Uracil is a nitrogenous base found in RNA that is not present in DNA.
An enzyme that catalyzes the HYDROLYSIS of the N-glycosidic bond between sugar phosphate backbone and URACIL residue during DNA synthesis.
Uracil nucleotides are nitrogenous bases that are components of RNA molecules, playing a crucial role in various cellular processes.
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.
A class of enzymes involved in the hydrolysis of the N-glycosidic bond of nitrogen-linked sugars.
Proteins involved in the transport of NUCLEOTIDES across cellular membranes.
Uracil nucleotides which contain deoxyribose as the sugar moiety.
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.
Thymine is a nitrogenous base found in DNA and RNA that pairs with adenine during DNA replication and transcription.
Enzymes of the transferase class that catalyze the transfer of a pentose group from one compound to another.
Nitrogen mustard derivative of URACIL. It is a alkylating antineoplastic agent that is used in lymphatic malignancies, and causes mainly gastrointestinal and bone marrow damage.
5'-Uridylic acid. A uracil nucleotide containing one phosphate group esterified to the sugar moiety in the 2', 3' or 5' position.
A pyrimidine base that is a fundamental unit of nucleic acids.
The removal of an amino group (NH2) from a chemical compound.
An enzyme that catalyzes the transfer of ribose from uridine to orthophosphate, forming uracil and ribose 1-phosphate.
An oxidoreductase involved in pyrimidine base degradation. It catalyzes the catabolism of THYMINE; URACIL and the chemotherapeutic drug, 5-FLUOROURACIL.
Congener of FLUOROURACIL with comparable antineoplastic action. It has been suggested especially for the treatment of breast neoplasms.
A pyrimidine nucleoside formed in the body by the deamination of CYTARABINE.
Uridine is a nucleoside that plays a role in RNA synthesis and metabolism.
Occurs in seeds of Brassica and Crucifera species. Thiouracil has been used as antithyroid, coronary vasodilator, and in congestive heart failure although its use has been largely supplanted by other drugs. It is known to cause blood dyscrasias and suspected of terato- and carcinogenesis.
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 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.
An enzyme that removes THYMINE and URACIL bases mispaired with GUANINE through hydrolysis of their N-glycosidic bond. These mispaired nucleotides generally occur through the hydrolytic DEAMINATION of 5-METHYLCYTOSINE to thymine.
Pyrimidines with a RIBOSE attached that can be phosphorylated to PYRIMIDINE NUCLEOTIDES.
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.
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.
Orotic acid is a metabolic intermediate involved in the biosynthesis of nucleotides and is important for DNA and RNA synthesis.
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.
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 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).
Inorganic salts of sulfurous acid.
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.
A group of enzymes within the class EC 3.6.1.- that catalyze the hydrolysis of diphosphate bonds, chiefly in nucleoside di- and triphosphates. They may liberate either a mono- or diphosphate. EC 3.6.1.-.
An enzyme that catalyzes the deamination of cytidine, forming uridine. EC 3.5.4.5.
A nutritional condition produced by a deficiency of FOLIC ACID in the diet. Many plant and animal tissues contain folic acid, abundant in green leafy vegetables, yeast, liver, and mushrooms but destroyed by long-term cooking. Alcohol interferes with its intermediate metabolism and absorption. Folic acid deficiency may develop in long-term anticonvulsant therapy or with use of oral contraceptives. This deficiency causes anemia, macrocytic anemia, and megaloblastic anemia. It is indistinguishable from vitamin B 12 deficiency in peripheral blood and bone marrow findings, but the neurologic lesions seen in B 12 deficiency do not occur. (Merck Manual, 16th ed)
5-Hydroxymethyl-6-methyl- 2,4-(1H,3H)-pyrimidinedione. Uracil derivative used in combination with toxic antibiotics to lessen their toxicity; also to stimulate leukopoiesis and immunity. Synonyms: pentoksil; hydroxymethylmethyluracil.
A purine base and a fundamental unit of ADENINE NUCLEOTIDES.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Inhibitor of DNA replication in gram-positive bacteria.
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.

Base excision repair of oxidative DNA damage activated by XPG protein. (1/1786)

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)

Synthesis of bacteriophage phi6 double-stranded ribonucleic acid. (2/1786)

Uracil was incorporated into all three bacteriophage phi6 dsRNA segments throughout the infection cycle; the rates of incorporation into each of the three segments were approx. constant for the first 15 to 20 min and then increased rapidly until 50 min after infection. The medium and small dsRNA segments were produced in greater amounts than the large dsRNA segment at all times in the infection cycle. Inhibition of host RNA and protein synthesis with rifampin and chloramphenicol revealed that virus dsRNA synthesis immediately after infection was independent of either host function.  (+info)

Phase I study of eniluracil, a dihydropyrimidine dehydrogenase inactivator, and oral 5-fluorouracil with radiation therapy in patients with recurrent or advanced head and neck cancer. (3/1786)

5-Fluorouracil (5-FU) is an effective enhancer of radiation therapy (RT) in head and neck cancers. Due to rapid, predominantly hepatic metabolism by dihydropyrimidine dehydrogenase (DPD) and suggested clinical benefit from prolonged drug exposure, 5-FU is commonly given by continuous infusion. Eniluracil is a novel DPD-inactivator designed to prolong the half-life of 5-FU and provide sustained plasma concentrations of 5-FU with oral dosing. We conducted a Phase I study of the safety and efficacy of eniluracil given with oral 5-FU in patients receiving concurrent RT for recurrent or advanced squamous cell carcinomas of the head and neck. Thirteen patients with recurrent, metastatic, or high-risk (defined as an expected 2-year survival rate of <10%) head and neck cancer were enrolled and treated with concomitant chemoradiotherapy on an every-other-week schedule. Eniluracil at a fixed dose [20 mg twice a day (BID)] was given for 7 consecutive days (days 1-7). 5-FU and RT were given on 5 consecutive days (days 2-6). One patient was treated with once-daily RT (2.0 Gy fractions). The remaining patients received hyperfractionated RT (1.5-Gy fractions BID). The initial dose of 5-FU was 2.5 mg/m2 given BID. Dose escalation in patient cohorts was scheduled at 2.5-mg/m2 increments, with intrapatient dose escalation permitted. Lymphocyte DPD activity and serum 5-FU and uracil concentrations were monitored during two cycles. DPD activity was completely or nearly completely inactivated in all patients. Sustained, presumed therapeutic concentrations of 5-FU were observed at a dose of 5.0 mg/m2 given BID. Cumulative dose-limiting myelosuppression (both neutropenia and thrombocytopenia) was observed during the fourth and fifth cycles following administration of 5.0 mg/m2 5-FU BID. One patient died of neutropenic sepsis during cycle 4. Other late cycle toxicities included diarrhea, fatigue, and mucositis. Grade 3 mucositis was observed in 4 patients, but no grade 4 mucositis or grade 3 or 4 dermatitis was observed. A second patient death occurred during cycle 1 of treatment. No specific cause of death was identified. The study was subsequently discontinued. Cumulative myelosupression was the significant dose-limiting toxicity of oral 5-FU given with the DPD-inactivator eniluracil on an every-other-week schedule. Clinical radiation sensitization was not observed, based on the absence of dose-limiting mucositis and dermatitis. Alternative dosing schedules need to be examined to determine the most appropriate use of eniluracil and 5-FU as radiation enhancers.  (+info)

Base pairing of anhydrohexitol nucleosides with 2,6-diaminopurine, 5-methylcytosine and uracil asbase moiety. (4/1786)

Hexitol nucleic acids (HNAs) with modified bases (5-methylcytosine, 2,6-diaminopurine or uracil) were synthesized. The introduction of the 5-methylcytosine base demonstrates that N -benzoylated 5-methylcytosyl-hexitol occurs as the imino tautomer. The base pairing systems (G:CMe, U:D, T:D and U:A) obey Watson-Crick rules. Substituting hT for hU, hCMefor hC and hD for hA generally leads to increased duplex stability. In a single case, replacement of hC by hCMedid not result in duplex stabilization. This sequence-specific effect could be explained by the geometry of the model duplex used for carrying out the thermal stability study. Generally, polypurine HNA sequences give more stable duplexes with their RNA complement than polypyrimidine HNA sequences. This observation supports the hypothesis that, besides changes in stacking pattern, the difference in conformational stress between purine and pyrimidine nucleosides may contribute to duplex stability. Introduction of hCMeand hD in HNA sequences further increases the potential of HNA to function as a steric blocking agent.  (+info)

Smoothing of the thermal stability of DNA duplexes by using modified nucleosides and chaotropic agents. (5/1786)

The effect of alkyltrimethylammonium ions on the thermostability of natural and modified DNA duplexes has been investigated. We have shown that the use of tetramethylammonium ions TMA+along with the chemical modification of duplexes allow the fine adjustment of T m and the possibility of obtaining several duplex systems with varied isostabilizedtemperatures, some of which show greater stability than those of natural DNA. This approach could be very useful for DNA sequencing by hybridization.  (+info)

Five caffeine metabolite ratios to measure tobacco-induced CYP1A2 activity and their relationships with urinary mutagenicity and urine flow. (6/1786)

To choose a sensitive protocol to discriminate populations exposed and not exposed to inducers, five urinary metabolite ratios (MRs) [MR1 (17X + 17U)/137X, MR2 (5-acetylamino-6-formylamino-3-methyluracil [AFMU] + 1X + 1U)/17U, MR3 (17X/137X), MR4 (AFMU + 1X + 1U + 17X + 17U)/137X, and MR5 (AFMU + 1X + 1U)/17X] were calculated in 4-5 h and 0-24 h urine samples after caffeine intake. One hundred twenty-five healthy volunteers (59 nonsmokers and 66 smokers) were included in the study. All ratios showed a log-normal distribution. MR2 in the two time intervals was the only ratio nondependent on the urine flow. Differences between nonsmokers and smokers could be detected with all ratios at 4-5 h. However, only MR2 and, to a lesser extent, MR5 allowed the discrimination of higher cytochrome P450 1A2 (CYP1A2) activity in smokers in the 0-24 h sample. Although smokers had increased urinary mutagenicity in relation to nonsmokers, a significant association between MRs and urine mutagenicity was observed only with MR2 in the 4-5 h interval; this ratio/time schedule being that of higher association with tobacco consumption. The most flow-dependent ratios, MR1, MR3, and MR4, were closely correlated with each other at the two intervals. The flow dependency profile of each ratio may explain their different power to indicate both tobacco exposure and tobacco-derived mutagenicity. In conclusion, MR2 in the period of 4-5 h after caffeine intake seems preferable, especially at high urine flow rates.  (+info)

Uracil-induced down-regulation of the yeast uracil permease. (7/1786)

In Saccharomyces cerevisiae the FUR4-encoded uracil permease catalyzes the first step of the pyrimidine salvage pathway. The availability of uracil has a negative regulatory effect upon its own transport. Uracil causes a decrease in the level of uracil permease, partly by decreasing the FUR4 mRNA level in a promoter-independent fashion, probably by increasing its instability. Uracil entry also triggers more rapid degradation of the existing permease by promoting high efficiency of ubiquitination of the permease that signals its internalization. A direct binding of intracellular uracil to the permease is possibly involved in this feedback regulation, as the behavior of the permease is similar in mutant cells unable to convert intracellular uracil into UMP. We used cells impaired in the ubiquitination step to show that the addition of uracil produces rapid inhibition of uracil transport. This may be the first response prior to the removal of the permease from the plasma membrane. Similar down-regulation of uracil uptake, involving several processes, was observed under adverse conditions mainly corresponding to a decrease in the cellular content of ribosomes. These results suggest that uracil of exogenous or catabolic origin down-regulates the cognate permease to prevent buildup of excess intracellular uracil-derived nucleotides.  (+info)

Only one of the charged amino acids located in membrane-spanning regions is important for the function of the Saccharomyces cerevisiae uracil permease. (8/1786)

The transport of uracil into the yeast Saccharomyces cerevisiae is mediated by uracil permease, a specific co-transporter encoded by the FUR4 gene. Uracil permease is a multispan membrane protein that is delivered to the plasma membrane via the secretory pathway. Experimental results led to the proposal of a two-dimensional model of the protein's topology. According to this model, the membrane domain of Fur4p contains three charged amino acid residues (Glu-243, Lys-272 and Glu-539) that are conserved in the members of the FUR family of yeast transporters. We have previously shown that a mis-sense mutation leading to the replacement of Lys-272 by Glu severely impairs the function of uracil permease. In the present paper, the role of the three charged residues present in the membrane-spanning regions of Fur4p was further investigated by using site-directed mutagenesis. The variant permeases were correctly targeted to the plasma membrane and their stabilities were similar to that of the wild-type permease. The effect of the mutations was studied by measuring the uptake constants for uracil on whole cells and equilibrium binding parameters on plasma membrane-enriched fractions. We found no evidence for ionic interaction between either of the glutamic residues in transmembrane segments 3 and 9 and the lysine residue in transmembrane segment 4. Of the three charged residues, only Lys-272 was important for the transport activity of the transporter. Its replacement by Ala, Glu or even Arg strongly impaired both the binding and the translocation of uracil.  (+info)

Uracil is a nitrogenous base that is found in RNA, but not in DNA. It is one of the four nitrogenous bases that make up the RNA molecule, along with adenine, guanine, and cytosine. Uracil is a pyrimidine base, which means that it has a six-membered ring structure with two nitrogen atoms and two carbon atoms. It is important for the function of RNA because it is involved in the process of transcription, in which the genetic information in DNA is copied into RNA. In addition, uracil is also involved in the process of translation, in which the information in RNA is used to synthesize proteins.

Uracil-DNA glycosidase (UDG) is an enzyme that plays a crucial role in maintaining the integrity of DNA. It is responsible for removing uracil, a pyrimidine base that is not normally present in DNA, from the DNA molecule. Uracil is a byproduct of DNA replication and can accumulate in DNA if not properly removed. UDG is a type of glycosylase enzyme that recognizes and binds to uracil in DNA. Once bound, it cleaves the sugar-phosphate backbone of the DNA molecule, releasing the uracil and leaving behind an apurinic/apyrimidinic (AP) site. This AP site can then be repaired by other enzymes in the cell, such as AP endonuclease and DNA polymerase, to restore the integrity of the DNA molecule. In the medical field, UDG is of particular interest because it is involved in the repair of DNA damage caused by mutagens and carcinogens. Mutagens are substances that can cause changes in DNA, leading to mutations that can contribute to the development of cancer. Carcinogens are substances that can cause cancer by damaging DNA. UDG is thought to play a role in protecting against the harmful effects of these substances by removing uracil from DNA before it can cause mutations. UDG is also used as a tool in molecular biology research. It is often used in techniques such as uracil-specific excision reagent (USER) PCR, which is a method for introducing a specific sequence of DNA into a sample. In this technique, UDG is used to remove uracil from a DNA template, creating an AP site that can be filled in by DNA polymerase with a complementary DNA sequence.

Uracil nucleotides are a type of nucleotide that contains the nitrogenous base uracil. They are one of the four types of nitrogenous bases found in RNA (ribonucleic acid), along with adenine, guanine, and cytosine. In RNA, uracil is paired with adenine through hydrogen bonding, similar to the way that thymine is paired with adenine in DNA (deoxyribonucleic acid). Uracil nucleotides play important roles in various biological processes, including transcription, translation, and regulation of gene expression. They are also involved in the metabolism of nucleic acids and the repair of DNA damage. In the medical field, uracil nucleotides are used as components of various drugs and therapies. For example, they are used in the treatment of certain types of cancer, such as bladder cancer, by inhibiting the growth and proliferation of cancer cells. They are also used in the treatment of viral infections, such as hepatitis B and C, by inhibiting the replication of the virus.

DNA glycosylases are a class of enzymes that play a crucial role in the repair of damaged DNA. These enzymes recognize and remove damaged or inappropriate nucleotides from the DNA strand, creating an abasic site (also known as an AP site) that can be further processed by other DNA repair enzymes. There are several types of DNA glycosylases, each with a specific substrate specificity. For example, some DNA glycosylases recognize and remove damaged bases such as thymine glycol, 8-oxoguanine, and uracil, while others recognize and remove bulky adducts such as benzo[a]pyrene diol epoxide. DNA glycosylases are important for maintaining the integrity of the genome and preventing mutations that can lead to cancer and other diseases. Mutations in DNA glycosylase genes have been linked to an increased risk of certain types of cancer, such as colon cancer and lung cancer.

N-Glycosyl Hydrolases (NGHs) are a group of enzymes that hydrolyze (break down) the glycosidic bonds in complex carbohydrates, also known as glycans. These enzymes play important roles in various biological processes, including cell signaling, protein folding, and immune response. In the medical field, NGHs are of particular interest due to their involvement in diseases such as cancer, diabetes, and infectious diseases. For example, some NGHs are overexpressed in cancer cells, leading to increased cell proliferation and invasion. In diabetes, NGHs are involved in the breakdown of glycans in the body, which can lead to hyperglycemia (high blood sugar levels). In infectious diseases, NGHs are produced by pathogens to evade the host immune system. NGHs are also being studied as potential therapeutic targets for various diseases. For example, inhibitors of NGHs have been developed as potential treatments for cancer and diabetes. Additionally, NGHs are being investigated as potential biomarkers for disease diagnosis and prognosis.

Nucleotide transport proteins are a group of proteins that are responsible for the transport of nucleotides across cell membranes. These proteins play a crucial role in the metabolism of nucleotides, which are the building blocks of DNA and RNA. There are several types of nucleotide transport proteins, including concentrative nucleoside transporters (CNTs), equilibrative nucleoside transporters (ENTs), and nucleotide-specific transporters (NSTs). These proteins are found in various tissues and cells throughout the body, and they are involved in a wide range of physiological processes, including energy metabolism, immune function, and neurotransmission. Mutations in nucleotide transport proteins can lead to a variety of diseases, including inherited disorders of metabolism and cancer.

Deoxyuracil nucleotides are a type of nucleotide that contains the nitrogenous base deoxyuracil (dU) instead of thymine (T). They are found in DNA and RNA, and are involved in various biological processes such as DNA replication, repair, and transcription. Deoxyuracil nucleotides are important for maintaining the integrity of the genetic material and ensuring proper cell function. In the medical field, deoxyuracil nucleotides are used as components of antiviral and anticancer drugs, as well as in the treatment of certain genetic disorders.

Bromouracil is a medication that is used to treat certain types of cancer, including leukemia and lymphoma. It works by interfering with the production of DNA and RNA, which are essential for the growth and reproduction of cancer cells. Bromouracil is usually given as a pill or a liquid, and it is usually taken in combination with other medications. It can cause side effects such as nausea, vomiting, and a decrease in the number of white blood cells.

Thymine is a nitrogenous base that is one of the four nucleobases found in DNA and RNA. It is a pyrimidine base, meaning it has a six-membered ring structure with two nitrogen atoms and four carbon atoms. Thymine is essential for the proper functioning of DNA and RNA, as it is involved in the storage and transmission of genetic information. In the medical field, thymine is often studied in the context of DNA replication and repair, as well as in the development of antiviral and anticancer drugs.

Pentosyltransferases are a group of enzymes that transfer a pentose sugar moiety from one molecule to another. In the medical field, pentosyltransferases are important in the metabolism of carbohydrates, nucleic acids, and other biomolecules. They play a role in the synthesis of various compounds, including nucleotides, glycosaminoglycans, and other complex carbohydrates. Pentosyltransferases are also involved in the breakdown of certain molecules, such as heparan sulfate and dermatan sulfate. Mutations in genes encoding pentosyltransferases can lead to various diseases, including mucopolysaccharidoses and other lysosomal storage disorders.

Uracil mustard is a type of chemotherapy drug that is used to treat certain types of cancer, including leukemia and lymphoma. It works by damaging the DNA of cancer cells, which can cause them to die or stop dividing. Uracil mustard is usually given intravenously, and it can cause side effects such as nausea, vomiting, hair loss, and a low white blood cell count. It is important to note that uracil mustard is not a cure for cancer, but it can help to slow the growth of cancer cells and improve a person's quality of life.

Uridine Monophosphate (UMP) is a nucleotide that plays a crucial role in various biological processes, including DNA and RNA synthesis, energy metabolism, and the regulation of gene expression. It is a building block of RNA, and its synthesis involves the conversion of uracil, ribose, and phosphoric acid. UMP is also a precursor for the synthesis of other nucleotides, such as Uridine Triphosphate (UTP), which is an essential energy source for cells. Additionally, UMP is involved in the synthesis of purine nucleotides, which are essential for DNA and RNA synthesis. In the medical field, UMP is used as a diagnostic tool to measure the activity of certain enzymes involved in nucleotide metabolism, such as uridine phosphorylase. It is also used as a component in certain medications, such as uridine, which is used to treat certain neurological disorders and liver diseases.

Cytosine is a nitrogenous base that is one of the four main building blocks of DNA and RNA. It is a pyrimidine base, meaning it has a six-membered ring structure with two nitrogen atoms and four carbon atoms. In DNA, cytosine is always paired with thymine, while in RNA, it is paired with uracil. Cytosine plays a crucial role in the storage and transmission of genetic information, as it is involved in the formation of the genetic code. In the medical field, cytosine is often studied in the context of genetics and molecular biology, as well as in the development of new drugs and therapies.

Uridine Phosphorylase (UP) is an enzyme that plays a crucial role in the metabolism of pyrimidine nucleotides in the body. It catalyzes the reversible phosphorolysis of uridine to uracil and ribose-1-phosphate. This reaction is an important step in the salvage pathway for pyrimidine nucleotides, which allows the body to recycle and reuse these molecules rather than relying solely on de novo synthesis. UP is found in many tissues throughout the body, including the liver, kidney, and small intestine. It is also present in certain types of cancer cells, where it has been shown to play a role in tumor growth and progression. In the medical field, UP is of interest as a potential therapeutic target for the treatment of certain types of cancer. Inhibitors of UP have been shown to selectively target cancer cells that overexpress the enzyme, leading to cell death and potentially slowing or stopping tumor growth. Additionally, UP has been proposed as a biomarker for certain types of cancer, as its levels in the blood or other bodily fluids may be elevated in patients with these conditions.

Tegafur is a chemotherapy drug that is used to treat various types of cancer, including colorectal cancer, breast cancer, and lung cancer. It is a prodrug of 5-fluorouracil (5-FU), which is a medication that works by slowing or stopping the growth of cancer cells in the body. Tegafur is usually given in combination with other chemotherapy drugs, such as leucovorin, to increase its effectiveness and reduce the risk of side effects. It is usually taken orally, although it can also be given intravenously or by injection. Tegafur is a potent medication that can cause a range of side effects, including nausea, vomiting, diarrhea, loss of appetite, fatigue, and hair loss. It can also cause more serious side effects, such as bone marrow suppression, which can lead to anemia, neutropenia, and thrombocytopenia. It is important to note that tegafur is not suitable for everyone, and its use should be carefully considered by a healthcare professional based on the individual's medical history and current health status.

Arabinofuranosyluracil, also known as araU or ara-U, is a nucleoside that is a component of DNA and RNA. It is a modified form of uracil, with an arabinofuranosyl group attached to the nitrogen atom at position 5 of the pyrimidine ring. In DNA, araU is incorporated into the sugar-phosphate backbone as araU dT, where dT is thymidine. In RNA, araU is incorporated into the sugar-phosphate backbone as araU A, where A is adenine.

Uridine is a nucleoside that is a component of RNA (ribonucleic acid). It is composed of a uracil base attached to a ribose sugar through a glycosidic bond. In RNA, uridine is one of the four nitrogenous bases, along with adenine, cytosine, and guanine. Uridine plays a crucial role in RNA metabolism, including transcription and translation. It is also involved in various cellular processes, such as energy metabolism and signal transduction. In the medical field, uridine is sometimes used as a supplement or medication to treat certain conditions, such as liver disease, depression, and nerve damage.

Thiouracil is a medication that is used to treat certain types of goiter, which is an enlargement of the thyroid gland. It works by reducing the production of thyroid hormones in the gland. Thiouracil is also used to treat hyperthyroidism, which is a condition in which the thyroid gland produces too much thyroid hormone. It is usually taken by mouth in the form of tablets. Side effects of thiouracil may include nausea, vomiting, diarrhea, and skin rash. It is important to follow the instructions of your healthcare provider when taking thiouracil.

Dihydropyrimidine dehydrogenase (DPD) deficiency is a rare genetic disorder that affects the metabolism of certain medications, including some chemotherapy drugs. DPD is an enzyme that is responsible for breaking down pyrimidine molecules, which are important building blocks of DNA and RNA. In individuals with DPD deficiency, the enzyme is not functioning properly, leading to a buildup of pyrimidine molecules in the body. This buildup can cause a range of symptoms, including nausea, vomiting, abdominal pain, and skin rash. It can also lead to serious side effects when certain medications, such as 5-fluorouracil (5-FU), are used to treat cancer. These medications are converted into active forms by the body, and the buildup of pyrimidine molecules can interfere with this process, leading to toxic levels of the active forms. DPD deficiency is typically diagnosed through genetic testing and is usually treated by avoiding medications that are known to be metabolized by DPD. In some cases, alternative medications may be used, or the dose of the medication may be adjusted to minimize the risk of side effects.

Thymine DNA Glycosylase (TDG) is an enzyme that plays a role in DNA repair. It is involved in the base excision repair pathway, which is a mechanism that corrects small DNA lesions caused by damage from various sources, such as oxidation, alkylation, and deamination. TDG recognizes and removes a specific type of damaged base called thymine glycol, which is formed when thymine is damaged by reactive oxygen species or other environmental factors. TDG removes the damaged base and leaves behind an abasic site, which is a gap in the DNA backbone. The abasic site is then repaired by other enzymes in the base excision repair pathway. TDG is important for maintaining the integrity of the DNA and preventing mutations that can lead to cancer and other diseases. Mutations in the TDG gene have been associated with an increased risk of certain types of cancer, such as breast and ovarian cancer.

Pyrimidine nucleosides are a type of nucleoside that contains a pyrimidine base, which is one of the two types of nitrogen-containing bases found in DNA and RNA. Pyrimidine nucleosides are important components of nucleic acids, and they play a crucial role in the function and regulation of cellular processes. There are several different pyrimidine nucleosides, including cytosine, thymine, and uracil, which are found in DNA and RNA, respectively. Pyrimidine nucleosides are also used as precursors for the synthesis of nucleotides, which are the building blocks of nucleic acids. In the medical field, pyrimidine nucleosides are used as antiviral drugs to treat viral infections, and they are also being studied for their potential use in the treatment of cancer and other diseases.

Deoxyuridine (dU) is a nucleoside that is a component of DNA. It is formed by the removal of a hydroxyl group from thymidine, another nucleoside found in DNA. Deoxyuridine is not found in RNA, which is the other type of nucleic acid found in cells. In the medical field, deoxyuridine is sometimes used as a medication. For example, it has been used to treat certain types of cancer, such as breast cancer and non-Hodgkin's lymphoma. It works by inhibiting the synthesis of DNA, which can slow the growth of cancer cells. Deoxyuridine is also used as a diagnostic tool in the laboratory. It can be incorporated into DNA during replication, and then detected using techniques such as PCR (polymerase chain reaction) or sequencing. This can be useful for studying the function and regulation of genes, as well as for identifying genetic mutations that may be associated with disease.

Orotidine-5'-Phosphate Decarboxylase (OMPDC) is an enzyme that plays a crucial role in the biosynthesis of pyrimidine nucleotides, which are essential components of DNA and RNA. It catalyzes the decarboxylation of orotidine-5'-phosphate (OMP) to form uridine-5'-phosphate (UMP), which is a key intermediate in the de novo synthesis of pyrimidine nucleotides. OMPDC is a member of the pyrimidine biosynthesis pathway, which is a series of enzymatic reactions that occur in the cytoplasm and mitochondria of cells. The pathway begins with the conversion of aspartate to carbamoyl phosphate, which is then used to synthesize OMP. OMPDC catalyzes the decarboxylation of OMP to form UMP, which is then converted to cytidine-5'-phosphate (CMP) and thymidine-5'-phosphate (TMP) through a series of subsequent reactions. OMPDC is encoded by the ODC1 gene, which is located on chromosome 17 in humans. Mutations in the ODC1 gene can lead to a deficiency in OMPDC activity, which can result in a rare genetic disorder called orotic aciduria. This disorder is characterized by the accumulation of orotic acid in the urine and can cause a range of symptoms, including developmental delays, seizures, and intellectual disability.

Orotic acid is a naturally occurring organic compound that is involved in the biosynthesis of nucleotides, which are the building blocks of DNA and RNA. It is a six-carbon compound that contains a keto group and a hydroxyl group. In the medical field, orotic acid is sometimes used as a supplement to treat certain genetic disorders that affect the metabolism of nucleotides. For example, orotic acid has been used to treat Lesch-Nyhan syndrome, a rare genetic disorder that causes high levels of uric acid in the blood and leads to neurological problems. Orotic acid is also involved in the metabolism of certain medications, including some antiviral drugs. In some cases, high levels of orotic acid can interfere with the effectiveness of these medications. Overall, orotic acid plays an important role in the metabolism of nucleotides and is involved in a number of biological processes in the body. However, its use as a supplement or medication should only be done under the guidance of a healthcare professional.

Orotate phosphoribosyltransferase (OPRTase) is an enzyme that plays a crucial role in the biosynthesis of the nucleotide uridine monophosphate (UMP) in the human body. UMP is a key intermediate in the synthesis of all nucleotides, including DNA and RNA. OPRTase catalyzes the transfer of a phosphoribosyl group from phosphoribosylpyrophosphate (PRPP) to orotic acid, forming orotidine monophosphate (OMP). This reaction is the first step in the de novo synthesis of UMP, which is necessary for the production of all other nucleotides. Mutations in the gene encoding OPRTase can lead to a deficiency in the enzyme, resulting in a rare genetic disorder called orotic aciduria. This disorder is characterized by the accumulation of orotic acid and its toxic metabolites in the body, leading to neurological and developmental problems in affected individuals.

DNA, or deoxyribonucleic acid, is a molecule that carries genetic information in living organisms. It is composed of four types of nitrogen-containing molecules called nucleotides, which are arranged in a specific sequence to form the genetic code. In the medical field, DNA is often studied as a tool for understanding and diagnosing genetic disorders. Genetic disorders are caused by changes in the DNA sequence that can affect the function of genes, leading to a variety of health problems. By analyzing DNA, doctors and researchers can identify specific genetic mutations that may be responsible for a particular disorder, and develop targeted treatments or therapies to address the underlying cause of the condition. DNA is also used in forensic science to identify individuals based on their unique genetic fingerprint. This is because each person's DNA sequence is unique, and can be used to distinguish one individual from another. DNA analysis is also used in criminal investigations to help solve crimes by linking DNA evidence to suspects or victims.

Sulfites are compounds that contain the sulfur ion (S2-) and are commonly used as preservatives in food and beverages. They are also used in the production of certain drugs and as a bleaching agent in textiles. In the medical field, sulfites can cause allergic reactions in some people, particularly those with sulfite sensitivity or asthma. Symptoms of a sulfite allergy can include hives, itching, difficulty breathing, and anaphylaxis, which is a severe and potentially life-threatening allergic reaction. Sulfites are also used as a treatment for certain medical conditions, such as rheumatoid arthritis and psoriasis. In these cases, sulfites are administered in low doses and are closely monitored by a healthcare provider to ensure their safety and effectiveness. Overall, sulfites have both medical and non-medical uses, and their effects can vary depending on the individual and the context in which they are used.

Pyrimidines are a class of nitrogen-containing heterocyclic compounds that are important in the field of medicine. They are composed of six carbon atoms arranged in a planar ring, with four nitrogen atoms and two carbon atoms in the ring. Pyrimidines are found in many biological molecules, including nucleic acids (DNA and RNA), and are involved in a variety of cellular processes, such as DNA replication and repair, gene expression, and metabolism. In the medical field, pyrimidines are often used as drugs to treat a variety of conditions, including cancer, viral infections, and autoimmune diseases. For example, the drug 5-fluorouracil is a pyrimidine analog that is used to treat a variety of cancers, including colon cancer and breast cancer. Pyrimidines are also used as components of antiviral drugs, such as acyclovir, which is used to treat herpes simplex virus infections.

Pyrophosphatases are a group of enzymes that catalyze the hydrolysis of pyrophosphate (PPi) to inorganic phosphate (Pi) and orthophosphate (P). These enzymes are important in many biological processes, including energy metabolism, nucleic acid synthesis, and signal transduction. In the medical field, pyrophosphatases are often studied in relation to various diseases and disorders. For example, mutations in certain pyrophosphatase genes have been linked to inherited disorders such as pyrophosphate diastase deficiency, which can cause joint pain, stiffness, and deformities. Pyrophosphatases are also involved in the regulation of bone mineralization, and changes in their activity have been implicated in osteoporosis and other bone diseases. In addition, pyrophosphatases are being investigated as potential therapeutic targets for a variety of conditions, including cancer, cardiovascular disease, and neurodegenerative disorders. For example, some studies have suggested that inhibiting pyrophosphatase activity may help to prevent the formation of blood clots and reduce the risk of stroke and heart attack.

Cytidine deaminase is an enzyme that plays a crucial role in the metabolism of nucleosides and nucleotides in the body. It catalyzes the conversion of cytidine, a nucleoside found in DNA and RNA, into uridine, another nucleoside. This reaction is an important step in the synthesis of deoxyribonucleotides, which are the building blocks of DNA. Cytidine deaminase is encoded by the CDA gene and is found in many tissues throughout the body, including the liver, spleen, and bone marrow. It is also expressed in certain types of cancer cells, where it can contribute to the development and progression of the disease. In the medical field, cytidine deaminase is of interest because it is involved in the metabolism of several drugs and is a potential target for the development of new therapies. For example, some drugs that are used to treat certain types of cancer, such as gemcitabine and cytarabine, are nucleoside analogs that are activated by cytidine deaminase. By inhibiting this enzyme, it may be possible to increase the effectiveness of these drugs or reduce their toxicity. In addition, cytidine deaminase has been implicated in the development of certain genetic disorders, such as adenosine deaminase deficiency and Cockayne syndrome. In these conditions, mutations in the CDA gene can lead to a deficiency in the enzyme, which can result in a range of symptoms, including developmental delays, neurological problems, and an increased risk of infections.

Folic acid deficiency is a condition in which the body does not have enough folic acid, a B vitamin that is essential for the production of red blood cells and the proper functioning of the nervous system. Folic acid is also important for DNA synthesis and repair, and for the formation of new cells. Folic acid deficiency can occur due to a lack of folic acid in the diet, malabsorption of folic acid from the gut, or the use of certain medications that interfere with folic acid absorption. It can also occur during pregnancy, as the developing fetus requires large amounts of folic acid for proper growth and development. Symptoms of folic acid deficiency can include fatigue, weakness, shortness of breath, pale skin, and anemia. In severe cases, folic acid deficiency can lead to megaloblastic anemia, a condition in which the red blood cells are abnormally large and do not function properly. Treatment for folic acid deficiency typically involves increasing dietary intake of folic acid-rich foods, such as leafy green vegetables, citrus fruits, and fortified cereals, or taking folic acid supplements. In some cases, treatment may also involve addressing the underlying cause of the deficiency, such as treating a digestive disorder or discontinuing the use of certain medications.

Pentoxyl is a medication that is used to treat a variety of conditions, including acne, rosacea, and psoriasis. It is a topical cream or gel that contains the active ingredient retinol, which is a form of vitamin A that is known to have anti-inflammatory and skin-renewing properties. Pentoxyl is typically applied to the affected area of the skin once or twice a day, and it can help to improve the appearance of fine lines, wrinkles, and other signs of aging. It can also help to reduce the redness and inflammation associated with certain skin conditions.

Adenine is a nitrogenous base that is found in DNA and RNA. It is one of the four nitrogenous bases that make up the genetic code, along with guanine, cytosine, and thymine (in DNA) or uracil (in RNA). Adenine is a purine base, which means it has a double ring structure with a six-membered ring fused to a five-membered ring. It is one of the two purine bases found in DNA and RNA, the other being guanine. Adenine is important in the function of DNA and RNA because it forms hydrogen bonds with thymine (in DNA) or uracil (in RNA) to form the base pairs that make up the genetic code.

Hydroxyphenylazouracil (HPA) is a synthetic compound that has been studied for its potential use in the treatment of various medical conditions, including cancer. It is a derivative of uracil, a nitrogenous base found in RNA and DNA, and contains a hydroxyphenyl group attached to the azouracil ring. HPA has been shown to have antitumor activity in preclinical studies, and it has been proposed as a potential treatment for various types of cancer, including breast cancer, prostate cancer, and lung cancer. It is thought to work by inhibiting the growth and proliferation of cancer cells, as well as by inducing apoptosis (cell death) in these cells. In addition to its potential use in cancer treatment, HPA has also been studied for its potential use in the treatment of other medical conditions, such as inflammatory bowel disease and viral infections. However, more research is needed to fully understand the potential therapeutic applications of HPA and to determine its safety and efficacy in humans.

In DNA, the uracil nucleobase is replaced by thymine (T). Uracil is a demethylated form of thymine. Uracil is a common and ... Uracil can also be used in the synthesis of caffeine. Uracil has also shown potential as a HIV viral capsid inhibitor. Uracil ... In yeast, uracil concentrations are inversely proportional to uracil permease. Mixtures containing uracil are also commonly ... Uracil is a weak acid. The first site of ionization of uracil is not known. The negative charge is placed on the oxygen anion ...
... (EC 1.1.99.19, uracil oxidase) is an enzyme with systematic name uracil:(acceptor) oxidoreductase. This ... Uracil+dehydrogenase at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Portal: Biology (Articles with ... Hayaishi O, Kornberg A (May 1952). "Metabolism of cytosine, thymine, uracil, and barbituric acid by bacterial enzymes". The ... enzyme catalyses the following chemical reaction uracil + acceptor ⇌ {\displaystyle \rightleftharpoons } barbiturate + reduced ...
... is a major oxidation product of cytosine in DNA. It can be readily bypassed by E. coli DNA polymerase I (unlike ... "Enzymatic Processing of Uracil Glycol, a Major Oxidative Product of DNA Cytosine". Jbc.org. Retrieved July 20, 2015. (Articles ...
... is an enzyme which creates UMP from uracil and phosphoribosylpyrophosphate. This protein may ... Uracil+phosphoribosyltransferase at the U.S. National Library of Medicine Medical Subject Headings (MeSH) EC 2.4.2.9 Portal: ...
UDG cleaves the uracil base from the phosphodiester backbone of uracil-containing DNA, but has no effect on natural (i.e., ... One important function of uracil-DNA glycosylases is to prevent mutagenesis by eliminating uracil from DNA molecules by ... carry-over contamination of PCRs can be controlled effectively if the contaminants contain uracils in place of thymines. Uracil ... Uracil N glycosylase has also been used in a method for cloning of PCR amplified DNA fragments. In this method the primers used ...
... uracil-forming). Other names in common use include uracil-5-carboxylic acid decarboxylase, and uracil-5-carboxylate carboxy- ... The enzyme uracil-5-carboxylate decarboxylase (EC 4.1.1.66) catalyzes the chemical reaction uracil 5-carboxylate ⇌ {\ ... Palmatier RD, McCroskey RP, Abbott MT (1970). "The enzymatic conversion of uracil 5-carboxylic acid to uracil and carbon ... The systematic name of this enzyme class is uracil-5-carboxylate carboxy-lyase ( ...
Other names in common use include ribothymidyl synthase, transfer RNA uracil 5-methyltransferase, transfer RNA uracil methylase ... In enzymology, a tRNA (uracil-5-)-methyltransferase (EC 2.1.1.35) is an enzyme that catalyzes the chemical reaction S-adenosyl- ... The systematic name of this enzyme class is S-adenosyl-L-methionine:tRNA (uracil-5-)-methyltransferase. ... tRNA uracil 5-methyltransferase, m5U-methyltransferase, tRNA:m5U54-methyltransferase, and RUMT. Hurwitz J, Gold M, Anders M ( ...
The systematic name of this enzyme class is 5,10-methylenetetrahydrofolate:tRNA (uracil-5-)-methyl-transferase. Other names in ... In enzymology, a methylenetetrahydrofolate-tRNA-(uracil-5-)-methyltransferase (EC 2.1.1.74) is an enzyme that catalyzes the ... uracil-5-)-methyl-transferase. Delk AS, Nagle DP, Rabinowitz JC (1980). "Methylenetetrahydrofolate-dependent biosynthesis of ... methylenetetrahydrofolate-transfer ribonucleate uracil, 5-methyltransferase, 5,10-methylenetetrahydrofolate:tRNA-UPsiC, and ( ...
... (EC 3.2.2.28, Mug, double-strand uracil-DNA glycosylase, Dug, dsUDG, double-stranded DNA ... Sung JS, Mosbaugh DW (August 2000). "Escherichia coli double-strand uracil-DNA glycosylase: involvement in uracil-mediated DNA ... is an enzyme with systematic name uracil-double-stranded DNA deoxyribohydrolase (uracil-releasing). This enzyme catalyses a ... Double-stranded+uracil-DNA+glycosylase at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Portal: Biology ...
... uracil + NADPH + H+ Thus, the two substrates of this enzyme are 5-amino-6-(5-phosphoribitylamino)uracil and NADP+, whereas its ... In enzymology, a 5-amino-6-(5-phosphoribosylamino)uracil reductase (EC 1.1.1.193) is an enzyme that catalyzes the chemical ... The systematic name of this enzyme class is 5-amino-6-(5-phosphoribitylamino)uracil:NADP+ 1'-oxidoreductase. This enzyme is ... 3 products are 5-amino-6-(5-phosphoribosylamino)uracil, NADPH, and H+. This enzyme belongs to the family of oxidoreductases, ...
Adenine readily binds uracil or thymine. Uracil is, however, one product of damage to cytosine that makes RNA particularly ... Chemically, uracil is similar to thymine, differing only by a methyl group, and its production requires less energy. In terms ... "Uracil". Archived from the original on 2015-09-08. Retrieved 2020-07-24. Lindahl T (April 1993). "Instability and decay of the ... RNA also uses a different set of bases than DNA-adenine, guanine, cytosine and uracil, instead of adenine, guanine, cytosine ...
"Uracil". Genome.gov. Retrieved 21 November 2019. Russell P (2001). iGenetics. New York: Benjamin Cummings. ISBN 0-8053-4553-1. ... Complex DNA and RNA organic compounds of life, including uracil, cytosine, and thymine, have also been formed in the laboratory ... Most of these are modifications of the canonical bases plus uracil. Modified Adenine N6-carbamoyl-methyladenine N6-methyadenine ... uracil (U), usually takes the place of thymine in RNA and differs from thymine by lacking a methyl group on its ring. In ...
5a Uracil; 5 Uracil dimer; 6a 2-pyridoxine; 6b 2-aminopyridine; 6 2-pyridoxine/2-aminopyridine; 7a Adenine; 7b Thymine; 7 ... 13 Uracil dimer; 14a Indole; 14 Indole/benzene; 15 Adenine/thymine stack; 16b Ethyne; 16 Ethene/ethyne; 17 Benzene/water; 18 ...
Enzymatic pathways of uracil anabolism". J. Biol. Chem. 227 (1): 329-38. doi:10.1016/S0021-9258(18)70818-1. PMID 13449076. ... PAEGE LM, SCHLENK F (1952). "Bacterial uracil riboside phosphorylase". Arch. Biochem. Biophys. 40 (1): 42-9. doi:10.1016/0003- ... uracil + alpha-D-ribose 1-phosphate Thus, the two substrates of this enzyme are uridine and phosphate, whereas its two products ... are uracil and alpha-D-ribose 1-phosphate. This enzyme belongs to the family of glycosyltransferases, specifically the ...
Mol CD, Harris JM, McIntosh EM, Tainer JA (September 1996). "Human dUTP pyrophosphatase: uracil recognition by a beta hairpin ... Lack or inhibition of dUTPase action leads to harmful perturbations in the nucleotide pool resulting in increased uracil ... Vassylyev DG, Morikawa K (1996). "Precluding uracil from DNA". Structure. 4 (12): 1381-5. doi:10.1016/S0969-2126(96)00145-1. ... "Keeping uracil out of DNA". Accounts of Chemical Research. 42 (1): 97-106. doi:10.1021/ar800114w. PMC 2732909. PMID 18837522. ...
RNA contains uracil instead of thymine. It has been proved in the laboratory that a single strand of DNA of one species can ...
This causes a U:G mispair which is detected by Uracil DNA glycosylase. The uracil base is flipped out into the glycosylase ... An example of base excision repair occurs when a cytosine base is deaminated and becomes a uracil base. ... Research has demonstrated both mechanisms: uracil-DNA glycosylase follows the passive mechanism and Tn10 transposase follows ... "Uracil in DNA - occurrence, consequences and repair". Oncogene. 21 (58): 8935-8948. doi:10.1038/sj.onc.1205996. PMID 12483510. ...
The Murchison meteorite contains the organic molecules uracil and xanthine, which must therefore already have been present in ... "Uracil in the carbonaceous asteroid (162173) Ryugu". Nature Communications. 14 (1): 1292. Bibcode:2023NatCo..14.1292O. doi: ...
Uracil forms a base pair with adenine. In DNA, uracil is not used at all, and is instead replaced with thymine. uridine (U, Urd ... Cytosine (C), thymine (T), and uracil (U) are classified as pyrimidines. The letter Y is sometimes used to indicate a generic ... In RNA, thymine is not used at all, and is instead replaced with uracil. thymine dimer See pyrimidine dimer. tissue tissue- ... A set of five particular nitrogenous bases - adenine (A), guanine (G), cytosine (C), thymine (T), and uracil (U) - are ...
These symbols are also valid for RNA, except with U (uracil) replacing T (thymine). Apart from adenine (A), cytosine (C), ... Similarly, deamination of cytosine results in uracil. Example of comparing and determining the % difference between two ... guanine (G), thymine (T) and uracil (U), DNA and RNA also contain bases that have been modified after the nucleic acid chain ...
However, uracil is only found in RNA. Therefore, after UTP is synthesized, it is must be converted into a deoxy form to be ... In contrast to uracil, thymine bases are found mostly in DNA, not RNA. Cells do not normally contain thymine bases that are ... Other DNA and RNA nucleotide bases that are linked to the ribose sugar via a glycosidic bond are thymine, cytosine and uracil ( ... This reaction transfers a methyl group onto the uracil base of dUMP to generate dTMP. The thymidylate synthase reaction, dUMP ...
The reaction of C3O and urea is predicted to form uracil. The pathway for this, is that firstly the two molecules react to form ... Then a final cyclisation occurs to make uracil. The C3O molecules do not last long. At the low pressure of 1 pascal, they ... Wang, Tianfang; Bowie, John H. (2012). "Can cytosine, thymine and uracil be formed in interstellar regions? A theoretical study ...
While spontaneous deamination of cytosine forms uracil, which is recognized and removed by DNA repair enzymes, deamination of 5 ... quite distinct from conventional cytosine and uracil. After seven decades, it turned out that it is also a common feature in ... cytosine deaminates to uracil (U) under similar conditions. 5-methylcytosine is resistant to deamination by bisulfite treatment ...
This enzyme dephosphorylates the 5'- and 2'(3')-phosphates of uracil and thymine deoxyribonucleotides. The gene is located ... This enzyme functions in dephosphorylating nucleoside triphosphates, especially the 5′- and 2′(3′)-phosphates of uracil and ... mdN binds and dephosphorylates uracil and thymine deoxyribonucleotides. NT5C GRCh38: Ensembl release 89: ENSG00000205309 - ...
Studies of the 12C/13C isotopic ratios of organic compounds in the Murchison meteorite suggest that the RNA component uracil ... DNA and RNA components including uracil, cytosine and thymine can be synthesized under outer space conditions, using starting ... There were initial difficulties in the explanation of the abiotic synthesis of the nucleotides cytosine and uracil. Subsequent ... Robertson, Michael P.; Miller, Stanley L. (29 June 1995). "An efficient prebiotic synthesis of cytosine and uracil". Nature. ...
Rashtchian A, Thornton CG, Heidecker G (November 1992). "A novel method for site-directed mutagenesis using PCR and uracil DNA ... This DNA polymerase, similar to other DNA polymerases from Archaebacteria is sensitive to Uracil residues in DNA and is ... This polymerase breaks when reaching erroneous uracil in DNA from the chain extension and, through this readahead function, ... Lasken RS, Schuster DM, Rashtchian A (July 1996). "Archaebacterial DNA polymerases tightly bind uracil-containing DNA". The ...
Brunschweiger A, Müller CE (2006). "P2 receptors activated by uracil nucleotides--an update". Curr. Med. Chem. 13 (3): 289-312 ...
Uracil is located at the interface between the two domains. Uracil permease, UraA UraA with bound uracil at 2.8Å resolution PDB ... Uracil permeases, including UraA of E. coli (TC# 2.A.40.1.1), which facilitates Uracil uptake. Pyrimidine permeases, including ... biosynthesis operon of the thermophile Bacillus caldolyticus includes genes for uracil phosphoribosyltransferase and uracil ... "Structure and mechanism of the uracil transporter UraA". Nature. 472 (7342): 243-6. Bibcode:2011Natur.472..243L. doi:10.1038/ ...
The four nucleobases in DNA are guanine, adenine, cytosine and thymine; in RNA, uracil is used in place of thymine. Nucleotides ... Ramesh, Deepthi; Vijayakumar, Balaji Gowrivel; Kannan, Tharanikkarasu (December 2020). "Therapeutic potential of uracil and its ... and uracil (in RNA) occur in just one. Adenine forms a base pair with thymine with two hydrogen bonds, while guanine pairs with ... "Contribution of de-novo and salvage synthesis to the uracil nucleotide pool in mouse tissues and tumors in vivo". European ...
In RNA, the complement of adenine (A) is uracil (U) instead of thymine (T), so the pairs that form are adenine:uracil and ... Very rarely, thymine can appear in RNA, or uracil in DNA, but when the other three major pyrimidine bases are represented, some ... 4, p. 336 Nuevo, M.; Milam, S. N.; Sandford, S. A.; Elsila, J. E.; Dworkin, J. P. (2009). "Formation of uracil from the ... Pyrimidine biosynthesis creates derivatives -like orotate, thymine, cytosine, and uracil- de novo from carbamoyl phosphate and ...
It is composed of the compounds Adenine, Uracil, Guanine, and Cytosine. This product includes one Adenine and one Uracil ... It is composed of the compounds Adenine, Uracil, Guanine, and Cytosine.. This product includes one Adenine and one Uracil ...
Permease for cytosine/purines; uracil; thiamine; allantoin. 98. gb,AAW53058.1,. Sk04. 2999-3883. 885. None. Ribokinase. 98. gb, ...
Uracil-DNA glycosylase acts by substrate autocatalysis. Nature. 2001 Oct 18; 413(6857):752-5. ...
Counterions effect on uracil-silver coordination. Authors: Tahirbegi, I. B.; Pérez, Y.; Mir, M.; Samitier, J. ...
5-Bromo-6-methyl-3-(1-methylpropyl)uracil. 314-40-9. YQ9100000. ...
Synthesis, Base Pairing Properties, and Biological Activity Studies of Platinum(II) Complexes Based on Uracil Nucleosides. ...
Dive into the research topics of Affinity purification and comparative analysis of two distinct human uracil-DNA glycosylases ... Affinity purification and comparative analysis of two distinct human uracil-DNA glycosylases. ...
... which is involved in the breakdown of molecules called uracil and thymine. Uracil and thymine are pyrimidines, which are one ... It is unclear how the excess uracil and thymine are related to the specific signs and symptoms of dihydropyrimidine ... Dihydropyrimidine dehydrogenase deficiency interferes with the breakdown of uracil and thymine, and results in excess ...
Uracil *. 5.76 × 107 ± 1.19 × 107 B. 1.08 × 108 ± 1.39 × 107 A. 0.02. ... and uracil, respectively [24,25]; these metabolites are related to feed efficiency parameters. Clemmons et al. [26] found that ...
... ... Structural Role of Uracil DNA Glycosylase for the Recognition of Uracil in DNA Duplexes. Clues from Atomistic Simulations / ... In the first stage of the base excision repair pathway the enzyme uracil DNA glycosylase (UNG) recognizes and excises uracil (U ... In the first stage of the base excision repair pathway the enzyme uracil DNA glycosylase (UNG) recognizes and excises uracil (U ...
CM Glucose Plates minus Uracil. 100mm, 20 Plates per Sleeve, Sterile.. CM Glucose Plates minus Uracil. 100mm, 20 Plates per ...
Biochemical and kinetic characterization of uracil cleavage by human uracil DNA glycosylase in the context of mitochondrial DNA ... Biochemical and kinetic characterization of uracil..., 2019. Download whole document (PDF) (2.11 MB) ...
2,4-Dichloro-4-methoxy uracil. 0 out of 5. $0.00. Read more Add to wishlist ...
Originally discovered and isolated from a range of bacterial species, specifically Actinomyces, Pepstatin A is able to inhibit pepsin using picomolar concentrations. Often used to study HIV proteases, Pepstatin is used to better understand the mechanisms of HIV-infected cells. It also helps prevent the degradation of hemoglobin.. ...
Option to remove uracil (deaminated cytosine) artifacts. *Ready-to-use DNA for PCR, digital PCR (dPCR) and next-generation ... The EZ1&2 DNA FFPE protocol uses double lysis to recover DNA effectively, while the optional uracil-N-glycosylase (UNG) step ... The most common artifact in FFPE tissues is the deamination of cytosine to uracil, which results in a single nucleotide ... optimized lysis conditions that additionally allow the specific removal of deaminated cytosine residues by the enzyme Uracil-N- ...
Folate deficiency causes uracil misincorporation into human DNA and chromosome breakage: implications for cancer and neuronal ... which folic acid deficiency led to increased carcinogenesis included chromosomal breaks due to massive incorporation of uracil ...
Stability of uracil and thymine cations. 15th Symposium on Atomic and Surface Physics and Related Topics (SASP 2006), Obergurgl ... Stability of uracil and thymine cations. DPG - Frühjahrstagung des Arbeitskreises Atome, Moleküle, Quantenoptik und Plasmen ( ... Stability of uracil and thymine cations. 17th International Mass Spectrometry Conference (IMSC), Prague (2006) ...
1993) Consensus sequences for good and poor removal of uracil from double stranded DNA by uracil-DNA glycosylase. Nucleic Acids ... 1993) Consensus sequences for good and poor removal of uracil from double stranded DNA by uracil-DNA glycosylase. Nucleic Acids ... 1995) Sequence specificity for removal of uracil from U.A pairs and U.G mismatches by uracil-DNA glycosylase from Escherichia ... 1995) Sequence specificity for removal of uracil from U.A pairs and U.G mismatches by uracil-DNA glycosylase from Escherichia ...
PDB Compounds: (B:) 23s rRNA (uracil-5-)-methyltransferase ruma. SCOPe Domain Sequences for d2bh2b2:. Sequence; same for both ... Protein rRNA (Uracil-5-)-methyltransferase RumA, catalytic domain [102582] (1 species). includes an iron-sulfur cluster-binding ... Family c.66.1.40: (Uracil-5-)-methyltransferase [102581] (1 protein). Pfam PF05958. ... d2bh2b2 c.66.1.40 (B:75-431) rRNA (Uracil-5-)-methyltransferase RumA, catalytic domain {Escherichia coli [TaxId: 562]} ...
The mixture is incubated for at least 30 min at room temperature, facilitating the conversion of an unstable uracil metabolite ...
The mixture is incubated for at least 30 min at room temperature, facilitating the conversion of an unstable uracil metabolite ...
Uracil, this is because RNA has cytosine and uracil as the pyrimidine bases. This is compared to DNA, which has cytosine and ... Since RNA has uracil instead of thymine, uracil bonds with adenine in RNA. ... RNA has uracil in it instead of thymine. When DNA bonds together, its bases always pair the same way. Adenine bonds with ...
Uracil-triphosphate had no relaxant ability, which suggested that relaxation was not mediated by a nucleotide receptor. 8- ...
ABHD5 blunts the sensitivity of colorectal cancer to fluorouracil via promoting autophagic uracil yield. Nature Commun. (2019) ... promotes autophagy degradation of RNAs to form uracil, and thus maintains cell survival. The absence or inactivation of RNase ...
ADDITIONAL NAMES: Levovir; L-FMAU; 2-Fluoro-5-methyl-β-L-arabinofuranosyl-uracil ...
The nucleobases of RNA can be two different purines (adenine and guanine) or two different pyrimidines (cytosine and uracil). ...
COOL HREK7.KS ON THE URACIL. Itaiamliiit, Iohvch Kockaway at 4 :*, P. At.. Earn lor iTie whole excuraiou Vi cu.ita. t ONTi.KNO ...
For testing the agents, we used 5-hydroxymethyl uracil, 5-hydroxymethyl cytosine as model molecules. In addition, we ...
  • The EZ1&2 DNA FFPE protocol uses double lysis to recover DNA effectively, while the optional uracil-N-glycosylase (UNG) step removes deaminated cytosine artifacts to limit the risk of nucleotide read errors. (qiagen.com)
  • Uracil, this is because RNA has cytosine and uracil as the pyrimidine bases. (databasefootball.com)
  • RNA is composed of a sugar-phosphate backbone and four bases as well, though one of them is different: adenine, guanine, cytosine, and uracil. (databasefootball.com)
  • For testing the agents, we used 5-hydroxymethyl uracil, 5-hydroxymethyl cytosine as model molecules. (helsinki.fi)
  • This gene provides instructions for making an enzyme called dihydropyrimidine dehydrogenase, which is involved in the breakdown of molecules called uracil and thymine. (medlineplus.gov)
  • Dihydropyrimidine dehydrogenase deficiency interferes with the breakdown of uracil and thymine, and results in excess quantities of these molecules in the blood, urine, and the fluid that surrounds the brain and spinal cord ( cerebrospinal fluid ). (medlineplus.gov)
  • It is unclear how the excess uracil and thymine are related to the specific signs and symptoms of dihydropyrimidine dehydrogenase deficiency. (medlineplus.gov)
  • RNA has uracil in it instead of thymine. (databasefootball.com)
  • Since RNA has uracil instead of thymine, uracil bonds with adenine in RNA. (databasefootball.com)
  • Uracil-DNA glycosylase acts by substrate autocatalysis. (uchicago.edu)
  • Structural Role of Uracil DNA Glycosylase for the Recognition of Uracil in DNA Duplexes. (sissa.it)
  • In the first stage of the base excision repair pathway the enzyme uracil DNA glycosylase (UNG) recognizes and excises uracil (U) from DNA filaments. (sissa.it)
  • Cross-contamination can therefore be prevented by a pretreatment of dUTP containing DNA with heat-labile Uracil-DNA Glycosylase before amplification. (sigmaaldrich.com)
  • Synthesis, Base Pairing Properties, and Biological Activity Studies of Platinum(II) Complexes Based on Uracil Nucleosides. (bvsalud.org)
  • The mixture is incubated for at least 30 min at room temperature, facilitating the conversion of an unstable uracil metabolite into a more stable form. (cdc.gov)
  • This gene provides instructions for making an enzyme called dihydropyrimidine dehydrogenase, which is involved in the breakdown of molecules called uracil and thymine. (medlineplus.gov)
  • Dihydropyrimidine dehydrogenase deficiency interferes with the breakdown of uracil and thymine, and results in excess quantities of these molecules in the blood, urine, and the fluid that surrounds the brain and spinal cord ( cerebrospinal fluid ). (medlineplus.gov)
  • It is unclear how the excess uracil and thymine are related to the specific signs and symptoms of dihydropyrimidine dehydrogenase deficiency. (medlineplus.gov)
  • 1. Uracil-DNA glycosylases SMUG1 and UNG2 coordinate the initial steps of base excision repair by distinct mechanisms. (nih.gov)
  • 2. Strikingly different properties of uracil-DNA glycosylases UNG2 and SMUG1 may explain divergent roles in processing of genomic uracil. (nih.gov)
  • 12. [Uracil-DNA glycosylases]. (nih.gov)
  • GF RN [2] #=GF RM 11178247 #=GF RT The alpha/beta fold uracil DNA glycosylases: a common origin #=GF RT with diverse fates. (genome.jp)
  • UDG depletion sensitizes cells to high APOBEC3B deaminase and to pemetrexed (PEM) and floxuridine (5-FdU), which are toxic to tumor cells through incorporation of uracil and 5-FU into DNA. (nih.gov)
  • Combination with irreversible inhibitors of dihydropyrimidine dehydrogenase (DPD), such as brivudine, sorivudine and their analogues or uracil, a reversible DPD inhibitor, is contraindicated (see Section 4.4). (who.int)
  • 14. DNA-uracil and human pathology. (nih.gov)
  • 6. Uracil in DNA--occurrence, consequences and repair. (nih.gov)
  • but, no evidence for uracils in immunoglobulin loci. (nih.gov)