proteins and/or functioning as SR-specific splicing enhancers.  (+info)

Base excision repair of oxidative DNA damage activated by XPG protein. (3/8131)

Oxidized pyrimidines in DNA are removed by a distinct base excision repair pathway initiated by the DNA glycosylase--AP lyase hNth1 in human cells. We have reconstituted this single-residue replacement pathway with recombinant proteins, including the AP endonuclease HAP1/APE, DNA polymerase beta, and DNA ligase III-XRCC1 heterodimer. With these proteins, the nucleotide excision repair enzyme XPG serves as a cofactor for the efficient function of hNth1. XPG protein promotes binding of hNth1 to damaged DNA. The stimulation of hNth1 activity is retained in XPG catalytic site mutants inactive in nucleotide excision repair. The data support the model that development of Cockayne syndrome in XP-G patients is related to inefficient excision of endogenous oxidative DNA damage.  (+info)

A correlation between changes in gamma-aminobutyric acid metabolism and seizures induced by antivitamin B6. (4/8131)

The effects of DL-penicillamine (DL-PeA), hydrazine and toxopyrimidine (TXP, 2-methyl-6-amino-5-hydroxymethylpyrimidine) on gamma-aminobutyric acid (GABA) metabolism in mouse brain were studied. All these compounds inhibited the activity of glutamate decarboxylase [EC 4.1.1.15] (GAD) and slightly inhibited that of 4-aminobutyrate: 2-oxoglutarate aminotransferase [EC 2.6.1.19] (GABA-T). In contrast, very different effects were observed on GABA levels; hydrazine caused a marked increase, DL-PeA had no effect, and TXP caused a slight decrease in the content of the amino acid. These results could be described by an equation which related the excitable state to changes in the flux of the GABA bypass. Since the values obtained from the equation clearly reflect the seizure activity, it is suggested that the decreased GABA flux might be a cause of convulsions induced by these drugs.  (+info)

Selective antiaggressive effects of alnespirone in resident-intruder test are mediated via 5-hydroxytryptamine1A receptors: A comparative pharmacological study with 8-hydroxy-2-dipropylaminotetralin, ipsapirone, buspirone, eltoprazine, and WAY-100635. (5/8131)

The present study characterized the effects of the novel, selective, and potent 5-hydroxytryptamine1A (serotonin) (5-HT1A) receptor agonist, alnespirone [S-20499, (S)-N-4-[5-methoxychroman-3-yl)propylamino)butyl- 8-azaspiro-(4,5)-diacetamide, hydrochloride] on offensive and defensive resident-intruder aggression in wild-type rats and compared its actions with those of the prototypical full 5-HT1A agonist 8-hydroxy-2- dipropylaminotetralin (8-OH-DPAT), the partial 5-HT1A agonists ipsapirone and buspirone, and the mixed 5-HT1A/1B agonist eltoprazine. All five agonists exerted effective dose-dependent decreases of offensive aggressive behavior in resident rats; 8-OH-DPAT was the most potent (ID50 = 0.074 mg/kg), followed by eltoprazine (0.24), buspirone (0.72), ipsapirone (1.08), and alnespirone (1.24). However, in terms of selectivity of the antiaggressive effects as determined by the absence of decrements in social interest and general motor activity, alnespirone appeared to be superior. In the defensive aggression test, neither alnespirone nor any of the other four agonists changed defensive behaviors in the intruder rats. The involvement of 5-HT1A receptors in the antiaggressive actions of these drugs was confirmed by showing that the selective 5-HT1A receptor antagonist WAY-100635 (N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2- pyridinyl)cyclohexanecarboxamide trihydrochloride), which was inactive alone, fully prevented the antiaggressive effects of alnespirone, 8-OH-DPAT, and buspirone and partly reversed those of ipsapirone and eltoprazine. The data clearly indicate that alnespirone effectively suppresses offensive aggression with an advantageous profile of action compared with other full or partial 5-HT1A agonists. These selective antiaggressive actions of alnespirone are mediated by stimulating 5-HT1A receptors, presumably the somatodendritic autoreceptors at the raphe nuclei. Furthermore, the data provide evidence for a major involvement of these 5-HT1A receptors in the modulation of aggressive behavior by 8-OH-DPAT, ipsapirone, buspirone, and eltoprazine.  (+info)

Increased lipophilicity and subsequent cell partitioning decrease passive transcellular diffusion of novel, highly lipophilic antioxidants. (6/8131)

Oxidative stress is considered a cause or propagator of acute and chronic disorders of the central nervous system. Novel 2, 4-diamino-pyrrolo[2,3-d]pyrimidines are potent inhibitors of iron-dependent lipid peroxidation, are cytoprotective in cell culture models of oxidative injury, and are neuroprotective in brain injury and ischemia models. The selection of lead candidates from this series required that they reach target cells deep within brain tissue in efficacious amounts after oral dosing. A homologous series of 26 highly lipophilic pyrrolopyrimidines was examined using cultured cell monolayers to understand the structure-permeability relationship and to use this information to predict brain penetration and residence time. Pyrrolopyrimidines were shown to be a more permeable structural class of membrane-interactive antioxidants where transepithelial permeability was inversely related to lipophilicity or to cell partitioning. Pyrrole substitutions influence cell partitioning where bulky hydrophobic groups increased partitioning and decreased permeability and smaller hydrophobic groups and more hydrophilic groups, especially those capable of weak hydrogen bonding, decreased partitioning, and increased permeability. Transmonolayer diffusion for these membrane-interactive antioxidants was limited mostly by desorption from the receiver-side membrane into the buffer. Thus, in this case, these in vitro cell monolayer models do not adequately mimic the in vivo situation by underestimating in vivo bioavailability of highly lipophilic compounds unless acceptors, such as serum proteins, are added to the receiving buffer.  (+info)

Novel, highly lipophilic antioxidants readily diffuse across the blood-brain barrier and access intracellular sites. (7/8131)

In an accompanying article, an in vitro assay for permeability predicts that membrane-protective, antioxidant 2,4-diamino-pyrrolo[2, 3-d]pyrimidines should have improved blood-brain barrier (BBB) permeation over previously described lipophilic antioxidants. Using a first-pass extraction method and brain/plasma quantification, we show here that two of the pyrrolopyrimidines, one of which is markedly less permeable, readily partition into rat brain. The efficiency of extraction was dependent on serum protein binding, and in situ efflux confirms the in vitro data showing that PNU-87663 is retained in brain longer than PNU-89843. By exploiting inherent fluorescence properties of PNU-87663, its distribution within brain and within cells in culture was demonstrated using confocal scanning laser microscopy. PNU-87663 rapidly partitioned into the cell membrane and equilibrates with cytoplasmic compartments via passive diffusion. Although partitioning of PNU-87663 favors intracytoplasmic lipid storage droplets, the compound was readily exchangeable as shown by efflux of compound from cells to buffer when protein was present. The results demonstrated that pyrrolopyrimidines were well suited for quickly accessing target cells within the central nervous system as well as in other target tissues.  (+info)

Channeling of carbamoyl phosphate to the pyrimidine and arginine biosynthetic pathways in the deep sea hyperthermophilic archaeon Pyrococcus abyssi. (8/8131)

The kinetics of the coupled reactions between carbamoyl-phosphate synthetase (CPSase) and both aspartate transcarbamoylase (ATCase) and ornithine transcarbamoylase (OTCase) from the deep sea hyperthermophilic archaeon Pyrococcus abyssi demonstrate the existence of carbamoyl phosphate channeling in both the pyrimidine and arginine biosynthetic pathways. Isotopic dilution experiments and coupled reaction kinetics analyzed within the context of the formalism proposed by Ovadi et al. (Ovadi, J., Tompa, P., Vertessy, B., Orosz, F., Keleti, T., and Welch, G. R. (1989) Biochem. J. 257, 187-190) are consistent with a partial channeling of the intermediate at 37 degrees C, but channeling efficiency increases dramatically at elevated temperatures. There is no preferential partitioning of carbamoyl phosphate between the arginine and pyrimidine biosynthetic pathways. Gel filtration chromatography at high and low temperature and in the presence and absence of substrates did not reveal stable complexes between P. abyssi CPSase and either ATCase or OTCase. Thus, channeling must occur during the dynamic association of coupled enzymes pairs. The interaction of CPSase-ATCase was further demonstrated by the unexpectedly weak inhibition of the coupled reaction by the bisubstrate analog, N-(phosphonacetyl)-L-aspartate (PALA). The anomalous effect of PALA suggests that, in the coupled reaction, the effective concentration of carbamoyl phosphate in the vicinity of the ATCase active site is 96-fold higher than the concentration in the bulk phase. Channeling probably plays an essential role in protecting this very unstable intermediate of metabolic pathways performing at extreme temperatures.  (+info)

Some common examples of purine-pyrimidine metabolism, inborn errors include:

1. Adenine sulfate accumulation: This disorder is caused by a deficiency of the enzyme adenylosuccinase, which is needed to break down adenine sulfate. The build-up of this compound can lead to developmental delays, intellectual disability, and seizures.
2. Hypoxanthine-guanine phosphoribosyltransferase (HGPRT) deficiency: This disorder is caused by a lack of the enzyme HGPRT, which is needed to break down hypoxanthine and guanine. The build-up of these compounds can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
3. Phosphoribosylpyrophosphate synthase (PRPS) deficiency: This disorder is caused by a lack of the enzyme PRPS, which is needed to break down phosphoribosylpyrophosphate. The build-up of this compound can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
4. Purine nucleotide phosphorylase (PNP) deficiency: This disorder is caused by a lack of the enzyme PNP, which is needed to break down purine nucleotides. The build-up of these compounds can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
5. Adenylosuccinate lyase (ADSL) deficiency: This disorder is caused by a lack of the enzyme ADSL, which is needed to break down adenylosuccinate. The build-up of this compound can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
6. Leukemia-lymphoma-related gene (LRG) deficiency: This disorder is caused by a lack of the LRG gene, which is needed for the development of immune cells. The build-up of abnormal immune cells can lead to an increased risk of leukemia and lymphoma.
7. Methylmalonyl-CoA mutase (MUT) deficiency: This disorder is caused by a lack of the enzyme MUT, which is needed to break down methylmalonyl-CoA. The build-up of this compound can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
8. Mycobacterium avium intracellulare infection: This disorder is caused by an infection with the bacteria Mycobacterium avium intracellulare. The infection can lead to a variety of symptoms, including fever, fatigue, and weight loss.
9. NAD+ transhydrogenase (NAT) deficiency: This disorder is caused by a lack of the enzyme NAT, which is needed to break down NAD+. The build-up of this compound can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
10. Neuronal ceroid lipofuscinosis (NCL) diseases: These disorders are caused by a lack of the enzyme ALDH7A1, which is needed to break down certain fats in the body. The build-up of these fats can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
11. Phenylketonuria (PKU): This disorder is caused by a lack of the enzyme phenylalanine hydroxylase (PAH), which is needed to break down the amino acid phenylalanine. The build-up of phenylalanine can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
12. Propionic acidemia: This disorder is caused by a lack of the enzyme propionyl-CoA carboxytransferase (PCC), which is needed to break down the amino acid propionate. The build-up of propionate can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
13. Methylmalonic acidemia: This disorder is caused by a lack of the enzyme methylmalonyl-CoA mutase (MCM), which is needed to break down the amino acid methionine. The build-up of methylmalonyl-CoA can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
14. Homocystinuria: This disorder is caused by a lack of the enzyme cystathionine beta-synthase (CBS), which is needed to break down the amino acid homocysteine. The build-up of homocysteine can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
15. maple syrup urine disease (MSUD): This disorder is caused by a lack of the enzyme branched-chain alpha-keto acid dehydrogenase (BCKDH), which is needed to break down the amino acids leucine, isoleucine, and valine. The build-up of these amino acids can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
16. Tyrosinemia type I: This disorder is caused by a lack of the enzyme fumarylacetoacetate hydrolase (FAH), which is needed to break down the amino acid tyrosine. The build-up of tyrosine can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
17. Hereditary tyrosinemia type II: This disorder is caused by a lack of the enzyme tyrosine ammonia lyase (TAL), which is needed to break down the amino acid tyrosine. The build-up of tyrosine can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
18. Galactosemia: This disorder is caused by a lack of the enzyme galactose-1-phosphate uridylyltransferase (GALT), which is needed to break down the sugar galactose. The build-up of galactose can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
19. Phenylketonuria (PKU): This disorder is caused by a lack of the enzyme phenylalanine hydroxylase (PAH), which is needed to break down the amino acid phenylalanine. The build-up of phenylalanine can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.
20. Methylmalonic acidemia (MMA): This disorder is caused by a lack of the enzyme methylmalonyl-CoA mutase (MCM), which is needed to break down the amino acids methionine and homocysteine. The build-up of these amino acids can lead to developmental delays, intellectual disability, and an increased risk of certain cancers.

In addition to these specific disorders, there are also many other inborn errors of metabolism that can affect various aspects of the body, including the nervous system, the skin, and the muscles. These disorders can be caused by a variety of genetic mutations, and they can have a wide range of symptoms and effects on the body.

Overall, inborn errors of metabolism are a group of rare genetic disorders that can affect various aspects of the body and can have serious health consequences if left untreated. These disorders are often diagnosed through newborn screening programs, and they can be managed with dietary changes, medication, and other treatments. With appropriate treatment, many individuals with inborn errors of metabolism can lead active and productive lives.

The main symptoms of XP include:

1. Extremely sensitive skin that burns easily and develops freckles and age spots at an early age.
2. Premature aging of the skin, including wrinkling and thinning.
3. Increased risk of developing skin cancers, especially melanoma, which can be fatal if not treated early.
4. Poor wound healing and scarring.
5. Eye problems such as cataracts, glaucoma, and poor vision.
6. Neurological problems such as intellectual disability, seizures, and difficulty with coordination and balance.

XP is usually inherited in an autosomal recessive pattern, which means that a child must inherit two copies of the mutated gene, one from each parent, to develop the condition. The diagnosis of XP is based on clinical features, family history, and genetic testing. There is no cure for XP, but treatment options include:

1. Avoiding UV radiation by staying out of the sun, using protective clothing, and using sunscreens with high SPF.
2. Regular monitoring and early detection of skin cancers.
3. Chemoprevention with drugs that inhibit DNA replication.
4. Photoprotection with antioxidants and other compounds that protect against UV damage.
5. Managing neurological problems with medications and therapy.

The prognosis for XP is poor, with most patients dying from skin cancer or other complications before the age of 20. However, with early diagnosis and appropriate treatment, some patients may be able to survive into their 30s or 40s. There is currently no cure for XP, but research is ongoing to develop new treatments and improve the quality of life for affected individuals.

There are several types of erythema, including:

1. Erythema migrans (Lyme disease): A rash that occurs due to an infection with the bacteria Borrelia burgdorferi and is characterized by a red, expanding rash with a central clearing.
2. Erythema multiforme: A condition that causes small, flat or raised red lesions on the skin, often triggered by an allergic reaction to medication or infection.
3. Erythema nodosum: A condition that causes small, painful lumps under the skin, usually due to an allergic reaction to medication or infection.
4. Erythema infectiosum (Fifth disease): A viral infection that causes a red rash on the face, arms, and legs.
5. Erythema annulare centrifugum: A condition that causes a ring-shaped rash with raised borders, often seen in people with autoimmune disorders or taking certain medications.

Treatment for erythema depends on the underlying cause, and may include topical creams or ointments, oral medications, or antibiotics. It is important to seek medical attention if you experience any unusual skin changes or symptoms, as some types of erythema can be a sign of a more serious underlying condition.

Without this enzyme, the medications build up in the body and can cause severe side effects, including nausea, vomiting, diarrhea, and a low white blood cell count. In severe cases, DPD deficiency can lead to life-threatening complications, such as sepsis and organ failure.

DPD deficiency is usually diagnosed through a genetic test that measures the presence and function of the dihydropyrimidine dehydrogenase enzyme. Treatment for DPD deficiency typically involves avoiding medications that trigger the condition and using alternative treatments that do not require the presence of the enzyme. In some cases, medications may be given to help reduce the risk of complications.

The exact prevalence of DPD deficiency is not well established, but it is estimated to affect about 1 in 300 people of European ancestry and a higher percentage of people with certain genetic conditions, such as hereditary colon cancer syndromes. The condition is usually diagnosed in adulthood, although it can sometimes be detected in children who have a family history of DPD deficiency.

Overall, dihydropyrimidine dehydrogenase deficiency is a rare genetic disorder that can cause severe side effects from certain medications used to treat cancer and other conditions. It is important for healthcare providers to be aware of this condition and to test for it in individuals who are being prescribed these medications.

Favism is characterized by a sudden and severe anemia, often triggered by exposure to certain foods or medications that contain a chemical called quinine. Quinine is found in the bark of the cinchona tree, which is used to make antimalarial drugs. In individuals with favism, quinine can cause red blood cells to rupture and die prematurely, leading to anemia and other complications.

Symptoms of favism usually begin within 24 hours of exposure to quinine and may include fatigue, jaundice, dark urine, and a low platelet count. In severe cases, favism can lead to life-threatening complications such as kidney failure and cardiac arrest.

Favism is most commonly found in individuals of Mediterranean or African descent, particularly those from Greece, Italy, Turkey, and the Middle East. It is estimated that approximately 10% of these populations carry the G6PD deficiency that causes favism.

There is no cure for favism, but certain medications and dietary changes can help manage symptoms and prevent complications. Individuals with favism are advised to avoid consuming foods or medications containing quinine, and may require regular monitoring of their red blood cell count and other clinical parameters.

In conclusion, favism is a rare genetic disorder that affects the metabolism of hemoglobin and can cause sudden and severe anemia in certain populations. It is important to be aware of this condition and take necessary precautions to prevent complications, particularly when consuming certain foods or medications containing quinine.

Symptoms of hemolytic anemia may include fatigue, weakness, shortness of breath, dizziness, headaches, and pale or yellowish skin. Treatment options depend on the underlying cause but may include blood transfusions, medication to suppress the immune system, antibiotics for infections, and removal of the spleen (splenectomy) in severe cases.

Prevention strategies for hemolytic anemia include avoiding triggers such as certain medications or infections, maintaining good hygiene practices, and seeking early medical attention if symptoms persist or worsen over time.

It is important to note that while hemolytic anemia can be managed with proper treatment, it may not be curable in all cases, and ongoing monitoring and care are necessary to prevent complications and improve quality of life.

Prevalence: Anemia, hemolytic, congenital is a rare disorder, affecting approximately 1 in 100,000 to 1 in 200,000 births.

Causes: The condition is caused by mutations in genes that code for proteins involved in hemoglobin synthesis or red blood cell membrane structure. These mutations can lead to abnormal hemoglobin formation, red blood cell membrane instability, and increased susceptibility to oxidative stress, which can result in hemolytic anemia.

Symptoms: Symptoms of anemia, hemolytic, congenital may include jaundice (yellowing of the skin and eyes), fatigue, weakness, pale skin, and shortness of breath. In severe cases, the condition can lead to life-threatening complications such as anemia, infections, and kidney failure.

Diagnosis: Anemia, hemolytic, congenital is typically diagnosed through a combination of physical examination, medical history, and laboratory tests, including blood smear examination, hemoglobin electrophoresis, and mutation analysis.

Treatment: Treatment for anemia, hemolytic, congenital depends on the specific underlying genetic cause and may include blood transfusions, folic acid supplements, antibiotics, and/or surgery to remove the spleen. In some cases, bone marrow transplantation may be necessary.

Prognosis: The prognosis for anemia, hemolytic, congenital varies depending on the specific underlying genetic cause and the severity of the condition. With appropriate treatment, many individuals with this condition can lead relatively normal lives, but in severe cases, the condition can be life-threatening.

1. Rabies: A deadly viral disease that affects the central nervous system and is transmitted through the saliva of infected animals, usually through bites.
2. Distemper: A highly contagious viral disease that affects dogs, raccoons, and other carnivorous animals, causing symptoms such as seizures, vomiting, and diarrhea.
3. Parvo: A highly contagious viral disease that affects dogs and other animals, causing severe gastrointestinal symptoms and dehydration.
4. Heartworm: A parasitic infection caused by a worm that infects the heart and blood vessels of animals, particularly dogs and cats.
5. Feline immunodeficiency virus (FIV): A viral disease that weakens the immune system of cats, making them more susceptible to other infections and diseases.
6. Avian influenza: A type of flu that affects birds, including chickens and other domesticated fowl, as well as wild birds.
7. Tuberculosis: A bacterial infection that can affect a wide range of animals, including cattle, pigs, and dogs.
8. Leptospirosis: A bacterial infection that can affect a wide range of animals, including dogs, cats, and wildlife, and can cause symptoms such as fever, kidney failure, and death.
9. Lyme disease: A bacterial infection transmitted through the bite of an infected tick, primarily affecting dogs and humans.
10. Fungal infections: Fungal infections can affect a wide range of animals, including dogs, cats, and livestock, and can cause symptoms such as skin lesions, respiratory problems, and death.

Animal diseases can have a significant impact on animal health and welfare, as well as human health and the economy. They can also be transmitted between animals and humans, making it important to monitor and control animal disease outbreaks to prevent their spread.

Vaccination is an effective way to prevent animal diseases in pets and livestock. Regular vaccinations can help protect against common diseases such as distemper, hepatitis, parvovirus, and rabies, among others. Vaccines can be administered orally, through injection, or through a nasal spray.

Preventative care is key in avoiding animal disease outbreaks. Some of the best ways to prevent animal diseases include:

1. Regular vaccinations: Keeping pets and livestock up to date on their vaccinations can help protect against common diseases.
2. Proper sanitation and hygiene: Keeping living areas clean and free of waste can help prevent the spread of disease-causing bacteria and viruses.
3. Avoiding contact with wild animals: Wild animals can carry a wide range of diseases that can be transmitted to domesticated animals, so it's best to avoid contact with them whenever possible.
4. Proper nutrition: Providing pets and livestock with a balanced diet can help keep their immune systems strong and better able to fight off disease.
5. Monitoring for signs of illness: Regularly monitoring pets and livestock for signs of illness, such as fever, vomiting, or diarrhea, can help identify and treat diseases early on.
6. Quarantine and isolation: Isolating animals that are showing signs of illness can help prevent the spread of disease to other animals and humans.
7. Proper disposal of animal waste: Properly disposing of animal waste can help prevent the spread of disease-causing bacteria and viruses.
8. Avoiding overcrowding: Overcrowding can contribute to the spread of disease, so it's important to provide adequate living space for pets and livestock.
9. Regular veterinary care: Regular check-ups with a veterinarian can help identify and treat diseases early on, and also provide guidance on how to prevent animal diseases.
10. Emergency preparedness: Having an emergency plan in place for natural disasters or other unexpected events can help protect pets and livestock from disease outbreaks.

Hemoglobinuria can be caused by a variety of factors, including:

1. Blood disorders such as sickle cell disease, thalassemia, and von Willebrand disease.
2. Inherited genetic disorders such as hemophilia.
3. Autoimmune disorders such as autoimmune hemolytic anemia.
4. Infections such as septicemia or meningococcemia.
5. Toxins such as lead, which can damage red blood cells and cause hemoglobinuria.
6. Certain medications such as antibiotics and nonsteroidal anti-inflammatory drugs (NSAIDs).
7. Kidney disease or failure.
8. Transfusion-related acute lung injury (TRALI), which can occur after blood transfusions.
9. Hemolytic uremic syndrome (HUS), a condition that occurs when red blood cells are damaged and broken down, leading to kidney failure.

The symptoms of hemoglobinuria may include:

1. Red or brown-colored urine
2. Frequent urination
3. Pale or yellowish skin
4. Fatigue
5. Shortness of breath
6. Nausea and vomiting
7. Headache
8. Dizziness or lightheadedness
9. Confusion or loss of consciousness in severe cases.

Diagnosis of hemoglobinuria is typically made through urine testing, such as a urinalysis, which can detect the presence of hemoglobin in the urine. Additional tests may be ordered to determine the underlying cause of hemoglobinuria, such as blood tests, imaging studies, or biopsies.

Treatment of hemoglobinuria depends on the underlying cause and severity of the condition. In some cases, treatment may involve addressing the underlying condition that is causing the hemoglobinuria, such as managing an infection or stopping certain medications. Other treatments may include:

1. Fluid and electrolyte replacement to prevent dehydration and maintain proper fluid balance.
2. Medications to help remove excess iron from the body.
3. Blood transfusions to increase the number of red blood cells in the body and improve oxygen delivery.
4. Dialysis to filter waste products from the blood when the kidneys are unable to do so.
5. Supportive care, such as oxygen therapy and pain management.

In severe cases of hemoglobinuria, complications can include:

1. Kidney damage or failure
2. Septicemia (blood infection)
3. Respiratory failure
4. Heart problems
5. Increased risk of infections and other complications.

Prevention of hemoglobinuria involves managing any underlying medical conditions, such as diabetes or infections, and avoiding certain medications that can cause the condition. It is also important to seek medical attention if symptoms of hemoglobinuria develop, as early treatment can help prevent complications and improve outcomes.

There are several types of skin neoplasms, including:

1. Basal cell carcinoma (BCC): This is the most common type of skin cancer, and it usually appears as a small, fleshy bump or a flat, scaly patch. BCC is highly treatable, but if left untreated, it can grow and invade surrounding tissue.
2. Squamous cell carcinoma (SCC): This type of skin cancer is less common than BCC but more aggressive. It typically appears as a firm, flat, or raised bump on sun-exposed areas. SCC can spread to other parts of the body if left untreated.
3. Melanoma: This is the most serious type of skin cancer, accounting for only 1% of all skin neoplasms but responsible for the majority of skin cancer deaths. Melanoma can appear as a new or changing mole, and it's essential to recognize the ABCDE signs (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving size, shape, or color) to detect it early.
4. Sebaceous gland carcinoma: This rare type of skin cancer originates in the oil-producing glands of the skin and can appear as a firm, painless nodule on the forehead, nose, or other oily areas.
5. Merkel cell carcinoma: This is a rare and aggressive skin cancer that typically appears as a firm, shiny bump on the skin. It's more common in older adults and those with a history of sun exposure.
6. Cutaneous lymphoma: This type of cancer affects the immune system and can appear as a rash, nodules, or tumors on the skin.
7. Kaposi sarcoma: This is a rare type of skin cancer that affects people with weakened immune systems, such as those with HIV/AIDS. It typically appears as a flat, red or purple lesion on the skin.

While skin cancers are generally curable when detected early, it's important to be aware of your skin and notice any changes or unusual spots, especially if you have a history of sun exposure or other risk factors. If you suspect anything suspicious, see a dermatologist for an evaluation and potential biopsy. Remember, prevention is key to avoiding the harmful effects of UV radiation and reducing your risk of developing skin cancer.

Symptoms of argininosuccinic aciduria typically appear during infancy or early childhood and may include seizures, developmental delays, intellectual disability, vision loss, and poor muscle tone. Treatment for this condition involves a strict diet that limits the intake of certain amino acids, as well as medication to manage seizures and other symptoms. In some cases, liver transplantation may be necessary.

Argininosuccinic aciduria is diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment is usually coordinated by a multidisciplinary team of healthcare professionals, including pediatricians, neurologists, metabolism specialists, dietitians, and psychologists. With appropriate treatment and management, many individuals with argininosuccinic aciduria are able to lead active and fulfilling lives.

Overall, argininosuccinic aciduria is a rare and complex genetic disorder that requires careful management and monitoring to prevent complications and improve quality of life for affected individuals.

The term "Sarcoma 180" was coined by a German surgeon named Otto Kunkel in the early 20th century. He described this type of cancer as a highly malignant tumor that grows slowly but is resistant to treatment with surgery, radiation therapy, and chemotherapy.

The exact cause of Sarcoma 180 is not known, but it is believed to be linked to genetic mutations and exposure to certain chemicals or radiation. The disease typically affects middle-aged adults and is more common in men than women.

The symptoms of Sarcoma 180 can vary depending on the location of the tumor, but they may include pain, swelling, redness, and limited mobility in the affected area. If left untreated, the cancer can spread to other parts of the body and be fatal.

Treatment for Sarcoma 180 usually involves a combination of surgery, radiation therapy, and chemotherapy. In some cases, amputation of the affected limb may be necessary. The prognosis for this disease is generally poor, with a five-year survival rate of less than 50%.

In summary, Sarcoma 180 is a rare and aggressive form of cancer that affects connective tissue and has a poor prognosis. It is important for medical professionals to be aware of this condition and its symptoms in order to provide proper diagnosis and treatment.

Although pyrimidine derivatives such as alloxan were known in the early 19th century, a laboratory synthesis of a pyrimidine ... Pyrimidine is also found in meteorites, but scientists still do not know its origin. Pyrimidine also photolytically decomposes ... some minor pyrimidine bases can also occur in nucleic acids. These minor pyrimidines are usually methylated versions of major ... such as pyrimidine, found in meteorites. Pyrimidine, like polycyclic aromatic hydrocarbons (PAHs), the most carbon-rich ...
Pyrimidine+oxygenase at the US National Library of Medicine Medical Subject Headings (MeSH) Portal: Biology (EC 1.14.99). ... Pyrimidine oxygenase (EC 1.14.99.46, RutA) is an enzyme with systematic name uracil,FMNH2:oxygen oxidoreductase (uracil ... Kim KS, Pelton JG, Inwood WB, Andersen U, Kustu S, Wemmer DE (August 2010). "The Rut pathway for pyrimidine degradation: novel ...
... s are antimetabolites which mimic the structure of metabolic pyrimidines. Nucleobase analogues Fluorouracil ... Gemcitabine Nucleotide analogues Pyrimidine Fluorouracil Floxuridine Gemcitabine Pyrimidine antimetabolites are commonly used ... Parker, William B. (2009). "Enzymology of Purine and Pyrimidine Antimetabolites Used in the Treatment of Cancer". Chem Rev. 109 ...
... may refer to: Thymidine phosphorylase Uridine phosphorylase This article includes a list of related ...
... s are the primary cause of melanomas in humans. A cyclobutane pyrimidine dimer (CPD) contains a four membered ... A 6-4 photoproduct (6-4 pyrimidine-pyrimidone or 6-4 pyrimidine-pyrimidinone) is an alternate dimer consisting of a single ... The number of pyrimidine dimers induced per haploid genome at this dose was measured as 27,000. A mutant yeast strain defective ... It is a base excision repair enzyme specific for pyrimidine dimers. It is then able to cut open the AP site. A study by Hanson ...
Pyrimidine biosynthesis occurs both in the body and through organic synthesis. De Novo biosynthesis of a pyrimidine is ... Pyrimidines are ultimately catabolized (degraded) to CO2, H2O, and urea. Cytosine can be broken down to uracil, which can be ... Pyrimidine synthesis inhibitors are used in active moderate to severe rheumatoid arthritis and psoriatic arthritis, as well as ... showed how pyrimidine nucleosides can be synthesized from small molecules and ribose, driven solely by wet-dry cycles. ...
... (EC 3.1.25.1, endodeoxyribonuclease (pyrimidine dimer), bacteriophage T4 ... Deoxyribonuclease+(pyrimidine+dimer) at the US National Library of Medicine Medical Subject Headings (MeSH) Portal: Biology v t ... Mechanism of action of two endonucleases specific for DNA containing pyrimidine dimers". The Journal of Biological Chemistry. ... This enzyme catalyses the following chemical reaction Endonucleolytic cleavage near pyrimidine dimers to products with 5'- ...
... a pyrimidine base + alpha-D-ribose 1-phosphate Thus, the two substrates of this enzyme are pyrimidine nucleoside and phosphate ... In enzymology, a pyrimidine-nucleoside phosphorylase (EC 2.4.2.2) is an enzyme that catalyzes the chemical reaction a ... This enzyme participates in pyrimidine metabolism. As of late 2007, two structures have been solved for this class of enzymes, ... The systematic name of this enzyme class is pyrimidine-nucleoside:phosphate alpha-D-ribosyltransferase. This enzyme is also ...
In enzymology, a pyrimidine-deoxynucleoside 1'-dioxygenase (EC 1.14.11.10) is an enzyme that catalyzes the chemical reaction 2 ...
Other names in common use include pyrimidine nucleotide N-ribosidase, and Pyr5N. This enzyme participates in pyrimidine ... Imada A (1967). "Degradation of pyrimidine nucleotides by enzyme systems of Streptomyces. II. Pyrimidine 5'-nucleotide ... a pyrimidine base Thus, the two substrates of this enzyme are pyrimidine 5'-nucleotide and H2O, whereas its two products are D- ... In enzymology, a pyrimidine-5'-nucleotide nucleosidase (EC 3.2.2.10) is an enzyme that catalyzes the chemical reaction a ...
In enzymology, a pyrimidine-deoxynucleoside 2'-dioxygenase (EC 1.14.11.3) is an enzyme that catalyzes the chemical reaction 2'- ... pyrimidine deoxyribonucleoside 2'-hydroxylase, thymidine 2'-dioxygenase, thymidine 2'-hydroxylase, thymidine 2-oxoglutarate ...
April 1999). "1H-NMR spectroscopy of body fluids: inborn errors of purine and pyrimidine metabolism". Clin. Chem. 45 (4): 539- ... Inborn errors of purine-pyrimidine metabolism are a class of inborn error of metabolism disorders specifically affecting purine ... Inborn errors of purine-pyrimidine metabolism, All stub articles, Endocrine, nutritional and metabolic disease stubs, ... metabolism and pyrimidine metabolism. An example is Lesch-Nyhan syndrome. Urine tests may be of use in identifying some of ...
... is a metabolite in the purine metabolism, formed by the hydrolysis of ... 2,5-diamino-6-hydroxy-4-(5-phosphoribosylamino)pyrimidine is deaminated by Diaminohydroxyphosphoribosylaminopyrimidine ...
Pyrimidines. Part XIII. Electrophilic substitution at position 6 and a synthesis of divicine (2,4-diamino-5,6- ... Bendich, C. (1953). "A revision of the structural formulation of vicine and its pyrimidine aglucone, divicine". Biochim. ...
The complementary nitrogenous bases are divided into two groups, pyrimidines and purines. In DNA, the pyrimidines are thymine ... and the pyrimidines, the six-membered rings C and T. A fifth pyrimidine nucleobase, uracil (U), usually takes the place of ... such as pyrimidine, found in meteorites. Pyrimidine, like polycyclic aromatic hydrocarbons (PAHs), the most carbon-rich ... For example, UV light can damage DNA by producing thymine dimers, which are cross-links between pyrimidine bases. On the other ...
... such as pyrimidine, found in meteorites. Pyrimidine, like polycyclic aromatic hydrocarbons (PAHs), the most carbon-rich ... Uracil is a common and naturally occurring pyrimidine derivative. The name "uracil" was coined in 1885 by the German chemist ... Brown DJ, Evans RF, Cowden WB, Fenn MD (1994). Taylor EC (ed.). The Pyrimidines. Heterocyclic Compounds. Vol. 52. New York, NY ... pyrimidine‐2,4(1H,3H)‐diones against leishmaniasis and tuberculosis: Rationale, in vitro, ex vivo studies and mechanistic ...
Folkers, K.; Harwood, H. J.; Johnson, T. B. (1932). "Researches on Pyrimidines. Cxxx. Synthesis of 2-Keto-1,2,3,4- ... Folkers, K.; Johnson, T. B. (1933). "Researches on Pyrimidines. CXXXVI. The Mechanism of Formation of Tetrahydropyrimidines by ...
... purines and pyrimidines; and kerogen-type material. The organic inventories of primitive meteorites display large and variable ...
Urea gives pyrimidines. Condensation with two aryl- and alkylamines to gives NacNacs, wherein the oxygen atoms in acetylacetone ...
"Purines and pyrimidines". Retrieved 2008-03-27. {{cite journal}}: Cite journal requires ,journal= (help) Guanine was first ... With the formula C5H5N5O, guanine is a derivative of purine, consisting of a fused pyrimidine-imidazole ring system with ...
In 1918, he received the Nichols Medal of the American Chemical Society in recognition of his work on pyrimidines. and in 1919 ... Johnson, Treat B.; Coghill, Robert D. (1925). "Researches on Pyrimidines. C111. The Discovery of 5-Methyl-Cytosine in ... Johnson, Treat B.; Hahn, Dorothy A. (1933). "Pyrimidines: Their Amino and Aminoöxy Derivatives". Chemical Reviews. 13 (2): 193- ... Johnson, Treat B. (1918). "The Development of Pyrimidine Chemistry-Medal Address". Journal of Industrial & Engineering ...
Pyrimidine biosynthesis Cooper C, Wilson DW (1954). "Biosynthesis of pyrimidines". Fed. Proc. 13: 194. Lieberman I, Kornberg A ... April 1954). "Enzymatic synthesis and breakdown of a pyrimidine, orotic acid. I. Dihydroortic acid, ureidosuccinic acid, and 5- ... 5-dihydroorotic acid in the biosynthesis of pyrimidines. It forms a multifunctional enzyme with carbamoyl phosphate synthetase ...
Campbell LL (August 1957). "Reductive degradation of pyrimidines. III. Purification and properties of dihydrouracil ... pyrimidine reductase, thymine reductase, uracil reductase, and dihydrouracil dehydrogenase (NAD+). This enzyme participates in ... 3 metabolic pathways: pyrimidine metabolism, beta-alanine metabolism, and pantothenate and coa biosynthesis. ...
CAMPBELL LL (1960). "Reductive degradation of pyrimidines. 5. Enzymatic conversion of N-carbamyl-beta-alanine to beta-alanine, ... Traut TW, Loechel S (1984). "Pyrimidine catabolism: individual characterization of the three sequential enzymes with a new ... This enzyme participates in 3 metabolic pathways: pyrimidine metabolism, beta-alanine metabolism, and pantothenate and coenzyme ...
Sprague JM, Kissinger LW, Lincoln RM (1941). "Sulfonamido Derivatives of Pyrimidines". Journal of the American Chemical Society ... Pyrimidines, All stub articles, Antibiotic stubs, Dermatologic drug stubs). ...
Disruption of purine and pyrimidine production may impair energy storage and transport in cells. Impairment of these processes ... Kelley, Roger E.; Andersson, Hans C. (2014-01-01). Disorders of purines and pyrimidines. Handbook of Clinical Neurology. Vol. ... This enzyme is involved in producing purines and pyrimidines which are the building blocks of DNA, RNA, ATP and other molecules ...
Adenine and guanine are purines, while thymine, cytosine and uracil are pyrimidines. Purines are larger than pyrimidines. Both ... any pyrimidine) and M (amino) to K (keto). W (weak) and S (strong) are usually not swapped but have been swapped in the past by ...
Ralevic V, Burnstock G (Nov 1998). "Receptors for purines and pyrimidines". Pharmacol Rev. 50 (3): 413-92. PMID 9755289. ...
... a pyrimidine nucleotide, is an inhibitor of pyrimidine synthesis. This regulation helps to keep the purine/pyrimidine amounts ... Pyrimidine nucleosides include cytidine, uridine, and thymidine. The synthesis of any pyrimidine nucleotide begins with the ... Pyrimidine bases can also be salvaged. For example, the uracil base can be combined with ribose-1-phosphate to create uridine ... Purine and pyrimidine nucleosides can either be degraded to waste products and excreted or can be salvaged as nucleotide ...
Ralevic V, Burnstock G (September 1998). "Receptors for purines and pyrimidines". Pharmacological Reviews. 50 (3): 413-92. PMID ...
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A series of 4-(2,5-dichlorophenoxy)pyrimidine and cyclopropylmalonamide derivatives were synthesized as potent agonists of TGR5 ... Discovery of novel pyrimidine and malonamide derivatives as TGR5 agonists Bioorg Med Chem Lett. 2014 Sep 1;24(17):4271-5. doi: ... A series of 4-(2,5-dichlorophenoxy)pyrimidine and cyclopropylmalonamide derivatives were synthesized as potent agonists of TGR5 ...
... Sulfonyl Chlorides. Thiophenes, Benzothiophenes, and Thiophenols. (Trifluoromethyl) Pyridines. New Additions. ... 6-(2-Hydroxy-ethyl)-3-methyl-5-oxo-5,8-dihydro-[1,2,4]triazolo[4,3-a]pyrimidine-7-carboxylic acid. Catalog Number: 034176 ... 7-(1-Ethyl-3-methyl-1H-pyrazol-4-yl)-pyrazolo[1,5-a]pyrimidine-2-carboxylic acid. Catalog Number: 033988 ... 7-tert-Butyl-2-methyl-[1,2,4]triazolo[1,5-a]-pyrimidine-5-carboxylic acid. Catalog Number: 034088 ...
... pyrimidine , C12H11BrN2 , CID 26369947 - structure, chemical names, physical and chemical properties, classification, patents, ...
In this study, syntheses of new pyrimidine-coupled N-ß-glucosides and tetra-O-acetyl derivatives were carried out. All ... In this study, syntheses of new pyrimidine-coupled N-ß-glucosides and tetra-O-acetyl derivatives were carried out. All ... New pyrimidine-N-ß-D-glucosides: synthesis, biological evaluation, and molecular docking investigations ... 2, 4, 6-trisubstituted pyrimidine, N-ß-D-glucosides, biological activity, molecular docking ...
[147972-27-8], MFCD09834966, 4-Chloro-2-(trifluoromethyl)thieno[3,2-d]pyrimidine
7-Chloro-2,5-dimethyl-3-thiophen-2-ylpyrazolo[1,5-a]pyrimidine. Supplier: Matrix Scientific ...
Get Methyl 5,7-Dichloropyrazolo[1,5-a]Pyrimidine-3-Carboxylate molecular formula, CAS number, boiling point, melting point, ... Pyrazolo[1,5-a]Pyrimidine-3-Carboxylic Acid, 5,7-Dichloro-, Methyl Ester. ...
Pyrimidines may be absorbed or converted to pyrimidine nucleotides by pathways described.... A diet that may be rich in ... the pyrimidine bases 14: purine nucleotide came different... Acid bases pyrimidines purines 4 Sugars semi-essential for newborn ... 3 Nucleic Acid Bases Pyrimidines Purines 4 Sugars. The catabolism of pyrimidine nucleotides, like that of purine nucleotides, ... Is biosynthesis of purine and pyrimidine nucleotides slideshare to PRPP as positive modulators, while pyrimidine nucleotides ...
Details of Molecule 5-methoxyfuroxano[3,4-d]pyrimidine. For reactivities of structurally related compounds go to: Electrophiles ...
pyrimidine deoxyribonucleoside monophosphate biosynthetic process. GO:0009178. pyrimidine deoxyribonucleoside monophosphate ... pyrimidine deoxyribonucleoside monophosphate metabolic process. id: GO:0009176. name: pyrimidine deoxyribonucleoside ... Description: The chemical reactions and pathways involving pyrimidine deoxynucleoside monophosphate, a compound consisting of a ... pyrimidine base linked to a deoxyribose sugar esterified with phosphate on the sugar. ...
This page titled 5.14B: Purine and Pyrimidine Synthesis is shared under a CC BY-SA 4.0 license and was authored, remixed, and/ ... Pyrimidine_Synthesis : property get [Map MindTouch.Deki.Logic.ExtensionProcessorQueryProvider+,,c__DisplayClass228_0., ...
Antiproliferative activities of halogenated pyrrolo[3,2-d]pyrimidines. Kartik W. Temburnikar, Christina R. Ross, Gerald M. ... Upon screening of a series of pyrrolo[3,2-d]pyrimidines, the 2,4-Cl compound 1 was found to exhibit antiproliferative activity ... Upon screening of a series of pyrrolo[3,2-d]pyrimidines, the 2,4-Cl compound 1 was found to exhibit antiproliferative activity ... Upon screening of a series of pyrrolo[3,2-d]pyrimidines, the 2,4-Cl compound 1 was found to exhibit antiproliferative activity ...
Purine Bases, Pyrimidine Bases and Nucleosides (1) (DE-613). Purine bases, pyrimidine bases and nucleosides were analyzed using ... Purine Bases, Pyrimidine Bases and Nucleosides (2) (NN-814) Six components were separated using RSpak NN-814 with pH3.0 … ... Purine Bases and Pyrimidine Bases (3) (DE-613) Six components were completely separated using RSpak DE-613 (a … ...
Pyrimidine homeostasis is accomplished by directed overflow metabolism.. Title. Pyrimidine homeostasis is accomplished by ... Disruption of the directed overflow regulatory mechanism impairs growth in pyrimidine-rich environments. Thus, pyrimidine ... In a canonical example, the first committed enzyme in the pyrimidine pathway in Escherichia coli is allosterically inhibited by ... Here we identify an alternative regulatory strategy that enables precise control of pyrimidine pathway end-product levels, even ...
Product Spec: 4-Chloro-7H-pyrrolo[2,3-d]pyrimidine-5-carbaldehyde ...
You are here: Home1 / Small Molecules2 / 4-(1H-1,2,3,4-Tetrazol-5-yl)pyrimidine ...
Computational Estimation of the Acidities of Pyrimidines and Related Compounds. Joel Michalski Jan 7, 2022. ... This article highlights the use of ACD/pKa to obtain computed pKa values for the pyrimidines and related heterocycles in this ...
Immunosuppression after solid organ transplantation is complex. Over the past 50 years, the medical community has witnessed great advances in the care of patients receiving organ transplants.
In the present work, we report the synthesis of 1,4-disubstituted 1,2,3-triazoles and 1,2,4-triazolo[1, 5-a]pyrimidine ... Synthesis, characterization and cytotoxicity studies of 1,2,3-triazoles and 1,2,4-triazolo 1,5-a pyrimidines in human breast ... 5-a pyrimidines in human breast cancer cells. Bioorganic and Medicinal Chemistry Letters, 28 (13). pp. 2314-2319. ...
Mapping adenines, guanines, and pyrimidines in RNA.. Nucleic Acids Res. 1977; 4: 2527-2538 ...
Immunosuppression after solid organ transplantation is complex. Over the past 50 years, the medical community has witnessed great advances in the care of patients receiving organ transplants.
In this study, a series of nitric oxide (NO) -releasing 5-cyano-6-phenyl-2, 4-disubstituted pyrimidine derivatives were ... Design, synthesis and biological evaluation of nitric oxide-releasing 5-cyano-6-phenyl-2, 4-disubstituted pyrimidine ...
Adrucil - Get up-to-date information on Adrucil side effects, uses, dosage, overdose, pregnancy, alcohol and more. Learn more about Adrucil
Ronoxidil is a brand name medication included in a group of medications called Pyrimidine derivatives. For more information ...
Disorder of purine and pyrimidine metabolism, unspecified. E87.6. Hypokalemia. E87.6P. Prevent hypokalemia. ...
  • A series of 4-(2,5-dichlorophenoxy)pyrimidine and cyclopropylmalonamide derivatives were synthesized as potent agonists of TGR5 based on a bioisosteric replacement strategy. (nih.gov)
  • In this study, syntheses of new pyrimidine-coupled N-ß-glucosides and tetra-O-acetyl derivatives were carried out. (tubitak.gov.tr)
  • Humans synthesize the nucleic acids and their derivatives ATP, NAD +, coenzyme A, etc, from amphibolic intermediates.However, injected purine or pyrimidine analogs, including potential anticancer drugs, may nevertheless be incorporated into DNA. (myinfo.la)
  • In the present work, we report the synthesis of 1,4-disubstituted 1,2,3-triazoles and 1,2,4-triazolo[1, 5-a]pyrimidine derivatives via copper (I)-catalyzed azide-alkyne cycloaddition (CuAAC) reaction and screened for their anticancer activity against MCF7 cells. (uni-mysore.ac.in)
  • Ronoxidil is a brand name medication included in a group of medications called Pyrimidine derivatives . (rxwiki.com)
  • Design, synthesis and biological evaluation of nitric oxide-releasing 5-cyano-6-phenyl-2, 4-disubstituted pyrimidine derivatives. (bvsalud.org)
  • In this study, a series of nitric oxide (NO) -releasing 5-cyano-6-phenyl-2, 4-disubstituted pyrimidine derivatives were designed and synthesized. (bvsalud.org)
  • There are two major synthetic pathways, for purine and pyrimidine bases, respectively, both of which diverge towards their ends to produce the different variants. (myinfo.la)
  • No article was found for Purine-Pyrimidine Metabolism, Inborn Errors and UMOD[original query] . (cdc.gov)
  • The biosynthesis of pyrimidines is simpler than that of purines. (myinfo.la)
  • Pyrimidine homeostasis is accomplished by directed overflow metabolism. (princeton.edu)
  • Thus, pyrimidine homeostasis involves dual regulatory strategies, with classical feedback inhibition enhancing metabolic efficiency and directed overflow metabolism ensuring end-product homeostasis. (princeton.edu)
  • Detoxification is also mediated by CYP450s, forming a pyridinol (TCP) and a pyrimidine (IMHP), respectively. (cdc.gov)
  • 3 Nucleic Acid Bases Pyrimidines Purines 4 Sugars. (myinfo.la)
  • To uracil through multiple steps involving different enzymes ( purines and pyrimidines are converted back into triphosphate! (myinfo.la)
  • Plants possess metabolic pathways for the de novo synthesis of purine nucleotides generating AMP, as well as pyrimidine nucleotides yielding UMP. (myinfo.la)
  • The chemical reactions and pathways involving pyrimidine deoxynucleoside monophosphate, a compound consisting of a pyrimidine base linked to a deoxyribose sugar esterified with phosphate on the sugar. (systemsbiology.net)
  • In vitro evaluation of the halogenated pyrrolo[3,2-d]pyrimidines identified antiproliferative activities in compounds 1 and 2 against four different cancer cell lines. (johnshopkins.edu)
  • UMP, which is also the precursor of CMP, is synthesized in a six-reaction pathway However, in contrast to purine catabolism, the pyrimidine bases in most organisms are subjected to reduction rather than oxidation. (myinfo.la)
  • Welco Free pyrimidine bases without sugar residues cannot be recovered. (myinfo.la)
  • Upon screening of a series of pyrrolo[3,2-d]pyrimidines, the 2,4-Cl compound 1 was found to exhibit antiproliferative activity at low micromolar concentrations. (johnshopkins.edu)
  • New pyrimidine-N-ß-D-glucosides: synthesis, biological evaluation, and" by NURAN KAHRİMAN, KIVANÇ PEKER et al. (tubitak.gov.tr)
  • The pyrimidine analogues, used as antineoplastic agents, are a diverse group of agents with similar structures but somewhat different mechanisms of action, activities and spectra of activity. (nih.gov)
  • All of the pyrimidine analogues have some degree of direct hepatotoxic potential. (nih.gov)
  • Two pyrimidine analogues have been linked to unique forms of liver injury. (nih.gov)
  • Review Intracellular Pharmacokinetics of Pyrimidine Analogues used in Oncology and the Correlation with Drug Action. (nih.gov)
  • Fluorouracil is a fluorinated pyrimidine analog used in topical form to treat actinic keratoses. (medscape.com)
  • Identification of 2-Sulfonyl/Sulfonamide Pyrimidines as Covalent Inhibitors of WRN Using a Multiplexed High-Throughput Screening Assay. (bvsalud.org)
  • This screening campaign led to the discovery of 2-sulfonyl/ sulfonamide pyrimidine derivatives as novel covalent inhibitors of WRN helicase activity. (bvsalud.org)

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