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.
A transferase that catalyzes the addition of aliphatic, aromatic, or heterocyclic FREE RADICALS as well as EPOXIDES and arene oxides to GLUTATHIONE. Addition takes place at the SULFUR. It also catalyzes the reduction of polyol nitrate by glutathione to polyol and nitrite.
A somewhat heterogeneous class of enzymes that catalyze the transfer of alkyl or related groups (excluding methyl groups). EC 2.5.
A class of enzymes that transfers substituted phosphate groups. EC 2.7.8.
A non-template-directed DNA polymerase normally found in vertebrate thymus and bone marrow. It catalyzes the elongation of oligo- or polydeoxynucleotide chains and is widely used as a tool in the differential diagnosis of acute leukemias in man. EC 2.7.7.31.
Enzymes which transfer coenzyme A moieties from acyl- or acetyl-CoA to various carboxylic acceptors forming a thiol ester. Enzymes in this group are instrumental in ketone body metabolism and utilization of acetoacetate in mitochondria. EC 2.8.3.
Acyltransferases that use AMINO ACYL TRNA as the amino acid donor in formation of a peptide bond. There are ribosomal and non-ribosomal peptidyltransferases.
Enzymes that catalyze the transfer of N-acetylglucosamine from a nucleoside diphosphate N-acetylglucosamine to an acceptor molecule which is frequently another carbohydrate. EC 2.4.1.-.
Enzymes that transfer the ADP-RIBOSE group of NAD or NADP to proteins or other small molecules. Transfer of ADP-ribose to water (i.e., hydrolysis) is catalyzed by the NADASES. The mono(ADP-ribose)transferases transfer a single ADP-ribose. POLY(ADP-RIBOSE) POLYMERASES transfer multiple units of ADP-ribose to protein targets, building POLY ADENOSINE DIPHOSPHATE RIBOSE in linear or branched chains.
An enzyme that catalyzes the synthesis of geranylgeranyl diphosphate from trans, trans-farnesyl diphosphate and isopentenyl diphosphate.
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.
Enzymes from the transferase class that catalyze the transfer of acyl groups from donor to acceptor, forming either esters or amides. (From Enzyme Nomenclature 1992) EC 2.3.
A skin irritant that may cause dermatitis of both primary and allergic types. Contact sensitization with DNCB has been used as a measure of cellular immunity. DNCB is also used as a reagent for the detection and determination of pyridine compounds.
A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.
Enzymes that catalyze the transfer of galactose from a nucleoside diphosphate galactose to an acceptor molecule which is frequently another carbohydrate. EC 2.4.1.-.
Enzymes that catalyze the transfer of N-acetylgalactosamine from a nucleoside diphosphate N-acetylgalactosamine to an acceptor molecule which is frequently another carbohydrate. EC 2.4.1.-.
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.
A post-translational modification of proteins by the attachment of an isoprenoid to the C-terminal cysteine residue. The isoprenoids used, farnesyl diphosphate or geranylgeranyl diphosphate, are derived from the same biochemical pathway that produces cholesterol.
A class of enzymes that transfers nucleotidyl residues. EC 2.7.7.
An enzyme, sometimes called GGT, with a key role in the synthesis and degradation of GLUTATHIONE; (GSH, a tripeptide that protects cells from many toxins). It catalyzes the transfer of the gamma-glutamyl moiety to an acceptor amino acid.
Enzymes that catalyze the transfer of glycosyl groups to an acceptor. Most often another carbohydrate molecule acts as an acceptor, but inorganic phosphate can also act as an acceptor, such as in the case of PHOSPHORYLASES. Some of the enzymes in this group also catalyze hydrolysis, which can be regarded as transfer of a glycosyl group from the donor to water. Subclasses include the HEXOSYLTRANSFERASES; PENTOSYLTRANSFERASES; SIALYLTRANSFERASES; and those transferring other glycosyl groups. EC 2.4.
The rate dynamics in chemical or physical systems.
Enzymes that catalyze the incorporation of deoxyribonucleotides into a chain of DNA. EC 2.7.7.-.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Enzymes that catalyze the transfer of hexose groups. EC 2.4.1.-.
An enzyme that catalyzes the synthesis of UDPgalactose from UTP and galactose-1-phosphate. It is present in low levels in fetal and infant liver, but increases with age, thereby enabling galactosemic infants who survive to develop the capacity to metabolize galactose. EC 2.7.7.10.
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.
Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.
Enzymes of the transferase class that catalyze the transfer of a pentose group from one compound to another.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
The N-acetyl derivative of glucosamine.
A family of enzymes accepting a wide range of substrates, including phenols, alcohols, amines, and fatty acids. They function as drug-metabolizing enzymes that catalyze the conjugation of UDPglucuronic acid to a variety of endogenous and exogenous compounds. EC 2.4.1.17.
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.
Phosphoric or pyrophosphoric acid esters of polyisoprenoids.
Enzymes that catalyze the transfer of glucose from a nucleoside diphosphate glucose to an acceptor molecule which is frequently another carbohydrate. EC 2.4.1.-.
A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides.
The facilitation of a chemical reaction by material (catalyst) that is not consumed by the reaction.
The sequence of carbohydrates within POLYSACCHARIDES; GLYCOPROTEINS; and GLYCOLIPIDS.
The chemical or biochemical addition of carbohydrate or glycosyl groups to other chemicals, especially peptides or proteins. Glycosyl transferases are used in this biochemical reaction.
An enzyme that catalyzes the transfer of UMP from UDPglucose to galactose 1-phosphate, forming UDPgalactose and glucose 1-phosphate. Deficiency in this enzyme is the major cause of GALACTOSEMIA. EC 2.7.7.12.
An antitumor antibiotic produced by Streptomyces sparsogenes. It inhibits protein synthesis in 70S and 80S ribosomal systems.
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.
An enzyme that catalyzes the conversion of 5-phosphoribosyl-1-pyrophosphate and hypoxanthine, guanine, or 6-mercaptopurine to the corresponding 5'-mononucleotides and pyrophosphate. The enzyme is important in purine biosynthesis as well as central nervous system functions. Complete lack of enzyme activity is associated with the LESCH-NYHAN SYNDROME, while partial deficiency results in overproduction of uric acid. EC 2.4.2.8.
Enzymes that catalyze the transfer of mannose from a nucleoside diphosphate mannose to an acceptor molecule which is frequently another carbohydrate. The group includes EC 2.4.1.32, EC 2.4.1.48, EC 2.4.1.54, and EC 2.4.1.57.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
An enzyme that catalyzes reversibly the transfer of phosphoethanolamine from CDP-ethanolamine to diacylglycerol to yield phosphatidylethanolamine (cephalin) and CMP. The enzyme is found in the endoplasmic reticulum. EC 2.7.8.1.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Enzymes which transfer sulfur atoms to various acceptor molecules. EC 2.8.1.
Serves as the biological precursor of insect chitin, of muramic acid in bacterial cell walls, and of sialic acids in mammalian glycoproteins.
A nucleoside diphosphate sugar which serves as a source of N-acetylgalactosamine for glycoproteins, sulfatides and cerebrosides.
A subclass of enzymes of the transferase class that catalyze the transfer of a methyl group from one compound to another. (Dorland, 28th ed) EC 2.1.1.
Proteins prepared by recombinant DNA technology.
Proteins found in any species of bacterium.
Multicomponent ribonucleoprotein structures found in the CYTOPLASM of all cells, and in MITOCHONDRIA, and PLASTIDS. They function in PROTEIN BIOSYNTHESIS via GENETIC TRANSLATION.
An in situ method for detecting areas of DNA which are nicked during APOPTOSIS. Terminal deoxynucleotidyl transferase is used to add labeled dUTP, in a template-independent manner, to the 3 prime OH ends of either single- or double-stranded DNA. The terminal deoxynucleotidyl transferase nick end labeling, or TUNEL, assay labels apoptosis on a single-cell level, making it more sensitive than agarose gel electrophoresis for analysis of DNA FRAGMENTATION.
A group of inherited enzyme deficiencies which feature elevations of GALACTOSE in the blood. This condition may be associated with deficiencies of GALACTOKINASE; UDPGLUCOSE-HEXOSE-1-PHOSPHATE URIDYLYLTRANSFERASE; or UDPGLUCOSE 4-EPIMERASE. The classic form is caused by UDPglucose-Hexose-1-Phosphate Uridylyltransferase deficiency, and presents in infancy with FAILURE TO THRIVE; VOMITING; and INTRACRANIAL HYPERTENSION. Affected individuals also may develop MENTAL RETARDATION; JAUNDICE; hepatosplenomegaly; ovarian failure (PRIMARY OVARIAN INSUFFICIENCY); and cataracts. (From Menkes, Textbook of Child Neurology, 5th ed, pp61-3)
The region of an enzyme that interacts with its substrate to cause the enzymatic reaction.
Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
Established cell cultures that have the potential to propagate indefinitely.
A glutathione transferase that catalyzes the conjugation of electrophilic substrates to GLUTATHIONE. This enzyme has been shown to provide cellular protection against redox-mediated damage by FREE RADICALS.
Enzymes that catalyze the transfer of multiple ADP-RIBOSE groups from nicotinamide-adenine dinucleotide (NAD) onto protein targets, thus building up a linear or branched homopolymer of repeating ADP-ribose units i.e., POLY ADENOSINE DIPHOSPHATE RIBOSE.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
Enzymes catalyzing the transfer of an acetyl group, usually from acetyl coenzyme A, to another compound. EC 2.3.1.
An enzyme that catalyzes the first step of the pathway for histidine biosynthesis in Salmonella typhimurium. ATP reacts reversibly with 5-phosphoribosyl-1-pyrophosphate to yield N-1-(5'-phosphoribosyl)-ATP and pyrophosphate. EC 2.4.2.17.
Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.
A cinnamamido ADENOSINE found in STREPTOMYCES alboniger. It inhibits protein synthesis by binding to RNA. It is an antineoplastic and antitrypanosomal agent and is used in research as an inhibitor of protein synthesis.
Constituent of 50S subunit of prokaryotic ribosomes containing about 3200 nucleotides. 23S rRNA is involved in the initiation of polypeptide synthesis.
An enzyme that catalyzes the transfer of acetylgalactosamine from UDP N-acetylgalactosamine to various 2-fucosylgalactosides as acceptors. EC 2.4.1.40.
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.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Reduction of pharmacologic activity or toxicity of a drug or other foreign substance by a living system, usually by enzymatic action. It includes those metabolic transformations that make the substance more soluble for faster renal excretion.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Enzyme that catalyzes the movement of a methyl group from S-adenosylmethionone to a catechol or a catecholamine.
A group of enzymes that catalyze the transfer of carboxyl- or carbamoyl- groups. EC 2.1.3.
Closed vesicles of fragmented endoplasmic reticulum created when liver cells or tissue are disrupted by homogenization. They may be smooth or rough.
The functional hereditary units of BACTERIA.
The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. The degree of relatedness or homology between the sequences is predicted computationally or statistically based on weights assigned to the elements aligned between the sequences. This in turn can serve as a potential indicator of the genetic relatedness between the organisms.
The sum of the weight of all the atoms in a molecule.
Carbohydrates consisting of between two (DISACCHARIDES) and ten MONOSACCHARIDES connected by either an alpha- or beta-glycosidic link. They are found throughout nature in both the free and bound form.
Genetically engineered MUTAGENESIS at a specific site in the DNA molecule that introduces a base substitution, or an insertion or deletion.
Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.
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.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
An enzyme that, in the pathway of cholesterol biosynthesis, catalyzes the condensation of isopentenyl pyrophosphate and dimethylallylpyrophosphate to yield pyrophosphate and geranylpyrophosphate. The enzyme then catalyzes the condensation of the latter compound with another molecule of isopentenyl pyrophosphate to yield pyrophosphate and farnesylpyrophosphate. EC 2.5.1.1.
A species of halophilic archaea distinguished by its production of acid from sugar. This species was previously called Halobacterium marismortui.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.
Artifactual vesicles formed from the endoplasmic reticulum when cells are disrupted. They are isolated by differential centrifugation and are composed of three structural features: rough vesicles, smooth vesicles, and ribosomes. Numerous enzyme activities are associated with the microsomal fraction. (Glick, Glossary of Biochemistry and Molecular Biology, 1990; from Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
Any of various enzymatically catalyzed post-translational modifications of PEPTIDES or PROTEINS in the cell of origin. These modifications include carboxylation; HYDROXYLATION; ACETYLATION; PHOSPHORYLATION; METHYLATION; GLYCOSYLATION; ubiquitination; oxidation; proteolysis; and crosslinking and result in changes in molecular weight and electrophoretic motility.
An aldohexose that occurs naturally in the D-form in lactose, cerebrosides, gangliosides, and mucoproteins. Deficiency of galactosyl-1-phosphate uridyltransferase (GALACTOSE-1-PHOSPHATE URIDYL-TRANSFERASE DEFICIENCY DISEASE) causes an error in galactose metabolism called GALACTOSEMIA, resulting in elevations of galactose in the blood.
Enzymes that catalyze the transfer of an aminoacyl group from donor to acceptor resulting in the formation of an ester or amide linkage. EC 2.3.2.
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).
Enzymes that catalyze the transfer of N-acetylhexosaminyl groups to an acceptor molecule which is frequently another carbohydrate. EC 2.4.1.
Enzymes that catalyze the transfer of nitrogenous groups, primarily amino groups, from a donor, generally an amino acid, to an acceptor, usually a 2-oxoacid. EC 2.6.
An enzyme that catalyzes the acetylation of chloramphenicol to yield chloramphenicol 3-acetate. Since chloramphenicol 3-acetate does not bind to bacterial ribosomes and is not an inhibitor of peptidyltransferase, the enzyme is responsible for the naturally occurring chloramphenicol resistance in bacteria. The enzyme, for which variants are known, is found in both gram-negative and gram-positive bacteria. EC 2.3.1.28.
Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.
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 test used to determine whether or not complementation (compensation in the form of dominance) will occur in a cell with a given mutant phenotype when another mutant genome, encoding the same mutant phenotype, is introduced into that cell.
Enzymes that catalyze the transfer of hydroxymethyl or formyl groups. EC 2.1.2.
An inherited disorder transmitted as a sex-linked trait and caused by a deficiency of an enzyme of purine metabolism; HYPOXANTHINE PHOSPHORIBOSYLTRANSFERASE. Affected individuals are normal in the first year of life and then develop psychomotor retardation, extrapyramidal movement disorders, progressive spasticity, and seizures. Self-destructive behaviors such as biting of fingers and lips are seen frequently. Intellectual impairment may also occur but is typically not severe. Elevation of uric acid in the serum leads to the development of renal calculi and gouty arthritis. (Menkes, Textbook of Child Neurology, 5th ed, pp127)
Toxic proteins produced from the species CLOSTRIDIUM BOTULINUM. The toxins are synthesized as a single peptide chain which is processed into a mature protein consisting of a heavy chain and light chain joined via a disulfide bond. The botulinum toxin light chain is a zinc-dependent protease which is released from the heavy chain upon ENDOCYTOSIS into PRESYNAPTIC NERVE ENDINGS. Once inside the cell the botulinum toxin light chain cleaves specific SNARE proteins which are essential for secretion of ACETYLCHOLINE by SYNAPTIC VESICLES. This inhibition of acetylcholine release results in muscular PARALYSIS.
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)
Enzymes of the transferase class that catalyze the conversion of L-aspartate and 2-ketoglutarate to oxaloacetate and L-glutamate. EC 2.6.1.1.
Covalent attachment of LIPIDS and FATTY ACIDS to other compounds and PROTEINS.
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.
An increase in the rate of synthesis of an enzyme due to the presence of an inducer which acts to derepress the gene responsible for enzyme synthesis.
Leukemia associated with HYPERPLASIA of the lymphoid tissues and increased numbers of circulating malignant LYMPHOCYTES and lymphoblasts.
Electrophoresis in which a pH gradient is established in a gel medium and proteins migrate until they reach the site (or focus) at which the pH is equal to their isoelectric point.
Consists of a polypeptide chain and 4'-phosphopantetheine linked to a serine residue by a phosphodiester bond. Acyl groups are bound as thiol esters to the pantothenyl group. Acyl carrier protein is involved in every step of fatty acid synthesis by the cytoplasmic system.
A group of enzymes with the general formula CMP-N-acetylneuraminate:acceptor N-acetylneuraminyl transferase. They catalyze the transfer of N-acetylneuraminic acid from CMP-N-acetylneuraminic acid to an acceptor, which is usually the terminal sugar residue of an oligosaccharide, a glycoprotein, or a glycolipid. EC 2.4.99.-.
The study of crystal structure using X-RAY DIFFRACTION techniques. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Derivatives of adipic acid. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain a 1,6-carboxy terminated aliphatic structure.
The small RNA molecules, 73-80 nucleotides long, that function during translation (TRANSLATION, GENETIC) to align AMINO ACIDS at the RIBOSOMES in a sequence determined by the mRNA (RNA, MESSENGER). There are about 30 different transfer RNAs. Each recognizes a specific CODON set on the mRNA through its own ANTICODON and as aminoacyl tRNAs (RNA, TRANSFER, AMINO ACYL), each carries a specific amino acid to the ribosome to add to the elongating peptide chains.
A nucleoside diphosphate sugar which can be epimerized into UDPglucose for entry into the mainstream of carbohydrate metabolism. Serves as a source of galactose in the synthesis of lipopolysaccharides, cerebrosides, and lactose.
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.
Enzymes that catalyze the template-directed incorporation of ribonucleotides into an RNA chain. EC 2.7.7.-.
The addition of an organic acid radical into a molecule.
A group of derivatives of naphthyridine carboxylic acid, quinoline carboxylic acid, or NALIDIXIC ACID.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9.
An enzyme that catalyzes the transfer of a methyl group from S-adenosylmethionine to histamine, forming N-methylhistamine, the major metabolite of histamine in man. EC 2.1.1.8.
A nucleoside diphosphate sugar which can be converted to the deoxy sugar GDPfucose, which provides fucose for lipopolysaccharides of bacterial cell walls. Also acts as mannose donor for glycolipid synthesis.
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.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
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.
A set of genes descended by duplication and variation from some ancestral gene. Such genes may be clustered together on the same chromosome or dispersed on different chromosomes. Examples of multigene families include those that encode the hemoglobins, immunoglobulins, histocompatibility antigens, actins, tubulins, keratins, collagens, heat shock proteins, salivary glue proteins, chorion proteins, cuticle proteins, yolk proteins, and phaseolins, as well as histones, ribosomal RNA, and transfer RNA genes. The latter three are examples of reiterated genes, where hundreds of identical genes are present in a tandem array. (King & Stanfield, A Dictionary of Genetics, 4th ed)
Enzymes catalyzing the transfer of fucose from a nucleoside diphosphate fucose to an acceptor molecule which is frequently another carbohydrate, a glycoprotein, or a glycolipid molecule. Elevated activity of some fucosyltransferases in human serum may serve as an indicator of malignancy. The class includes EC 2.4.1.65; EC 2.4.1.68; EC 2.4.1.69; EC 2.4.1.89.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
5'-Uridylic acid. A uracil nucleotide containing one phosphate group esterified to the sugar moiety in the 2', 3' or 5' position.
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
The sole species of the genus Oxalobacter consisting of straight or curved gram-negative rods with rounded ends. Cells are nonmotile, nonsporing, and use oxylates as the only source of CARBON and energy, with formate and CARBON DIOXIDE as end products. They are isolated from lake sediments and from the rumen or large bowel of humans and animals. (From Bergey's Manual of Determinative Bacteriology, 9th ed)
S-Acyl coenzyme A. Fatty acid coenzyme A derivatives that are involved in the biosynthesis and oxidation of fatty acids as well as in ceramide formation.
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.
An enzyme that catalyzes the transfer of the propylamine moiety from 5'-deoxy-5'-S-(3-methylthiopropylamine)sulfonium adenosine to putrescine in the biosynthesis of spermidine. The enzyme has a molecular weight of approximately 73,000 kDa and is composed of two subunits of equal size.
The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).
Single-stranded complementary DNA synthesized from an RNA template by the action of RNA-dependent DNA polymerase. cDNA (i.e., complementary DNA, not circular DNA, not C-DNA) is used in a variety of molecular cloning experiments as well as serving as a specific hybridization probe.
Eicosamethyl octacontanonadecasen-1-o1. Polyprenol found in animal tissues that contains about 20 isoprene residues, the one carrying the alcohol group being saturated.
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.
Organic compounds that generally contain an amino (-NH2) and a carboxyl (-COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
A sequence of amino acids in a polypeptide or of nucleotides in DNA or RNA that is similar across multiple species. A known set of conserved sequences is represented by a CONSENSUS SEQUENCE. AMINO ACID MOTIFS are often composed of conserved sequences.
A coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). (Dorland, 27th ed)
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
An enzyme that catalyzes the conversion of L-alanine and 2-oxoglutarate to pyruvate and L-glutamate. (From Enzyme Nomenclature, 1992) EC 2.6.1.2.
Acetyl CoA participates in the biosynthesis of fatty acids and sterols, in the oxidation of fatty acids and in the metabolism of many amino acids. It also acts as a biological acetylating agent.
The extent to which an enzyme retains its structural conformation or its activity when subjected to storage, isolation, and purification or various other physical or chemical manipulations, including proteolytic enzymes and heat.
A chromatographic technique that utilizes the ability of biological molecules to bind to certain ligands specifically and reversibly. It is used in protein biochemistry. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
A thiol-containing non-essential amino acid that is oxidized to form CYSTINE.
A bile pigment that is a degradation product of HEME.
Separation technique in which the stationary phase consists of ion exchange resins. The resins contain loosely held small ions that easily exchange places with other small ions of like charge present in solutions washed over the resins.
Hydroxycinnamic acid and its derivatives. Act as activators of the indoleacetic acid oxidizing system, thereby producing a decrease in the endogenous level of bound indoleacetic acid in plants.
An analytical method used in determining the identity of a chemical based on its mass using mass analyzers/mass spectrometers.
A species of gram-negative, aerobic bacteria that is found in soil and which causes formation of root nodules on some, but not all, types of field pea, lentil, kidney bean, and clover.
An antibiotic produced by Streptomyces lincolnensis var. lincolnensis. It has been used in the treatment of staphylococcal, streptococcal, and Bacteroides fragilis infections.
The characteristic 3-dimensional shape of a carbohydrate.
An ester formed between the aldehydic carbon of RIBOSE and the terminal phosphate of ADENOSINE DIPHOSPHATE. It is produced by the hydrolysis of nicotinamide-adenine dinucleotide (NAD) by a variety of enzymes, some of which transfer an ADP-ribosyl group to target proteins.
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.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
A hexosaminidase specific for non-reducing N-acetyl-D-hexosamine residues in N-acetyl-beta-D-hexosaminides. It acts on GLUCOSIDES; GALACTOSIDES; and several OLIGOSACCHARIDES. Two specific mammalian isoenzymes of beta-N-acetylhexoaminidase are referred to as HEXOSAMINIDASE A and HEXOSAMINIDASE B. Deficiency of the type A isoenzyme causes TAY-SACHS DISEASE, while deficiency of both A and B isozymes causes SANDHOFF DISEASE. The enzyme has also been used as a tumor marker to distinguish between malignant and benign disease.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
An intermediate in the pathway of coenzyme A formation in mammalian liver and some microorganisms.
The facilitation of biochemical reactions with the aid of naturally occurring catalysts such as ENZYMES.
A stack of flattened vesicles that functions in posttranslational processing and sorting of proteins, receiving them from the rough ENDOPLASMIC RETICULUM and directing them to secretory vesicles, LYSOSOMES, or the CELL MEMBRANE. The movement of proteins takes place by transfer vesicles that bud off from the rough endoplasmic reticulum or Golgi apparatus and fuse with the Golgi, lysosomes or cell membrane. (From Glick, Glossary of Biochemistry and Molecular Biology, 1990)
The restriction of a characteristic behavior, anatomical structure or physical system, such as immune response; metabolic response, or gene or gene variant to the members of one species. It refers to that property which differentiates one species from another but it is also used for phylogenetic levels higher or lower than the species.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
Phosphoric acid esters of dolichol.
A drug-metabolizing, cytochrome P-450 enzyme which catalyzes the hydroxylation of aniline to hydroxyaniline in the presence of reduced flavoprotein and molecular oxygen. EC 1.14.14.-.
Mixture of 2- and 3-tert-butyl-4-methoxyphenols that is used as an antioxidant in foods, cosmetics, and pharmaceuticals.
Enzymes that catalyze the synthesis of FATTY ACIDS from acetyl-CoA and malonyl-CoA derivatives.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
Elements of limited time intervals, contributing to particular results or situations.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
A compound that inhibits symport of sodium, potassium, and chloride primarily in the ascending limb of Henle, but also in the proximal and distal tubules. This pharmacological action results in excretion of these ions, increased urinary output, and reduction in extracellular fluid. This compound has been classified as a loop or high ceiling diuretic.
An enzyme that catalyzes reversibly the conversion of palmitoyl-CoA to palmitoylcarnitine in the inner mitochondrial membrane. EC 2.3.1.21.
An enzyme that catalyzes the formation of acetoacetyl-CoA from two molecules of ACETYL COA. Some enzymes called thiolase or thiolase-I have referred to this activity or to the activity of ACETYL-COA C-ACYLTRANSFERASE.
Chromatography on thin layers of adsorbents rather than in columns. The adsorbent can be alumina, silica gel, silicates, charcoals, or cellulose. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Infection of ruminants with tapeworms of the genus Moniezia.
A genus of green nonsulfur bacteria in the family Chloroflexaceae. They are photosynthetic, thermophilic, filamentous gliding bacteria found in hot springs.
The major human blood type system which depends on the presence or absence of two antigens A and B. Type O occurs when neither A nor B is present and AB when both are present. A and B are genetic factors that determine the presence of enzymes for the synthesis of certain glycoproteins mainly in the red cell membrane.
Unsaturated hydrocarbons of the type Cn-H2n, indicated by the suffix -ene. (Grant & Hackh's Chemical Dictionary, 5th ed, p408)
A sulfur-containing essential L-amino acid that is important in many body functions.
Lipid A is the biologically active component of lipopolysaccharides. It shows strong endotoxic activity and exhibits immunogenic properties.
A flavoprotein that reversibly catalyzes the oxidation of NADH or NADPH by various quinones and oxidation-reduction dyes. The enzyme is inhibited by dicoumarol, capsaicin, and caffeine.
A species of the true toads, Bufonidae, widely distributed in the United States and Europe.
A single, unpaired primary lymphoid organ situated in the MEDIASTINUM, extending superiorly into the neck to the lower edge of the THYROID GLAND and inferiorly to the fourth costal cartilage. It is necessary for normal development of immunologic function early in life. By puberty, it begins to involute and much of the tissue is replaced by fat.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Compounds containing the -SH radical.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
Proteins obtained from ESCHERICHIA COLI.
Genus of coniferous yew trees or shrubs, several species of which have medicinal uses. Notable is the Pacific yew, Taxus brevifolia, which is used to make the anti-neoplastic drug taxol (PACLITAXEL).
The biosynthesis of PEPTIDES and PROTEINS on RIBOSOMES, directed by MESSENGER RNA, via TRANSFER RNA that is charged with standard proteinogenic AMINO ACIDS.

The Saccharomyces cerevisiae CWH8 gene is required for full levels of dolichol-linked oligosaccharides in the endoplasmic reticulum and for efficient N-glycosylation. (1/1662)

The Saccharomyces cerevisiae mutant cwh8 was previously found to have an anomalous cell wall. Here we show that the cwh8 mutant has an N -glycosylation defect. We found that cwh8 cells were resistant to vanadate and sensitive to hygromycin B, and produced glycoforms of invertase and carboxypeptidase Y with a reduced number of N -chains. We have cloned the CWH8 gene. We found that it was nonessential and encoded a putative transmembrane protein of 239 amino acids. Comparison of the in vitro oligosaccharyl transferase activities of membrane preparations from wild type or cwh8 Delta cells revealed no differences in enzyme kinetic properties indicating that the oligosaccharyl transferase complex of mutant cells was not affected. cwh8 Delta cells also produced normal dolichols and dolichol-linked oligosaccharide intermediates including the full-length form Glc3Man9GlcNAc2. The level of dolichol-linked oligosaccharides in cwh8 Delta cells was, however, reduced to about 20% of the wild type. We propose that inefficient N -glycosylation of secretory proteins in cwh8 Delta cells is caused by an insufficient supply of dolichol-linked oligosaccharide substrate.  (+info)

Isolation and characterization of two mouse L cell lines resistant to the toxic lectin ricin. (2/1662)

Two variant mouse L cell lines (termed CL 3 and CL 6) have been selected for resistant to ricin, a galactose-binding lectin with potent cytotoxic activity. The resistant lines exhibit a 50 to 70% decrease in ricin binding and a 300- to 500-fold increase in resistance to the toxic effects of ricin. Crude membrane preparations of CL 3 cells have increased sialic acid content (200% of control), while the galactose, mannose, and hexosamine content is within normal limits. Both the glycoproteins and glycolipids of CL 3 cells have increased sialic acid, with the GM3:lactosylceramide ratios for parent L and CL 3 cells being 0.29 and 1.5, respectively. In contrast, the membranes of CL 6 cells have a decrease in sialic acid, galactose, and hexosamine content with mannose being normal. Both cell lines have specific alterations in glycosyltransferase activities which can account for the observed membrane sugar changes. CL 3 cells have increased CMP-sialic acid:glycoprotein sialyltransferase and GM3 synthetase activities, while CL 6 cells have decrease UDP-GlcNAc:glycoproteinN-acetylglucosaminyltransferase and DPU-galactose:glycoprotein galactosyltransferase activities. The increased sialic acid content of CL 3 cells serves to mask ricin binding sites, since neuraminidase treatment of this cell line restores ricin binding to essentially normal levels. However, the fact that neuraminidase-treated CL 3 cells are still 45-fold resistant to ricin indicates that either a special class of productive ricin binding sites is not being exposed or that the cell line has a second mechanism for ricin resistance.  (+info)

Hyaluronan synthase expression in bovine eyes. (3/1662)

PURPOSE: Hyaluronan (HA), a high-molecular-weight linear glycosaminoglycan, is a component of the extracellular matrix (ECM). It is expressed in eyes and plays important roles in many biologic processes, including cell migration, proliferation, and differentiation. Hyaluronan is produced by HA synthase (HAS), which has three isoforms: HAS1, HAS2, and HAS3. In this study, the HAS expression in the anterior segment of bovine eyes was investigated to determine the significance of HA in eyes. METHODS: To obtain bovine HAS probes, degenerate oligonucleotide primers, based on well-conserved amino acid sequences including the catalytic region of each HAS isoform, were used for reverse transcription-polymerase chain reaction to amplify mRNA from bovine corneal endothelial cells (BCECs). Hyaluronan synthase-1 expression in the anterior segment of bovine eyes at the protein level was investigated by immunohistochemistry. RESULTS: All three HAS isoforms were expressed in BCECs at the mRNA level. Amplified cDNA fragments of HAS1, HAS2, and HAS3 from BCECs can be aligned to human counterparts, showing similarities of 100%, 97.3%, and 100%, respectively, at the amino acid level. Hyaluronan synthase 1 was expressed at the protein level in corneal epithelium, keratocyte, corneal endothelium, conjunctival epithelium, ciliary epithelium, capillary endothelium, and trabecular meshwork. CONCLUSIONS: Hyaluronan synthase isoforms were expressed in the ocular anterior segment and are speculated to be involved in HA production in situ.  (+info)

Behavior of transaldolase (EC 2.2.1.2) and transketolase (EC 2.2.1.1) Activities in normal, neoplastic, differentiating, and regenerating liver. (4/1662)

The objective of this investigation was to throw light on the biological behavior and metabolic regulation of hepatic enzymes of the nonoxidative branch of the pentose phosphate pathway. The activities of transaldolase (EC 2.2.1.2) and trasketolase (EC 2.2.1.1) Were compared in biological conditions that involve modulation of gene expression such as in starvation, in differentiation, after partial hepatectomy, and in a spectrum of hepatomas of different growth rates. The enzyme activities were determined under optimal kinetic conditions by spectrophotometric methods in the 100,000 X g supernatant fluids prepared from tissue homogenates. The kinetic properties of transaldolase and transketolase were similar in normal liver and in rapidly growing hepatoma 3924A. For transaldolase, apparent Km values of 0.13 mM (normal liver) and 0.17 mM (hepatoma) were observed for erythrose 4-phosphate and of 0.30 to 0.35 mM for fructose 6-phosphate. The pH optima in liver and hepatoma were at approximately 6.9 to 7.2. For the transketolase substrates, ribose 5-phosphate and xylulose 5-phosphate, the apparent Km values were 0.3 and 0.5 mM, respectively, in both liver and hepatoma. A broad pH optimum around 7.6 was observed in both tissues. In organ distribution studies, enzyme activities were measured in liver, intestinal mucosa, thymus, kidney, spleen, brain, adipose tissue, lung, heart, and skeletal muscle. Taking the specific activity of liver as 100%, transaldolase activity was the highest in intestinal mucosa (316%) and in thymus (219%); it was the lowest in heart (53%) and in skeletal muscle (21%). Transketolase activity was highest in kidney (155%) and lowest in heart (26%) and skeletal muscle (23%). Starvation decreased transaldolase and transketolase activities in 6 days to 69 and 74%, respectively, of those of the liver of the normal, fed rat. This was in the same range as the decrease in the protein concentration (66%y. In the liver tumors, transaldolase activity was increased 1.5- to 3.4-fold over the activities observed in normal control rat liver. Transketolase activity showed no relationship to tumor proliferation rate. In the regenerating liver at 24 hr after partial hepatectomy, the activity of both pentose phosphate pathway enzymes was in the same range as that of the sham-operated controls. In differentiation at the postnatal age of 5, 12, 23, and 32 days, hepatic transaldolase activities were 33, 44, 55, and 72%, respectively, of the activities observed in the 60-day-old, adult male rat. During the same period, transketolase activ-ties were 18, 21, 26, and 55% of the activities observed in liver of adult rat. The demonstration of increased transaldolase activity in hepatomas, irrespective of the degree of tumor malignancy, differentiation, or growth rate, suggests that the reprogramming of gene expression in malignant transformation is linked with an increase in the expression of this pentose phosphate pathway enzyme...  (+info)

A 20-kDa domain is required for phosphatidic acid-induced allosteric activation of phospholipase D from Streptomyces chromofuscus. (5/1662)

Two phospholipase D (PLD) enzymes with both hydrolase and transferase activities were isolated from Streptomyces chromofuscus. There were substantial differences in the kinetic properties of the two PLD enzymes towards monomeric, micellar, and vesicle substrates. The most striking difference was that the higher molecular weight enzyme (PLD57 approximately 57 kDa) could be activated allosterically with a low mole fraction of phosphatidic acid (PA) incorporated into a PC bilayer (Geng et al., J. Biol. Chem. 273 (1998) 12195-12202). PLD42/20, a tightly associated complex of two peptides, one of 42 kDa and the other 20 kDa, had a 4-6-fold higher Vmax toward PC substrates than PLD57 and was not activated by PA. N-Terminal sequencing of both enzymes indicated that both components of PLD42/20 were cleavage products of PLD57. The larger component included the N-terminal segment of PLD57 and contained the active site. The N-terminus of the smaller peptide corresponded to the C-terminal region of PLD57; this peptide had no PLD activity by itself. Increasing the pH of PLD42/20 to 8.9, followed by chromatography of PLD42/20 on a HiTrap Q column at pH 8.5 separated the 42- and 20-kDa proteins. The 42-kDa complex had about the same specific activity with or without the 20-kDa fragment. The lack of PA activation for the 42-kDa protein and for PLD42/20 indicates that an intact C-terminal region of PLD57 is necessary for activation by PA. Furthermore, the mechanism for transmission of the allosteric signal requires an intact PLD57.  (+info)

Serine transhydroxymethylase from rabbit liver. Sequence of anonapeptide at the pyridoxal-5'-phosphate-binding site. (6/1662)

The amino acid sequence of the coenzyme-binding site of serine transhydroxymethylase from rabbit liver has been determined. After reduction with NaBH4 and aminoethylation, a first sample of enzyme was digested with thermolysin and a single phosphopyridoxyl peptide was isolated. A second sample of similarly treated enzyme was digested with chymotrypsin and three phosphopyridoxyl peptides clearly originating from a unique coenzyme-binding site were isolated. Sequence analysis of these peptides indicate the following structure: Val-Val-Thr-Thr-His(Pxy)-Thr-Leu. Sequence homologies of the active site of various pyridoxalphosphate enzymes are discussed in terms of a possible catalytic role and of evolution of this class of proteins.  (+info)

Bordetella pertussis waaA encodes a monofunctional 2-keto-3-deoxy-D-manno-octulosonic acid transferase that can complement an Escherichia coli waaA mutation. (7/1662)

Bordetella pertussis lipopolysaccharide (LPS) contains a single 2-keto-3-deoxy-D-manno-octulosonic acid (Kdo) residue, whereas LPS from Escherichia coli contains at least two. Here we report that B. pertussis waaA encodes an enzyme capable of transferring only a single Kdo during the biosynthesis of LPS and that this activity is sufficient to complement an E. coli waaA mutation.  (+info)

Expression of prokaryotic 1-deoxy-D-xylulose-5-phosphatases in Escherichia coli increases carotenoid and ubiquinone biosynthesis. (8/1662)

Isopentenyl diphosphate (IPP) acts as the common, five-carbon building block in the biosynthesis of all isoprenoids. The first reaction of IPP biosynthesis in Escherichia coli is the formation of 1-deoxy-D-xylulose-5-phosphate, catalysed by 1-deoxy-D-xylulose-5-phosphate synthase (DXPS). E. coli engineered to produce lycopene, was transformed with dxps genes cloned from Bacillus subtilis and Synechocystis sp. 6803. Increases in lycopene levels were observed in strains expressing exogenous DXPS compared to controls. The recombinant strains also exhibited elevated levels of ubiquinone-8. These increases corresponded with enhanced DXP synthase activity in the recombinant E. coli strains.  (+info)

There are two main types of galactosemia:

1. Classical galactosemia: This is the most severe form of the disorder, and it is characterized by a complete lack of the enzyme galactose-1-phosphate uridylyltransferase (GALT). Without GALT, galactose builds up in the blood and tissues, leading to serious health problems.
2. Dialectical galactosemia: This form of the disorder is less severe than classical galactosemia, and it is characterized by a partial deficiency of GALT. People with dialectical galactosemia may experience some symptoms, but they are typically milder than those experienced by people with classical galactosemia.

Symptoms of galactosemia can include:

* Diarrhea
* Vomiting
* Jaundice (yellowing of the skin and eyes)
* Fatigue
* Poor feeding in infants
* Developmental delays

If left untreated, galactosemia can lead to a range of complications, including:

* Liver disease
* Kidney disease
* Increased risk of infections
* Delayed growth and development

The diagnosis of galactosemia is typically made through a combination of physical examination, medical history, and laboratory tests. Treatment for the disorder typically involves a strict diet that limits or eliminates galactose-containing foods, such as milk and other dairy products. In some cases, medication may also be prescribed to help manage symptoms.

Overall, early diagnosis and treatment of galactosemia are important for preventing or minimizing the risk of complications associated with this condition.

Term: Lesch-Nyhan Syndrome

Definition: A rare X-linked recessive genetic disorder caused by mutations in the HPRT1 gene, resulting in an impaired ability to metabolize uric acid and leading to symptoms such as gout, kidney stones, and other complications.

Etymology: Named after the physicians who first described the condition, Lesch and Nyhan.

Incidence: Approximately 1 in 165,000 male births.

Prevalence: Estimated to affect approximately 1 in 23,000 males worldwide.

Causes: Mutations in the HPRT1 gene, which codes for the enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT). This enzyme is involved in the metabolism of uric acid.

Symptoms: Gout attacks, kidney stones, joint pain and swelling, urate nephropathy (kidney damage), and other complications.

Diagnosis: Diagnosed through a combination of clinical evaluation, laboratory tests such as blood and urine analysis, and genetic testing to identify HPRT1 gene mutations.

Treatment: Medications to reduce uric acid levels, such as allopurinol or rasburicase, and management of symptoms such as pain and inflammation with nonsteroidal anti-inflammatory drugs (NSAIDs) or colchicine.

Prognosis: The condition is usually diagnosed in childhood, and patients often have a normal life expectancy if properly managed. However, untreated or poorly managed hyperuricemia can lead to complications such as kidney damage and cardiovascular disease.

Inheritance pattern: Autosomal recessive inheritance pattern, meaning that the individual must inherit two copies of the mutated HPRT1 gene (one from each parent) in order to develop the condition.

Other names: Hyperuricemia, gout, Lesch-Nyhan syndrome.

The two main types of lymphoid leukemia are:

1. Acute Lymphoblastic Leukemia (ALL): This type of leukemia is most commonly seen in children, but it can also occur in adults. It is characterized by a rapid increase in the number of immature white blood cells in the blood and bone marrow.
2. Chronic Lymphocytic Leukemia (CLL): This type of leukemia usually affects older adults and is characterized by the gradual buildup of abnormal white blood cells in the blood, bone marrow, and lymph nodes.

Symptoms of lymphoid leukemia include fatigue, fever, night sweats, weight loss, and swollen lymph nodes. Treatment options for lymphoid leukemia can vary depending on the type of cancer and the severity of symptoms, but may include chemotherapy, radiation therapy, or bone marrow transplantation.

Diagnosis of monieziasis typically involves a combination of physical examination, medical history, and laboratory tests such as fecal examination or endoscopy. Treatment typically involves the use of anthelmintic medications to kill the parasites, and supportive care to manage symptoms such as pain and diarrhea. In severe cases, hospitalization may be necessary to monitor and treat complications.

Prevention of monieziasis primarily involves good hygiene practices such as washing hands before eating or preparing food, avoiding close contact with individuals who have the infection, and avoiding consumption of undercooked or raw meat. In areas where the parasite is common, regular deworming programs can also help to reduce the risk of infection.

The prognosis for monieziasis is generally good if treatment is prompt and effective. However, complications such as intestinal obstruction, perforation, or abscesses can occur if left untreated, and can be life-threatening. It is important to seek medical attention if symptoms persist or worsen over time.

Overall, monieziasis is a rare but potentially serious condition that requires prompt diagnosis and treatment to prevent complications and ensure a good outcome.

Examples of experimental liver neoplasms include:

1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and can be induced experimentally by injecting carcinogens such as diethylnitrosamine (DEN) or dimethylbenz(a)anthracene (DMBA) into the liver tissue of animals.
2. Cholangiocarcinoma: This type of cancer originates in the bile ducts within the liver and can be induced experimentally by injecting chemical carcinogens such as DEN or DMBA into the bile ducts of animals.
3. Hepatoblastoma: This is a rare type of liver cancer that primarily affects children and can be induced experimentally by administering chemotherapy drugs to newborn mice or rats.
4. Metastatic tumors: These are tumors that originate in other parts of the body and spread to the liver through the bloodstream or lymphatic system. Experimental models of metastatic tumors can be studied by injecting cancer cells into the liver tissue of animals.

The study of experimental liver neoplasms is important for understanding the underlying mechanisms of liver cancer development and progression, as well as identifying potential therapeutic targets for the treatment of this disease. Animal models can be used to test the efficacy of new drugs or therapies before they are tested in humans, which can help to accelerate the development of new treatments for liver cancer.

Crigler-Najjar syndrome is a rare genetic disorder that affects the liver and causes it to be unable to break down bilirubin, a yellow pigment found in the blood. This results in a buildup of bilirubin in the blood and can lead to jaundice, which is characterized by a yellowish tint to the skin and whites of the eyes.

There are two types of Crigler-Najjar syndrome: type 1 and type 2. Type 1 is caused by a deficiency of the enzyme glucuronyltransferase, which is necessary for the breakdown of bilirubin. Type 2 is caused by a deficiency of the enzyme UDP-glucuronosyltransferase. Both types can be inherited from one's parents or can be acquired through mutations that occur spontaneously.

Symptoms of Crigler-Najjar syndrome include jaundice, yellowing of the skin and whites of the eyes, dark urine, itching all over the body, and a higher risk of liver disease. Treatment for Crigler-Najjar syndrome typically involves managing the symptoms and preventing complications. This may include phototherapy to help break down bilirubin, medications to reduce jaundice, and careful monitoring of the liver function. In severe cases, a liver transplant may be necessary.

Overall, Crigler-Najjar syndrome is a rare and potentially serious genetic disorder that affects the liver's ability to break down bilirubin. With proper management and care, individuals with this condition can lead relatively normal lives.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

There are several different types of leukemia, including:

1. Acute Lymphoblastic Leukemia (ALL): This is the most common type of leukemia in children, but it can also occur in adults. It is characterized by an overproduction of immature white blood cells called lymphoblasts.
2. Acute Myeloid Leukemia (AML): This type of leukemia affects the bone marrow's ability to produce red blood cells, platelets, and other white blood cells. It can occur at any age but is most common in adults.
3. Chronic Lymphocytic Leukemia (CLL): This type of leukemia affects older adults and is characterized by the slow growth of abnormal white blood cells called lymphocytes.
4. Chronic Myeloid Leukemia (CML): This type of leukemia is caused by a genetic mutation in a gene called BCR-ABL. It can occur at any age but is most common in adults.
5. Hairy Cell Leukemia: This is a rare type of leukemia that affects older adults and is characterized by the presence of abnormal white blood cells called hairy cells.
6. Myelodysplastic Syndrome (MDS): This is a group of disorders that occur when the bone marrow is unable to produce healthy blood cells. It can lead to leukemia if left untreated.

Treatment for leukemia depends on the type and severity of the disease, but may include chemotherapy, radiation therapy, targeted therapy, or stem cell transplantation.

Symptoms of OCTD typically appear during infancy and may include seizures, developmental delays, poor muscle tone, and abnormal brain activity (as detected by electroencephalogram (EEG)). Without treatment, OCTD can lead to serious health complications such as stroke, intellectual disability, and death. Treatment involves a strict diet that limits protein intake and supplementation with essential nutrients to support growth and development.

OCTD is usually diagnosed by measuring the activity of OCT enzyme in white blood cells or using genetic testing to identify mutations in the OCTD1 gene. Treatment options for OCTD are limited, but early detection and proper management can significantly improve outcomes for affected individuals.

There are several types of ketosis, including:

1. Nutritional ketosis: This is the most common type of ketosis and is achieved through a low-carb diet.
2. Therapeutic ketosis: This type of ketosis is used to treat medical conditions such as epilepsy, type 2 diabetes, and Alzheimer's disease.
3. Exogenous ketosis: This type of ketosis is achieved through the use of supplements that stimulate ketone production, such as ketone esters or medium-chain triglycerides (MCTs).
4. Endogenous ketosis: This type of ketosis is achieved through fasting or a very low-carb diet and is characterized by the body's natural production of ketones.

The benefits of ketosis include weight loss, improved blood sugar control, increased energy levels, and reduced inflammation. However, it can also have some drawbacks such as constipation, bad breath, and muscle cramps. It is important to consult a healthcare professional before starting any type of ketosis plan, especially if you have any underlying medical conditions.

The definition of DILI has been revised several times over the years, but the most recent definition was published in 2013 by the International Consortium for DILI Research (ICDCR). According to this definition, DILI is defined as:

"A clinically significant alteration in liver function that is caused by a medication or other exogenous substance, and is not related to underlying liver disease. The alteration may be biochemical, morphological, or both, and may be acute or chronic."

The ICDCR definition includes several key features of DILI, including:

1. Clinically significant alteration in liver function: This means that the liver damage must be severe enough to cause symptoms or signs of liver dysfunction, such as jaundice, nausea, vomiting, or abdominal pain.
2. Caused by a medication or other exogenous substance: DILI is triggered by exposure to certain drugs or substances that are not related to underlying liver disease.
3. Not related to underlying liver disease: This means that the liver damage must not be caused by an underlying condition such as hepatitis B or C, alcoholic liver disease, or other genetic or metabolic disorders.
4. May be acute or chronic: DILI can occur as a sudden and severe injury (acute DILI) or as a slower and more insidious process (chronic DILI).

The ICDCR definition provides a standardized way of defining and diagnosing DILI, which is important for clinicians and researchers to better understand the cause of liver damage in patients who are taking medications. It also helps to identify the drugs or substances that are most likely to cause liver injury and to develop strategies for preventing or treating DILI.

Myeloid leukemia can be classified into several subtypes based on the type of cell involved and the degree of maturity of the abnormal cells. The most common types of myeloid leukemia include:

1. Acute Myeloid Leukemia (AML): This is the most aggressive form of myeloid leukemia, characterized by a rapid progression of immature cells that do not mature or differentiate into normal cells. AML can be further divided into several subtypes based on the presence of certain genetic mutations or chromosomal abnormalities.
2. Chronic Myeloid Leukemia (CML): This is a slower-growing form of myeloid leukemia, characterized by the presence of a genetic abnormality known as the Philadelphia chromosome. CML is typically treated with targeted therapies or bone marrow transplantation.
3. Myelodysplastic Syndrome (MDS): This is a group of disorders characterized by the impaired development of immature blood cells in the bone marrow. MDS can progress to AML if left untreated.
4. Chronic Myelomonocytic Leukemia (CMML): This is a rare form of myeloid leukemia that is characterized by the accumulation of immature monocytes in the blood and bone marrow. CMML can be treated with chemotherapy or bone marrow transplantation.

The symptoms of myeloid leukemia can vary depending on the subtype and severity of the disease. Common symptoms include fatigue, weakness, fever, night sweats, and weight loss. Diagnosis is typically made through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment options for myeloid leukemia can include chemotherapy, targeted therapies, bone marrow transplantation, and supportive care to manage symptoms and prevent complications. The prognosis for myeloid leukemia varies depending on the subtype of the disease and the patient's overall health. With current treatments, many patients with myeloid leukemia can achieve long-term remission or even be cured.

There are many different types of liver diseases, including:

1. Alcoholic liver disease (ALD): A condition caused by excessive alcohol consumption that can lead to inflammation, scarring, and cirrhosis.
2. Viral hepatitis: Hepatitis A, B, and C are viral infections that can cause inflammation and damage to the liver.
3. Non-alcoholic fatty liver disease (NAFLD): A condition where there is an accumulation of fat in the liver, which can lead to inflammation and scarring.
4. Cirrhosis: A condition where the liver becomes scarred and cannot function properly.
5. Hemochromatosis: A genetic disorder that causes the body to absorb too much iron, which can damage the liver and other organs.
6. Wilson's disease: A rare genetic disorder that causes copper to accumulate in the liver and brain, leading to damage and scarring.
7. Liver cancer (hepatocellular carcinoma): Cancer that develops in the liver, often as a result of cirrhosis or viral hepatitis.

Symptoms of liver disease can include fatigue, loss of appetite, nausea, abdominal pain, dark urine, pale stools, and swelling in the legs. Treatment options for liver disease depend on the underlying cause and may include lifestyle changes, medication, or surgery. In severe cases, a liver transplant may be necessary.

Prevention of liver disease includes maintaining a healthy diet and lifestyle, avoiding excessive alcohol consumption, getting vaccinated against hepatitis A and B, and managing underlying medical conditions such as obesity and diabetes. Early detection and treatment of liver disease can help to prevent long-term damage and improve outcomes for patients.

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.

Liver neoplasms, also known as liver tumors or hepatic tumors, are abnormal growths of tissue in the liver. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant liver tumors can be primary, meaning they originate in the liver, or metastatic, meaning they spread to the liver from another part of the body.

There are several types of liver neoplasms, including:

1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and arises from the main cells of the liver (hepatocytes). HCC is often associated with cirrhosis and can be caused by viral hepatitis or alcohol abuse.
2. Cholangiocarcinoma: This type of cancer arises from the cells lining the bile ducts within the liver (cholangiocytes). Cholangiocarcinoma is rare and often diagnosed at an advanced stage.
3. Hemangiosarcoma: This is a rare type of cancer that originates in the blood vessels of the liver. It is most commonly seen in dogs but can also occur in humans.
4. Fibromas: These are benign tumors that arise from the connective tissue of the liver (fibrocytes). Fibromas are usually small and do not spread to other parts of the body.
5. Adenomas: These are benign tumors that arise from the glandular cells of the liver (hepatocytes). Adenomas are usually small and do not spread to other parts of the body.

The symptoms of liver neoplasms vary depending on their size, location, and whether they are benign or malignant. Common symptoms include abdominal pain, fatigue, weight loss, and jaundice (yellowing of the skin and eyes). Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and ultrasound, and a biopsy to confirm the presence of cancer cells.

Treatment options for liver neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery may be an option for some patients with small, localized tumors, while others may require chemotherapy or radiation therapy to shrink the tumor before surgery can be performed. In some cases, liver transplantation may be necessary.

Prognosis for liver neoplasms varies depending on the type and stage of the cancer. In general, early detection and treatment improve the prognosis, while advanced-stage disease is associated with a poorer prognosis.

AML is a fast-growing and aggressive form of leukemia that can spread to other parts of the body through the bloodstream. It is most commonly seen in adults over the age of 60, but it can also occur in children.

There are several subtypes of AML, including:

1. Acute promyelocytic leukemia (APL): This is a subtype of AML that is characterized by the presence of a specific genetic abnormality called the PML-RARA fusion gene. It is usually responsive to treatment with chemotherapy and has a good prognosis.
2. Acute myeloid leukemia, not otherwise specified (NOS): This is the most common subtype of AML and does not have any specific genetic abnormalities. It can be more difficult to treat and has a poorer prognosis than other subtypes.
3. Chronic myelomonocytic leukemia (CMML): This is a subtype of AML that is characterized by the presence of too many immature white blood cells called monocytes in the blood and bone marrow. It can progress slowly over time and may require ongoing treatment.
4. Juvenile myeloid leukemia (JMML): This is a rare subtype of AML that occurs in children under the age of 18. It is characterized by the presence of too many immature white blood cells called blasts in the blood and bone marrow.

The symptoms of AML can vary depending on the subtype and the severity of the disease, but they may include:

* Fatigue
* Weakness
* Shortness of breath
* Pale skin
* Easy bruising or bleeding
* Swollen lymph nodes, liver, or spleen
* Bone pain
* Headache
* Confusion or seizures

AML is diagnosed through a combination of physical examination, medical history, and diagnostic tests such as:

1. Complete blood count (CBC): This test measures the number and types of cells in the blood, including red blood cells, white blood cells, and platelets.
2. Bone marrow biopsy: This test involves removing a small sample of bone marrow tissue from the hipbone or breastbone to examine under a microscope for signs of leukemia cells.
3. Genetic testing: This test can help identify specific genetic abnormalities that are associated with AML.
4. Immunophenotyping: This test uses antibodies to identify the surface proteins on leukemia cells, which can help diagnose the subtype of AML.
5. Cytogenetics: This test involves staining the bone marrow cells with dyes to look for specific changes in the chromosomes that are associated with AML.

Treatment for AML typically involves a combination of chemotherapy, targeted therapy, and in some cases, bone marrow transplantation. The specific treatment plan will depend on the subtype of AML, the patient's age and overall health, and other factors. Some common treatments for AML include:

1. Chemotherapy: This involves using drugs to kill cancer cells. The most commonly used chemotherapy drugs for AML are cytarabine (Ara-C) and anthracyclines such as daunorubicin (DaunoXome) and idarubicin (Idamycin).
2. Targeted therapy: This involves using drugs that specifically target the genetic abnormalities that are causing the cancer. Examples of targeted therapies used for AML include midostaurin (Rydapt) and gilteritinib (Xospata).
3. Bone marrow transplantation: This involves replacing the diseased bone marrow with healthy bone marrow from a donor. This is typically done after high-dose chemotherapy to destroy the cancer cells.
4. Supportive care: This includes treatments to manage symptoms and side effects of the disease and its treatment, such as anemia, infection, and bleeding. Examples of supportive care for AML include blood transfusions, antibiotics, and platelet transfusions.
5. Clinical trials: These are research studies that involve testing new treatments for AML. Participating in a clinical trial may give patients access to innovative therapies that are not yet widely available.

It's important to note that the treatment plan for AML is highly individualized, and the specific treatments used will depend on the patient's age, overall health, and other factors. Patients should work closely with their healthcare team to determine the best course of treatment for their specific needs.

There are several possible causes of hyperbilirubinemia, including:

1. Hemolytic anemia: This is a condition where red blood cells are broken down faster than they can be replaced, leading to an accumulation of bilirubin in the blood.
2. Liver dysfunction: The liver plays a crucial role in processing and eliminating bilirubin from the body. If the liver is not functioning properly, bilirubin levels can become elevated.
3. Sepsis: This is a systemic infection that can cause inflammation throughout the body, including the liver, which can disrupt the normal processing of bilirubin.
4. Neonatal jaundice: This is a condition that affects newborn babies and is caused by an immature liver that is unable to process bilirubin quickly enough.

Symptoms of hyperbilirubinemia can include yellowing of the skin and whites of the eyes (jaundice), dark urine, pale or clay-colored stools, and fatigue. In severe cases, hyperbilirubinemia can lead to kernicterus, a condition that can cause brain damage and hearing loss.

Diagnosis of hyperbilirubinemia is typically made through blood tests that measure the level of bilirubin in the blood. Treatment depends on the underlying cause of the condition and may include blood transfusions, liver function tests, and phototherapy (exposure to light) to help break down bilirubin. In severe cases, hospitalization may be necessary to monitor and treat the condition.

Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.

There are several types of necrosis, including:

1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.

The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.

The main symptoms of choroideremia include:

1. Progressive vision loss: Patients with choroideremia experience a gradual decline in vision, starting with difficulty seeing in low light conditions and peripheral vision impairment.
2. Blind spots: Patients may develop blind spots or scotomas in their visual field, which can affect their ability to read, drive, or perform other daily tasks.
3. Eye movements: Choroideremia patients may experience abnormal eye movements, including nystagmus (involuntary eye movements) and photophobia (sensitivity to light).
4. Macular degeneration: As the condition progresses, patients may develop macular degeneration, which can lead to central vision loss.
5. Retinal degeneration: Choroideremia is characterized by progressive retinal degeneration, which can result in significant visual impairment and blindness.
6. Pigmentary changes: Patients with choroideremia may experience pigmentary changes in the retina, including the presence of hypopigmented or hyperpigmented spots.
7. Optic atrophy: Choroideremia can cause optic atrophy, which is the degeneration of the optic nerve and surrounding tissue.
8. Increased risk of other eye conditions: Patients with choroideremia may be at increased risk of developing other eye conditions, such as cataracts, glaucoma, and retinal detachment.
9. Impact on daily life: Choroideremia can significantly impact a patient's daily life, affecting their ability to perform daily activities, read, drive, and participate in social and recreational activities.
10. Limited treatment options: There is currently no cure for choroideremia, and treatment options are limited to management of symptoms and slowing the progression of the disease.

In summary, choroideremia is a rare genetic disorder that affects the retina and can cause significant visual impairment and blindness. It is characterized by progressive retinal degeneration, pigmentary changes, optic atrophy, increased risk of other eye conditions, and a significant impact on daily life. There are limited treatment options available for this condition, and research is ongoing to develop new therapies and improve patient outcomes.

There are several risk factors for developing HCC, including:

* Cirrhosis, which can be caused by heavy alcohol consumption, viral hepatitis (such as hepatitis B and C), or fatty liver disease
* Family history of liver disease
* Chronic obstructive pulmonary disease (COPD)
* Diabetes
* Obesity

HCC can be challenging to diagnose, as the symptoms are non-specific and can be similar to those of other conditions. However, some common symptoms of HCC include:

* Yellowing of the skin and eyes (jaundice)
* Fatigue
* Loss of appetite
* Abdominal pain or discomfort
* Weight loss

If HCC is suspected, a doctor may perform several tests to confirm the diagnosis, including:

* Imaging tests, such as ultrasound, CT scan, or MRI, to look for tumors in the liver
* Blood tests to check for liver function and detect certain substances that are produced by the liver
* Biopsy, which involves removing a small sample of tissue from the liver to examine under a microscope

Once HCC is diagnosed, treatment options will depend on several factors, including the stage and location of the cancer, the patient's overall health, and their personal preferences. Treatment options may include:

* Surgery to remove the tumor or parts of the liver
* Ablation, which involves destroying the cancer cells using heat or cold
* Chemoembolization, which involves injecting chemotherapy drugs into the hepatic artery to reach the cancer cells
* Targeted therapy, which uses drugs or other substances to target specific molecules that are involved in the growth and spread of the cancer

Overall, the prognosis for HCC is poor, with a 5-year survival rate of approximately 20%. However, early detection and treatment can improve outcomes. It is important for individuals at high risk for HCC to be monitored regularly by a healthcare provider, and to seek medical attention if they experience any symptoms.

There are several types of lymphoma, including:

1. Hodgkin lymphoma: This is a type of lymphoma that originates in the white blood cells called Reed-Sternberg cells. It is characterized by the presence of giant cells with multiple nucleoli.
2. Non-Hodgkin lymphoma (NHL): This is a type of lymphoma that does not meet the criteria for Hodgkin lymphoma. There are many subtypes of NHL, each with its own unique characteristics and behaviors.
3. Cutaneous lymphoma: This type of lymphoma affects the skin and can take several forms, including cutaneous B-cell lymphoma and cutaneous T-cell lymphoma.
4. Primary central nervous system (CNS) lymphoma: This is a rare type of lymphoma that develops in the brain or spinal cord.
5. Post-transplantation lymphoproliferative disorder (PTLD): This is a type of lymphoma that develops in people who have undergone an organ transplant, often as a result of immunosuppressive therapy.

The symptoms of lymphoma can vary depending on the type and location of the cancer. Some common symptoms include:

* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching

Lymphoma is diagnosed through a combination of physical examination, imaging tests (such as CT scans or PET scans), and biopsies. Treatment options for lymphoma depend on the type and stage of the cancer, and may include chemotherapy, radiation therapy, immunotherapy, or stem cell transplantation.

Overall, lymphoma is a complex and diverse group of cancers that can affect people of all ages and backgrounds. While it can be challenging to diagnose and treat, advances in medical technology and research have improved the outlook for many patients with lymphoma.

Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.

Types of Neoplasms

There are many different types of neoplasms, including:

1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.

Causes and Risk Factors of Neoplasms

The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:

1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.

Signs and Symptoms of Neoplasms

The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:

1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.

Diagnosis and Treatment of Neoplasms

The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.

The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:

1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.

Prevention of Neoplasms

While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:

1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.

It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.

Examples of inborn errors of metabolism include:

1. Phenylketonuria (PKU): A disorder that affects the body's ability to break down the amino acid phenylalanine, leading to a buildup of this substance in the blood and brain.
2. Hypothyroidism: A condition in which the thyroid gland does not produce enough thyroid hormones, leading to developmental delays, intellectual disability, and other health problems.
3. Maple syrup urine disease (MSUD): A disorder that affects the body's ability to break down certain amino acids, leading to a buildup of these substances in the blood and urine.
4. Glycogen storage diseases: A group of disorders that affect the body's ability to store and use glycogen, a form of carbohydrate energy.
5. Mucopolysaccharidoses (MPS): A group of disorders that affect the body's ability to produce and break down certain sugars, leading to a buildup of these substances in the body.
6. Citrullinemia: A disorder that affects the body's ability to break down the amino acid citrulline, leading to a buildup of this substance in the blood and urine.
7. Homocystinuria: A disorder that affects the body's ability to break down certain amino acids, leading to a buildup of these substances in the blood and urine.
8. Tyrosinemia: A disorder that affects the body's ability to break down the amino acid tyrosine, leading to a buildup of this substance in the blood and liver.

Inborn errors of metabolism can be diagnosed through a combination of physical examination, medical history, and laboratory tests such as blood and urine tests. Treatment for these disorders varies depending on the specific condition and may include dietary changes, medication, and other therapies. Early detection and treatment can help manage symptoms and prevent complications.

Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.

Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.

In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.

It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.

See also: Cancer, Tumor

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Examples of experimental leukemias include:

1. X-linked agammaglobulinemia (XLA): A rare inherited disorder that leads to a lack of antibody production and an increased risk of infections.
2. Diamond-Blackfan anemia (DBA): A rare inherited disorder characterized by a failure of red blood cells to mature in the bone marrow.
3. Fanconi anemia: A rare inherited disorder that leads to a defect in DNA repair and an increased risk of cancer, particularly leukemia.
4. Ataxia-telangiectasia (AT): A rare inherited disorder characterized by progressive loss of coordination, balance, and speech, as well as an increased risk of cancer, particularly lymphoma.
5. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21, which increases the risk of developing leukemia, particularly acute myeloid leukemia (AML).

These experimental leukemias are often used in research studies to better understand the biology of leukemia and to develop new treatments.

Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.

There are several ways to measure body weight, including:

1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.

It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.

There are several types of colonic neoplasms, including:

1. Adenomas: These are benign growths that are usually precursors to colorectal cancer.
2. Carcinomas: These are malignant tumors that arise from the epithelial lining of the colon.
3. Sarcomas: These are rare malignant tumors that arise from the connective tissue of the colon.
4. Lymphomas: These are cancers of the immune system that can affect the colon.

Colonic neoplasms can cause a variety of symptoms, including bleeding, abdominal pain, and changes in bowel habits. They are often diagnosed through a combination of medical imaging tests (such as colonoscopy or CT scan) and biopsy. Treatment for colonic neoplasms depends on the type and stage of the tumor, and may include surgery, chemotherapy, and/or radiation therapy.

Overall, colonic neoplasms are a common condition that can have serious consequences if left untreated. It is important for individuals to be aware of their risk factors and to undergo regular screening for colon cancer to help detect and treat any abnormal growths or tumors in the colon.

Jaundice is typically diagnosed through physical examination and laboratory tests such as blood tests to measure bilirubin levels. Treatment depends on the underlying cause, but may include medications to reduce bilirubin production or increase its excretion, or surgery to remove blockages in the bile ducts.

Here are some of the synonyms for Jaundice:

1. Yellow fever
2. Yellow jaundice
3. Hepatitis
4. Gallstones
5. Cholestasis
6. Obstruction of the bile ducts
7. Biliary tract disease
8. Hemochromatosis
9. Sickle cell anemia
10. Crigler-Najjar syndrome

Here are some of the antonyms for Jaundice:

1. Pinkness
2. Normal skin color
3. Healthy liver function
4. Bilirubin levels within normal range
5. No signs of liver disease or obstruction of bile ducts.

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... activity is carried out by the ribosome. Peptidyl transferase activity is not mediated by any ribosomal ... Enzyme Transferase Translation Tirumalai MR, Rivas M, Tran Q, Fox GE (November 2021). "The Peptidyl Transferase Center: a ... Pleuromutilins also bind to peptidyl transferase. Macrolide antibiotics are thought to inhibit peptidyl transferase, in ... ISBN 978-1-133-10629-6. "Peptidyl Transferase - Acyltransferases - Transferases - Enzymes - Products". www.axonmedchem.com. ...
... may refer to: UDP-N-acetylglucosamine-undecaprenyl-phosphate N-acetylglucosaminephosphotransferase, an enzyme ... an enzyme This disambiguation page lists articles associated with the title WecA transferase. If an internal link led you here ...
... may refer to: Lipid IVA 3-deoxy-D-manno-octulosonic acid transferase (KDO)-lipid IVA 3-deoxy-D-manno- ... octulosonic acid transferase (KDO)2-lipid IVA (2-8) 3-deoxy-D-manno-octulosonic acid transferase (KDO)3-lipid IVA (2-4) 3-deoxy ... manno-octulosonic acid transferase This disambiguation page lists articles associated with the title KDO transferase. If an ...
In molecular biology, the Cofactor transferase family is a family of protein domains that includes biotin protein ligases, ...
Other names in common use include formyl-coenzyme A transferase, and formyl-CoA oxalate CoA-transferase. As of late 2007, 4 ... This enzyme belongs to the family of transferases, specifically the CoA-transferases. The systematic name of this enzyme class ... In enzymology, a formyl-CoA transferase (EC 2.8.3.16) is an enzyme that catalyzes the chemical reaction formyl-CoA + oxalate ... Portal: Biology v t e (EC 2.8.3, Enzymes of known structure, All stub articles, Transferase stubs). ...
There are two recognised types of carboxyl transferase. One of them uses acyl-CoA and the other uses 2-oxo acid as the acceptor ... In molecular biology, proteins containing the carboxyl transferase domain include biotin-dependent carboxylases. This domain ...
... may stand for NAD(P)+ transhydrogenase (Re/Si-specific) NAD(P)+ transhydrogenase (Si-specific) ...
... (EC 2.8.4.2, ArsC1, ArsC2, mycothiol:arsenate transferase) is an enzyme with systematic name ... Wikimedia Commons has media related to Arsenate-mycothiol transferase. Arsenate-mycothiol+transferase at the US National ...
... (EC 2.1.1.165, MCT, methyl chloride transferase, S-adenosyl-L-methionine:halide/bisulfide ... Methyl+halide+transferase at the US National Library of Medicine Medical Subject Headings (MeSH) Portal: Biology (EC 2.1.1). ... Ni X, Hager LP (1999). "Expression of Batis maritima Methyl Chloride Transferase in Escherichia coli". Proc Natl Acad Sci USA. ... Ni X, Hager LP; Purification of the Enzyme (1998). "cDNA Cloning of Batis maritima Methyl Chloride Transferase". Proc Natl Acad ...
This enzyme belongs to the family of transferases, specifically the CoA-transferases. The systematic name of this enzyme class ... In enzymology, a glutaconate CoA-transferase (EC 2.8.3.12) is an enzyme that catalyzes the chemical reaction acetyl-CoA + (E)- ... Portal: Biology v t e (EC 2.8.3, Enzymes of unknown structure, All stub articles, Transferase stubs). ... Buckel W, Dorn U, Semmler R (1981). "Glutaconate CoA-transferase from Acidaminococcus fermentans". Eur. J. Biochem. 118 (2): ...
This enzyme belongs to the family of transferases, specifically the CoA-transferases. The systematic name of this enzyme class ... "Characterization of the isolated transferase subunit of citrate lyase as a CoA-Transferase. Evidence against a covalent enzyme- ... In enzymology, a citrate CoA-transferase (EC 2.8.3.10) is an enzyme that catalyzes the following chemical reaction: acetyl-CoA ... Portal: Biology v t e (EC 2.8.3, Enzymes of unknown structure, All stub articles, Transferase stubs). ...
This enzyme belongs to the family of transferases, specifically the CoA-transferases. The systematic name of this enzyme class ... In enzymology, a citramalate CoA-transferase (EC 2.8.3.11) is an enzyme that catalyzes the chemical reaction acetyl-CoA + ... Portal: Biology v t e (EC 2.8.3, Enzymes of unknown structure, All stub articles, Transferase stubs). ... is acetyl-CoA:citramalate CoA-transferase. This enzyme participates in c5-branched dibasic acid metabolism. Dimroth P, Buckel W ...
... acetate CoA transferase, butyryl coenzyme A transferase, and succinyl-CoA:acetate CoA transferase. This enzyme participates in ... This enzyme belongs to the family of transferases, specifically the CoA-transferases. The systematic name of this enzyme class ... In enzymology, an acetate CoA-transferase (EC 2.8.3.8) is an enzyme that catalyzes the chemical reaction acyl-CoA + acetate ... Media related to Acetato CoA-transferase at Wikimedia Commons Portal: Biology v t e (Articles with short description, Short ...
... lactoyl-CoA transferase, propionyl CoA:acetate CoA transferase, and propionyl-CoA transferase. This enzyme participates in 3 ... This enzyme belongs to the family of transferases, specifically the CoA-transferases. The systematic name of this enzyme class ... In enzymology, a propionate CoA-transferase (EC 2.8.3.1) is an enzyme that catalyzes the chemical reaction acetyl-CoA + ... Portal: Biology v t e (EC 2.8.3, Enzymes of unknown structure, All stub articles, Transferase stubs). ...
In enzymology, a xyloglucan:xyloglucosyl transferase (EC 2.4.1.207) is an enzyme that catalyzes the chemical reaction in which ... Nishitani K, Tominaga R (1992). "Endo-xyloglucan transferase, a novel class of glycosyltransferase that catalyzes transfer of a ... Other names in common use include endo-xyloglucan transferase, and xyloglucan endotransglycosylase. As of late 2007, two ...
This enzyme belongs to the family of transferases, specifically the CoA-transferases. The systematic name of this enzyme class ... Other names in common use include succinyl-beta-ketoacyl-CoA transferase, and oxalate coenzyme A-transferase. This enzyme ... In enzymology, an oxalate CoA-transferase (EC 2.8.3.2) is an enzyme that catalyzes the chemical reaction succinyl-CoA + oxalate ...
This enzyme belongs to the family of transferases, specifically the CoA-transferases. The systematic name of this enzyme class ... In enzymology, a malonate CoA-transferase (EC 2.8.3.3) is an enzyme that catalyzes the chemical reaction acetyl-CoA + malonate ... This enzyme is also called malonate coenzyme A-transferase. This enzyme participates in beta-alanine metabolism and propanoate ... Portal: Biology v t e (EC 2.8.3, Enzymes of unknown structure, All stub articles, Transferase stubs). ...
... (TdT), also known as DNA nucleotidylexotransferase (DNTT) or terminal transferase, is a ... In humans, terminal transferase is encoded by the DNTT gene. As a member of the X family of DNA polymerase enzymes, it works in ... Terminal transferase has applications in molecular biology. It can be used in RACE to add nucleotides that can then be used as ... Along with activity as a terminal transferase, it is known to also work in a more general template-dependent fashion. The ...
Glutathione transferases play a key role in catalyzing such reactions. Bacterial glutathione transferases of all classes are ... Bacterial glutathione transferases (GSTs; EC 2.5.1.18) are part of a superfamily of enzymes that play a crucial role in ... Bacterial glutathione transferases are not detected in anaerobic bacteria or archaea. These antioxidant enzymes are a part of ... Bacterial glutathione transferases are widely distributed in aerobic bacteria and are classified into several classes. These ...
Desosaminyl+transferase+EryCIII at the US National Library of Medicine Medical Subject Headings (MeSH) Portal: Biology (EC 2.4. ... Desosaminyl transferase EryCIII (EC 2.4.1.278, EryCIII) is an enzyme with systematic name dTDP-3-dimethylamino-4,6-dideoxy- ... "Reconstitution and characterization of a new desosaminyl transferase, EryCIII, from the erythromycin biosynthetic pathway". ...
... protein transferase, lipoate/octanoate transferase, lipoyltransferase, octanoyl-[acyl carrier protein]-protein N- ... In enzymology, a lipoyl(octanoyl) transferase (EC 2.3.1.181) is an enzyme that catalyzes the chemical reaction octanoyl-[acyl- ... This enzyme belongs to the family of transferases, specifically those acyltransferases transferring groups other than aminoacyl ... transferase". Protein Expr. Purif. 39 (2): 269-82. doi:10.1016/j.pep.2004.10.021. PMID 15642479. Vanden Boom TJ, Reed KE, ...
Affinity chromatography Bacterial glutathione transferase Glutathione S-transferase Mu 1 Glutathione S-transferase, C-terminal ... Overview of Glutathione S-Transferases Glutathione+S-Transferase at the US National Library of Medicine Medical Subject ... Glutathione S-transferases (GSTs), previously known as ligandins, are a family of eukaryotic and prokaryotic phase II metabolic ... Tew KD, Manevich Y, Grek C, Xiong Y, Uys J, Townsend DM (July 2011). "The role of glutathione S-transferase P in signaling ...
This enzyme belongs to the family of transferases, specifically the CoA-transferases. The systematic name of this enzyme class ... Other names in common use include 5-hydroxyvalerate CoA-transferase, and 5-hydroxyvalerate coenzyme A transferase. Eikmanns U, ... In enzymology, a 5-hydroxypentanoate CoA-transferase (EC 2.8.3.14) is an enzyme that catalyzes the chemical reaction acetyl-CoA ... Buckel W (1990). "Properties of 5-hydroxyvalerate CoA-transferase from Clostridium aminovalericum". Biol. Chem. Hoppe-Seyler. ...
This enzyme belongs to the family of transferases, specifically the CoA-transferases. The systematic name of this enzyme class ... Portal: Biology v t e (EC 2.8.3, Enzymes of unknown structure, All stub articles, Transferase stubs). ... In enzymology, a succinate-hydroxymethylglutarate CoA-transferase (EC 2.8.3.13) is an enzyme that catalyzes the chemical ... Other names in common use include hydroxymethylglutarate coenzyme A-transferase, and dicarboxyl-CoA:dicarboxylic acid coenzyme ...
... is an enzyme that in humans is encoded by the GSTA1 gene. Cytosolic and membrane-bound forms of ... This gene encodes a glutathione S-transferase belonging to the alpha class. The alpha class genes, located in a cluster mapped ... Board PG, Webb GC (1987). "Isolation of a cDNA clone and localization of human glutathione S-transferase 2 genes to chromosome ... Hayes JD, Kerr LA, Cronshaw AD (1990). "Evidence that glutathione S-transferases B1B1 and B2B2 are the products of separate ...
... , in short PST deficiency, is the lack or the reduced activity of the functional enzyme ... Phenol sulfur transferase, in short PST or SULT1, is a subfamily of the enzyme cytosolic sulfotransferases (SULTs) consisting ... phenol sulfur transferase, which is crucial in the detoxification of mainly phenolic compounds by catalysing the sulfate ...
O-GlcNAc transferase is a part of a host of biological functions within the human body. OGT is involved in the resistance of ... Protein O-GlcNAc transferase also known as OGT or O-linked N-acetylglucosaminyltransferase is an enzyme (EC 2.4.1.255) that in ... O-GlcNAc transferase is part of a dynamic competition for a serine or threonine hydroxyl functional group in a peptide unit. ... The crystal structure of O-GlcNAc transferase has not been well studied, but the structure of a binary complex with UDP and a ...
Glucuronyl transferase is a liver enzyme. It changes bilirubin into a form that can be removed from the body through the bile. ... Glucuronyl transferase is a liver enzyme. It changes bilirubin into a form that can be removed from the body through the bile. ... The skin can take on a yellow color (jaundice) if the body does not produce enough glucuronyl transferase. ...
More info for Superfamily c.26.1: Nucleotidylyl transferase. Timeline for Superfamily c.26.1: Nucleotidylyl transferase: * ... Superfamily c.26.1: Nucleotidylyl transferase appears in SCOP 1.69. *Superfamily c.26.1: Nucleotidylyl transferase appears in ... Lineage for Superfamily c.26.1: Nucleotidylyl transferase. *Root: SCOP 1.71 *. Class c: Alpha and beta proteins (a/b) [51349] ( ... Superfamily c.26.1: Nucleotidylyl transferase first appeared (with stable ids) in SCOP 1.55. * ...
Among them, the phosphopantetheinyl transferase (XaPPT, EC 2.7.8.7) enzyme plays an essential role to the development of X. ... Entre as enzimas dessa via, destaca-se a fosfopanteteinil transferase (XaPPT, E.C. 2.7.8.7), uma enzima essencial para o ... Estudos estruturais e moleculares da enzima fosfopanteteinil transferase de Xanthomonas albilineans: alvo molecular para o ... Structural and molecular studies of xanthomonas albilineans phosphopantetheinyl transferase enzyme: molecular target for new ...
... protein transferase (Escherichia coli IAI39). Find diseases associated with this biological target and compounds tested against ...
Abnormalities in other LFTs analyzed (alkaline phosphatase, gamma-glutamyl transferase, and total bilirubin) were not ...
QM/MM study of the reaction mechanism of the carboxyl transferase domain of pyruvate carboxylase from Staphylococcus aureus. by ... QM/MM study of the reaction mechanism of the carboxyl transferase domain of pyruvate carboxylase from Staphylococcus aureus. ... QM/MM study of the reaction mechanism of the carboxyl transferase domain of pyruvate carboxylase from Staphylococcus aureus.. ... In this article, the catalytic mechanism of the carboxyl transferase domain of PC from Staphylococcus aureus was investigated ...
ALT cancer cells are specifically sensitive to lysine acetyl transferase inhibition. Dalal Bakhos-Douaihy, Chantal Desmaze, ... suggesting that AA decreased the ALT mechanism through the inhibition of lysine transferase activity of PCAF, but not that of ...
The gamma-glutamyl transferase (GGT) blood test measures the level of the enzyme GGT in the blood. ... Gamma-glutamyl transferase (GGT) blood test. Gamma-GT; GGTP; GGT; Gamma-glutamyl transpeptidase ...
Harris M. J., Coggan M., Langton L., Wilson S. R., Board P. G. Polymorphism of the Pi class glutathione S-transferase in normal ... No Association between the I105V Polymorphism of the Glutathione S-Transferase P1 Gene (GSTP1) and Prostate Cancer Risk: A ... Hayes J. D., Pulford D. J. The glutathione S-transferase supergene family: regulation of GST and the contribution of the ... The abbreviations used are: GST, glutathione S-transferase; CaP, prostate cancer; OR, odds ratio; CI,confidence interval. ...
The role of apolipoprotein N-acyl transferase, Lnt, in the lipidation of factor H binding protein of Neisseria meningitidis ... The role of apolipoprotein N-acyl transferase, Lnt, in the lipidation of factor H binding protein of Neisseria meningitidis ... the transposon was located in the lnt gene which encodes apolipoprotein N-acyl transferase, Lnt, responsible for the addition ... The role of apolipoprotein N-acyl transferase, Lnt, in the lipidation of factor H binding protein of Neisseria meningitidis ...
Engineering orthogonal polypeptide GalNAc-Transferase and UDP-sugar pairs. Authors list. Junwon Choi Lauren JS Wagner Suzanne ...
... April 10, 2022. by Glucofort Glucofort is a dietary supplements that claims to treat diabetes. ...
Human variability in glutathione-S-transferase activities, tissue distribution and major polymorphic variants: Meta-analysis ... What are the major types of transferases? ... Where are transferases found in the cell?. Are enzymes lipids ... What kinds of reactions do transferases catalyze?. ... What are the major types of transferases? AboutPrivacyTerms of ...
Detection of TPMT genetic variants by genotyping is recommended prior to commencing the treatment of patients with Thiopurine drugs such as Azathioprine, 6-Mercaptopurine and 6-Thioguanine for Acute Lymphoblastic Leukemia ; autoimmune disorders like Crohns disease ; Rheumatoid arthritis.TPMT is an enzyme which converts these drugs in the body to an active form. Any genetic defect in this enzyme predisposes patients to a heightened risk of drug-induced bone marrow toxicity due to accumulation of unmetabolised drug. Approximately 0.3% of individuals lack TPMT activity while 11% show reduced activity (variants TPMT*2, 3A ; 3C). 89% of people have normal activity (variant TPMT*1).. ...
SGPT (Alanine Amino Transferase/ALT). January 10, 2023. Biochemistry Test Name:. SGPT (Alanine Amino Transferase/ALT). ... Test: SGPT (Alanine Amino Transferase/ALT). MRP: 315. Parameters: Method: Spectrophotometry. Sample Type: 2 ml. (1 ml. Minimum ...
LBXSGTSI - Gamma glutamyl transferase (U/L). Variable Name: LBXSGTSI. SAS Label: Gamma glutamyl transferase (U/L). English Text ... Gamma glutamyl transferase (U/L). Target: Both males and females 12 YEARS - 150 YEARS. Code or Value. Value Description. Count ...
2.5.1.18 Glutathione transferases in the IUPHAR/BPS Guide to PHARMACOLOGY. ... 2.5.1.18 Glutathione transferases. Unless otherwise stated all data on this page refer to the human proteins. Gene information ... glutathione S-transferase omega 1 Show summary »« Hide summary More detailed page ... 2.5.1.18 Glutathione transferases. Accessed on 10/06/2023. IUPHAR/BPS Guide to PHARMACOLOGY, http://www.guidetopharmacology.org ...
Please cite Turkarslan et al., 2017 Mol. Sys. Biol. if you find Syntrophy Portal useful.. Acknowledgement: "This material by ENIGMA- Ecosystems and Networks Integrated with Genes and Molecular Assemblies (http://enigma.lbl.gov), a Scientific Focus Area Program at Lawrence Berkeley National Laboratory is based upon work supported by the U.S. Department of Energy, Office of Science, Office of Biological & Environmental Research under contract number DE-AC02-05CH11231" ...
Changes related to "Histone Acetyl Transferases". From The School of Biomedical Sciences Wiki ...
So, what blood tests show alcoholism? The primary test measures the level of gamma-glutamyl transferase (GGT), which is an ... Gamma-glutamyl Transferase (GGT) Test. One of the tests used by doctors to determine if an individual is drinking excessively ... This is a blood test that measures the level of gamma-glutamyl transferase, a liver enzyme. This enzyme is produced at a higher ... is the Gamma-glutamyl Transferase (GGT) test. ... Gamma-glutamyl Transferase (GGT) Test. *Mean Corpuscular Volume ...
We have recently demonstrated reduced expression of glutathione S-transferase mu type 1 (Gstm1) in a rat model of hypertension ... Glutathione S-transferases are involved in defences against oxidative stress. ... Glutathione S-transferase variants and hypertension. Delles C., Padmanabhan S., Lee WK., Miller WH., McBride MW., McClure JD., ... OBJECTIVES: Glutathione S-transferases are involved in defences against oxidative stress. We have recently demonstrated reduced ...
Oryza; Domínio Catalítico; Oryza/genética; Oryza/metabolismo; Glutationa Transferase/genética; Glutationa Transferase/ ... Plant glutathione S-transferase (GST, EC 2.5.1.18) is an enzyme that detoxifies various electrophilic compounds including ... 3-Dimensional structure; Active site; Glutathione S-transferase; OsGSTF3; Serine residue; Site-directed mutagenesis ... Functional significance of serine 13 in the active site of glutathione S-transferase F3 from Oryza sativa. ...
EC2 Transferases (list). *EC3 Hydrolases (list). *EC4 Lyases (list). *EC5 Isomerases (list) ...
Mouse GSTa4(Glutathione S Transferase Alpha 4) ELISA Kit. Mouse GSTa4(Glutathione S Transferase Alpha 4) ELISA Kit ... Description: A sandwich ELISA kit for detection of Glutathione S Transferase Alpha 4 from Mouse in samples from blood, serum, ... Description: A sandwich quantitative ELISA assay kit for detection of Human Glutathione S Transferase Alpha 4 (GSTa4) in ... Description: A sandwich quantitative ELISA assay kit for detection of Human Glutathione S Transferase Alpha 4 (GSTa4) in ...
Gamma Glutamyl Transferase Testing Market, by Product (Elisa Based, Colorimetric Based), End User (Hospitals, Diagnostic ... The report offers market size and forecast by keenly evaluating every segment of the global gamma glutamyl transferase testing ... The report divides the global gamma glutamyl transferase testing market into four main regions including Europe, North America ... Furthermore, these regions are sub-divided to profile detailed panorama of the gamma glutamyl transferase testing market across ...
Aspartate transferase. 0-40 U/L. 271.3 (176.5-610.5). 13/16 (81). High. ...
Glutathione s-transferase p1-1 Coordinates. PDB Format Method. X-RAY DIFFRACTION 1.90 Å. Oligo State. homo-dimer. Ligands 2 x ... Oakley, A.J. et al., The ligandin (non-substrate) binding site of human Pi class glutathione transferase is located in the ...
Intramolecular Transferases / metabolism * Mutagenesis, Site-Directed * Mycobacterium tuberculosis / enzymology * Mycobacterium ...
  • Abnormalities in other LFTs analyzed (alkaline phosphatase, gamma-glutamyl transferase, and total bilirubin) were not associated with short-term mortality. (helsinki.fi)
  • The gamma-glutamyl transferase (GGT) blood test measures the level of the enzyme GGT in the blood. (adam.com)
  • One of the tests used by doctors to determine if an individual is drinking excessively is the Gamma-glutamyl Transferase (GGT) test. (brighthub.com)
  • This is a blood test that measures the level of gamma-glutamyl transferase, a liver enzyme. (brighthub.com)
  • The report offers comprehensive analysis of the global gamma glutamyl transferase testing market by thoroughly studying different aspects of the market including major segments, market statistics, market dynamics, regional market outlook, investment opportunities, and top players working towards the growth of the market. (researchdive.com)
  • The report offers market size and forecast by keenly evaluating every segment of the global gamma glutamyl transferase testing market. (researchdive.com)
  • The report divides the global gamma glutamyl transferase testing market into four main regions including Europe, North America, Asia-Pacific, and LAMEA. (researchdive.com)
  • Furthermore, these regions are sub-divided to profile detailed panorama of the gamma glutamyl transferase testing market across major countries in specific regions. (researchdive.com)
  • The report outlines the business overview including financial performance, latest strategic moves & developments, product portfolio, and SWOT analysis of the leading players of the gamma glutamyl transferase testing market. (researchdive.com)
  • Alcohol (ethanol) consumption and cigarette smoking can increase gamma-glutamyl transferase (GGT) levels. (medscape.com)
  • Glutathione S-transferase variants and hypertension. (ox.ac.uk)
  • OBJECTIVES: Glutathione S-transferases are involved in defences against oxidative stress. (ox.ac.uk)
  • We have recently demonstrated reduced expression of glutathione S-transferase mu type 1 (Gstm1) in a rat model of hypertension. (ox.ac.uk)
  • Functional significance of serine 13 in the active site of glutathione S-transferase F3 from Oryza sativa. (bvsalud.org)
  • Plant glutathione S-transferase (GST, EC 2.5.1.18) is an enzyme that detoxifies various electrophilic compounds including herbicides and organic pollutants by catalyzing the formation of conjugates with reduced glutathione (GSH). (bvsalud.org)
  • Description: A sandwich quantitative ELISA assay kit for detection of Human Glutathione S Transferase Alpha 4 (GSTa4) in samples from serum, plasma or other biological fluids. (wannabe-anthropologist.com)
  • Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Mouse Glutathione S Transferase Alpha 4 (GSTa4) in samples from Serum, plasma, tissue homogenates, cell lysates, cell culture supernates and other biological fluids. (wannabe-anthropologist.com)
  • The ligandin (non-substrate) binding site of human Pi class glutathione transferase is located in the electrophile binding site (H-site). (expasy.org)
  • Glutathione S-transferase Isoenzymes and the DDTase Activity in Two DDT-resistant Strains of Aedes aegypti. (who.int)
  • The glutathione S-transferases: influence of polymorphism on cancer susceptibility. (bvsalud.org)
  • Psychological Distress in Fibromyalgia Patients: A Role for Catechol-O-Methyl-Transferase Val158Met Polymorphism. (bvsalud.org)
  • 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). (bvsalud.org)
  • Entre as enzimas dessa via, destaca-se a fosfopanteteinil transferase (XaPPT, E.C. 2.7.8.7), uma enzima essencial para o desenvolvimento da X. albilineans . (usp.br)
  • Las transferases son enzimas que transfieren un grupo, por ejemplo, el grupo metilo o un grupo glucosilo, de un compuesto (generalmente considerado como donador) hacia otro compuesto (generalmente considerado aceptor). (bvsalud.org)
  • Alteration of pulmonary xenobiotic pathways was determined by monitoring the protein levels and activities of P-450 isozymes (CYP1A1 and CYP2B1), glutathioneS-transferase (GST), and NADPH:quinone oxidoreductase (QR). (cdc.gov)
  • In a mutant with markedly reduced binding, the transposon was located in the lnt gene which encodes apolipoprotein N-acyl transferase, Lnt, responsible for the addition of the third fatty acid to apolipoproteins prior to their sorting to the outer membrane. (nottingham.ac.uk)
  • AA treatment recapitulates the effect of PCAF knockdown on several ALT features, suggesting that AA decreased the ALT mechanism through the inhibition of lysine transferase activity of PCAF, but not that of GCN5. (oncotarget.com)
  • What are the major types of transferases? (aatbio.com)
  • There are 10 major types of transferases . (aatbio.com)