A flavoprotein amine oxidoreductase that catalyzes the reversible conversion of 5-methyltetrahydrofolate to 5,10-methylenetetrahydrofolate. This enzyme was formerly classified as EC 1.1.1.171.
An FAD-dependent oxidoreductase found primarily in BACTERIA. It is specific for the reduction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate. This enzyme was formerly listed as EC 1.1.1.68 and 1.1.99.15.
Enzymes catalyzing the dehydrogenation of secondary amines, introducing a C=N double bond as the primary reaction. In some cases this is later hydrolyzed.
An NADP-dependent oxidoreductase that catalyses the conversion of 5,10-methyleneterahydrofolate to 5,10-methenyl-tetrahydrofolate. In higher eukaryotes a trifunctional enzyme exists with additional METHENYLTETRAHYDROFOLATE CYCLOHYDROLASE and FORMATE-TETRAHYDROFOLATE LIGASE activity. The enzyme plays an important role in the synthesis of 5-methyltetrahydrofolate, the methyl donor for the VITAMIN B12-dependent remethylation of HOMOCYSTEINE to METHIONINE via METHIONINE SYNTHETASE.
A thiol-containing amino acid formed by a demethylation of METHIONINE.
A member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses (POACEAE). Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia.
Compounds based on 5,6,7,8-tetrahydrofolate.
The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
An enzyme that catalyzes the formation of methionine by transfer of a methyl group from 5-methyltetrahydrofolate to homocysteine. It requires a cobamide coenzyme. The enzyme can act on mono- or triglutamate derivatives. EC 2.1.1.13.
Condition in which the plasma levels of homocysteine and related metabolites are elevated (>13.9 µmol/l). Hyperhomocysteinemia can be familial or acquired. Development of the acquired hyperhomocysteinemia is mostly associated with vitamins B and/or folate deficiency (e.g., PERNICIOUS ANEMIA, vitamin malabsorption). Familial hyperhomocysteinemia often results in a more severe elevation of total homocysteine and excretion into the urine, resulting in HOMOCYSTINURIA. Hyperhomocysteinemia is a risk factor for cardiovascular and neurodegenerative diseases, osteoporotic fractures and complications during pregnancy.
A cobalt-containing coordination compound produced by intestinal micro-organisms and found also in soil and water. Higher plants do not concentrate vitamin B 12 from the soil and so are a poor source of the substance as compared with animal tissues. INTRINSIC FACTOR is important for the assimilation of vitamin B 12.
An enzyme that catalyzes the oxidation and reduction of FERREDOXIN or ADRENODOXIN in the presence of NADP. EC 1.18.1.2 was formerly listed as EC 1.6.7.1 and EC 1.6.99.4.
An individual in which both alleles at a given locus are identical.
Heat- and storage-labile plasma glycoprotein which accelerates the conversion of prothrombin to thrombin in blood coagulation. Factor V accomplishes this by forming a complex with factor Xa, phospholipid, and calcium (prothrombinase complex). Deficiency of factor V leads to Owren's disease.
A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.
A multifunctional pyridoxal phosphate enzyme. In the second stage of cysteine biosynthesis it catalyzes the reaction of homocysteine with serine to form cystathionine with the elimination of water. Deficiency of this enzyme leads to HYPERHOMOCYSTEINEMIA and HOMOCYSTINURIA. EC 4.2.1.22.
An enzyme of the transferase class that catalyzes the reaction 5,10-methylenetetrahydrofolate and dUMP to dihydrofolate and dTMP in the synthesis of thymidine triphosphate. (From Dorland, 27th ed) EC 2.1.1.45.
A disorder of HEMOSTASIS in which there is a tendency for the occurrence of THROMBOSIS.
Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.
A nutritional condition produced by a deficiency of FOLIC ACID in the diet. Many plant and animal tissues contain folic acid, abundant in green leafy vegetables, yeast, liver, and mushrooms but destroyed by long-term cooking. Alcohol interferes with its intermediate metabolism and absorption. Folic acid deficiency may develop in long-term anticonvulsant therapy or with use of oral contraceptives. This deficiency causes anemia, macrocytic anemia, and megaloblastic anemia. It is indistinguishable from vitamin B 12 deficiency in peripheral blood and bone marrow findings, but the neurologic lesions seen in B 12 deficiency do not occur. (Merck Manual, 16th ed)
The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.
A pyridoxal phosphate enzyme that catalyzes the reaction of glycine and 5,10-methylene-tetrahydrofolate to form serine. It also catalyzes the reaction of glycine with acetaldehyde to form L-threonine. EC 2.1.2.1.
Nutritional factor found in milk, eggs, malted barley, liver, kidney, heart, and leafy vegetables. The richest natural source is yeast. It occurs in the free form only in the retina of the eye, in whey, and in urine; its principal forms in tissues and cells are as FLAVIN MONONUCLEOTIDE and FLAVIN-ADENINE DINUCLEOTIDE.
A condensation product of riboflavin and adenosine diphosphate. The coenzyme of various aerobic dehydrogenases, e.g., D-amino acid oxidase and L-amino acid oxidase. (Lehninger, Principles of Biochemistry, 1982, p972)
Autosomal recessive inborn error of methionine metabolism usually caused by a deficiency of CYSTATHIONINE BETA-SYNTHASE and associated with elevations of homocysteine in plasma and urine. Clinical features include a tall slender habitus, SCOLIOSIS, arachnodactyly, MUSCLE WEAKNESS, genu varus, thin blond hair, malar flush, lens dislocations, an increased incidence of MENTAL RETARDATION, and a tendency to develop fibrosis of arteries, frequently complicated by CEREBROVASCULAR ACCIDENTS and MYOCARDIAL INFARCTION. (From Adams et al., Principles of Neurology, 6th ed, p979)
A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia.
The class of all enzymes catalyzing oxidoreduction reactions. The substrate that is oxidized is regarded as a hydrogen donor. The systematic name is based on donor:acceptor oxidoreductase. The recommended name will be dehydrogenase, wherever this is possible; as an alternative, reductase can be used. Oxidase is only used in cases where O2 is the acceptor. (Enzyme Nomenclature, 1992, p9)
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
A sulfur-containing essential L-amino acid that is important in many body functions.
A group of water-soluble vitamins, some of which are COENZYMES.
A carbon-nitrogen ligase that catalyzes the formation of 10-formyltetrahydrofolate from formate and tetrahydrofolate in the presence of ATP. In higher eukaryotes the enzyme also contains METHYLENETETRAHYDROFOLATE DEHYDROGENASE (NADP+) and METHENYLTETRAHYDROFOLATE CYCLOHYDROLASE activity.
Formerly a constituent republic of Yugoslavia, comprising the Yugoslav section of the region of Macedonia. It was made a constituent republic in the 1946 constitution. It became independent on 8 February 1994 and was recognized as The Former Yugoslav Republic of Macedonia by the United States Board on Geographic Names 16 February 1994.
A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair.
Physiologic methyl radical donor involved in enzymatic transmethylation reactions and present in all living organisms. It possesses anti-inflammatory activity and has been used in treatment of chronic liver disease. (From Merck, 11th ed)
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
VITAMIN B 6 refers to several PICOLINES (especially PYRIDOXINE; PYRIDOXAL; & PYRIDOXAMINE) that are efficiently converted by the body to PYRIDOXAL PHOSPHATE which is a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, and aminolevulinic acid. During transamination of amino acids, pyridoxal phosphate is transiently converted into PYRIDOXAMINE phosphate. Although pyridoxine and Vitamin B 6 are still frequently used as synonyms, especially by medical researchers, this practice is erroneous and sometimes misleading (EE Snell; Ann NY Acad Sci, vol 585 pg 1, 1990). Most of vitamin B6 is eventually degraded to PYRIDOXIC ACID and excreted in the urine.
An aminohydrolase that catalyzes the hydrolysis of 5,10-methenyltetrahydrofolate to 10-formyltetrahydrofolate. In most higher eucaryotic organisms this enzyme also includes METHYLENETETRAHYDROFOLATE DEHYDROGENASE (NADP) and FORMATE-TETRAHYDROFOLATE LIGASE activities.
The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases.
Congenital malformations of the central nervous system and adjacent structures related to defective neural tube closure during the first trimester of pregnancy generally occurring between days 18-29 of gestation. Ectodermal and mesodermal malformations (mainly involving the skull and vertebrae) may occur as a result of defects of neural tube closure. (From Joynt, Clinical Neurology, 1992, Ch55, pp31-41)
A naturally occurring compound that has been of interest for its role in osmoregulation. As a drug, betaine hydrochloride has been used as a source of hydrochloric acid in the treatment of hypochlorhydria. Betaine has also been used in the treatment of liver disorders, for hyperkalemia, for homocystinuria, and for gastrointestinal disturbances. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1341)
Compounds which increase the capacity of the male to induce conception.
An enzyme that utilizes NADH or NADPH to reduce FLAVINS. It is involved in a number of biological processes that require reduced flavin for their functions such as bacterial bioluminescence. Formerly listed as EC 1.6.8.1 and EC 1.5.1.29.
A ubiquitously expressed folic acid transporter that functions via an antiporter mechanism which is coupled to the transport of organic phosphates.
Oxidoreductases that are specific for the reduction of NITRATES.
A pyrimidine base that is a fundamental unit of nucleic acids.
Nicotinamide adenine dinucleotide phosphate. A coenzyme composed of ribosylnicotinamide 5'-phosphate (NMN) coupled by pyrophosphate linkage to the 5'-phosphate adenosine 2',5'-bisphosphate. It serves as an electron carrier in a number of reactions, being alternately oxidized (NADP+) and reduced (NADPH). (Dorland, 27th ed)
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
Individuals whose ancestral origins are in the southeastern and eastern areas of the Asian continent.
Congenital defects of closure of one or more vertebral arches, which may be associated with malformations of the spinal cord, nerve roots, congenital fibrous bands, lipomas, and congenital cysts. These malformations range from mild (e.g., SPINA BIFIDA OCCULTA) to severe, including rachischisis where there is complete failure of neural tube and spinal cord fusion, resulting in exposure of the spinal cord at the surface. Spinal dysraphism includes all forms of spina bifida. The open form is called SPINA BIFIDA CYSTICA and the closed form is SPINA BIFIDA OCCULTA. (From Joynt, Clinical Neurology, 1992, Ch55, p34)
An antineoplastic antimetabolite with immunosuppressant properties. It is an inhibitor of TETRAHYDROFOLATE DEHYDROGENASE and prevents the formation of tetrahydrofolate, necessary for synthesis of thymidylate, an essential component of DNA.
Three or more consecutive spontaneous abortions.
Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.
Variation occurring within a species in the presence or length of DNA fragment generated by a specific endonuclease at a specific site in the genome. Such variations are generated by mutations that create or abolish recognition sites for these enzymes or change the length of the fragment.
Disorders affecting amino acid metabolism. The majority of these disorders are inherited and present in the neonatal period with metabolic disturbances (e.g., ACIDOSIS) and neurologic manifestations. They are present at birth, although they may not become symptomatic until later in life.
A group of carrier proteins which bind with VITAMIN B12 in the BLOOD and aid in its transport. Transcobalamin I migrates electrophoretically as a beta-globulin, while transcobalamins II and III migrate as alpha-globulins.
The 4-methanol form of VITAMIN B 6 which is converted to PYRIDOXAL PHOSPHATE which is a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, aminolevulinic acid. Although pyridoxine and Vitamin B 6 are still frequently used as synonyms, especially by medical researchers, this practice is erroneous and sometimes misleading (EE Snell; Ann NY Acad Sci, vol 585 pg 1, 1990).
Products in capsule, tablet or liquid form that provide dietary ingredients, and that are intended to be taken by mouth to increase the intake of nutrients. Dietary supplements can include macronutrients, such as proteins, carbohydrates, and fats; and/or MICRONUTRIENTS, such as VITAMINS; MINERALS; and PHYTOCHEMICALS.
A subclass of enzymes which includes all dehydrogenases acting on primary and secondary alcohols as well as hemiacetals. They are further classified according to the acceptor which can be NAD+ or NADP+ (subclass 1.1.1), cytochrome (1.1.2), oxygen (1.1.3), quinone (1.1.5), or another acceptor (1.1.99).
Regular course of eating and drinking adopted by a person or animal.
Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.
5-Fluoro-2'-deoxyuridylate. An inhibitor of thymidylate synthetase. Formed from 5-fluorouracil or 5-fluorodeoxyuridine.
A FLAVOPROTEIN oxidoreductase that occurs both as a soluble enzyme and a membrane-bound enzyme due to ALTERNATIVE SPLICING of a single mRNA. The soluble form is present mainly in ERYTHROCYTES and is involved in the reduction of METHEMOGLOBIN. The membrane-bound form of the enzyme is found primarily in the ENDOPLASMIC RETICULUM and outer mitochondrial membrane, where it participates in the desaturation of FATTY ACIDS; CHOLESTEROL biosynthesis and drug metabolism. A deficiency in the enzyme can result in METHEMOGLOBINEMIA.
A group of enzymes that oxidize diverse nitrogenous substances to yield nitrite. (Enzyme Nomenclature, 1992) EC 1.
An individual having different alleles at one or more loci regarding a specific character.
An enzyme that catalyzes the reactivation by light of UV-irradiated DNA. It breaks two carbon-carbon bonds in PYRIMIDINE DIMERS in DNA.
A country spanning from central Asia to the Pacific Ocean.
Biochemical identification of mutational changes in a nucleotide sequence.
Addition of methyl groups to DNA. DNA methyltransferases (DNA methylases) perform this reaction using S-ADENOSYLMETHIONINE as the methyl group donor.
The analysis of a sequence such as a region of a chromosome, a haplotype, a gene, or an allele for its involvement in controlling the phenotype of a specific trait, metabolic pathway, or disease.
Catalyzes the oxidation of GLUTATHIONE to GLUTATHIONE DISULFIDE in the presence of NADP+. Deficiency in the enzyme is associated with HEMOLYTIC ANEMIA. Formerly listed as EC 1.6.4.2.
The rate dynamics in chemical or physical systems.
A FLAVOPROTEIN enzyme that catalyzes the oxidation of THIOREDOXINS to thioredoxin disulfide in the presence of NADP+. It was formerly listed as EC 1.6.4.5
An enzyme of the oxidoreductase class that catalyzes the reaction 7,8-dihyrofolate and NADPH to yield 5,6,7,8-tetrahydrofolate and NADPH+, producing reduced folate for amino acid metabolism, purine ring synthesis, and the formation of deoxythymidine monophosphate. Methotrexate and other folic acid antagonists used as chemotherapeutic drugs act by inhibiting this enzyme. (Dorland, 27th ed) EC 1.5.1.3.
A range of values for a variable of interest, e.g., a rate, constructed so that this range has a specified probability of including the true value of the variable.
A flavoprotein that catalyzes the reduction of heme-thiolate-dependent monooxygenases and is part of the microsomal hydroxylating system. EC 1.6.2.4.
Genotypic differences observed among individuals in a population.
A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).
A branch of genetics which deals with the genetic variability in individual responses to drugs and drug metabolism (BIOTRANSFORMATION).
Derivatives of folic acid (pteroylglutamic acid). In gamma-glutamyl linkage they are found in many tissues. They are converted to folic acid by the action of pteroylpolyglutamate hydrolase or synthesized from folic acid by the action of folate polyglutamate synthetase. Synthetic pteroylpolyglutamic acids, which are in alpha-glutamyl linkage, are active in bacterial growth assays.
The probability that an event will occur. It encompasses a variety of measures of the probability of a generally unfavorable outcome.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
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.
A subclass of enzymes which includes all dehydrogenases acting on carbon-carbon bonds. This enzyme group includes all the enzymes that introduce double bonds into substrates by direct dehydrogenation of carbon-carbon single bonds.
Pathological processes involving any of the BLOOD VESSELS in the cardiac or peripheral circulation. They include diseases of ARTERIES; VEINS; and rest of the vasculature system in the body.
An enzyme that catalyzes the reduction of 6,7-dihydropteridine to 5,6,7,8-tetrahydropteridine in the presence of NADP+. Defects in the enzyme are a cause of PHENYLKETONURIA II. Formerly listed as EC 1.6.99.7.
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.
The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the MAJOR HISTOCOMPATIBILITY COMPLEX.
Derivatives of the dimethylisoalloxazine (7,8-dimethylbenzo[g]pteridine-2,4(3H,10H)-dione) skeleton. Flavin derivatives serve an electron transfer function as ENZYME COFACTORS in FLAVOPROTEINS.
The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.
5'-S-(3-Amino-3-carboxypropyl)-5'-thioadenosine. Formed from S-adenosylmethionine after transmethylation reactions.
Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics.

There are several factors that can contribute to hyperhomocysteinemia, including:

1. Genetic mutations: Some individuals may have genetic mutations that affect the enzymes involved in homocysteine metabolism, leading to elevated levels of homocysteine.
2. Vitamin deficiencies: Deficiencies in vitamins B6, B12, and folate can interfere with the metabolism of homocysteine, leading to elevated levels.
3. Kidney disease: The kidneys play a critical role in removing homocysteine from the body. Any damage to the kidneys or impairment in their function can lead to hyperhomocysteinemia.
4. Other medical conditions: Certain medical conditions, such as thyroid disorders and autoimmune diseases, can also contribute to hyperhomocysteinemia.

Elevated levels of homocysteine have been linked to several health problems, including:

1. Cardiovascular disease: High levels of homocysteine have been associated with an increased risk of heart disease and stroke.
2. Blood clots: Homocysteine can interfere with the normal blood clotting process, leading to an increased risk of blood clots and deep vein thrombosis.
3. Bone loss: Elevated levels of homocysteine have been linked to bone loss and an increased risk of osteoporosis.
4. Cognitive decline: Some studies suggest that high levels of homocysteine may be associated with cognitive decline and an increased risk of dementia.

Treatment for hyperhomocysteinemia typically involves addressing any underlying medical conditions, such as kidney disease or thyroid disorders, and making dietary changes to increase the intake of vitamin B6, folate, and other nutrients that help regulate homocysteine levels. In some cases, medications may be prescribed to lower homocysteine levels. Regular monitoring of homocysteine levels can help healthcare providers track the effectiveness of treatment and make any necessary adjustments.

Explanation: Genetic predisposition to disease is influenced by multiple factors, including the presence of inherited genetic mutations or variations, environmental factors, and lifestyle choices. The likelihood of developing a particular disease can be increased by inherited genetic mutations that affect the functioning of specific genes or biological pathways. For example, inherited mutations in the BRCA1 and BRCA2 genes increase the risk of developing breast and ovarian cancer.

The expression of genetic predisposition to disease can vary widely, and not all individuals with a genetic predisposition will develop the disease. Additionally, many factors can influence the likelihood of developing a particular disease, such as environmental exposures, lifestyle choices, and other health conditions.

Inheritance patterns: Genetic predisposition to disease can be inherited in an autosomal dominant, autosomal recessive, or multifactorial pattern, depending on the specific disease and the genetic mutations involved. Autosomal dominant inheritance means that a single copy of the mutated gene is enough to cause the disease, while autosomal recessive inheritance requires two copies of the mutated gene. Multifactorial inheritance involves multiple genes and environmental factors contributing to the development of the disease.

Examples of diseases with a known genetic predisposition:

1. Huntington's disease: An autosomal dominant disorder caused by an expansion of a CAG repeat in the Huntingtin gene, leading to progressive neurodegeneration and cognitive decline.
2. Cystic fibrosis: An autosomal recessive disorder caused by mutations in the CFTR gene, leading to respiratory and digestive problems.
3. BRCA1/2-related breast and ovarian cancer: An inherited increased risk of developing breast and ovarian cancer due to mutations in the BRCA1 or BRCA2 genes.
4. Sickle cell anemia: An autosomal recessive disorder caused by a point mutation in the HBB gene, leading to defective hemoglobin production and red blood cell sickling.
5. Type 1 diabetes: An autoimmune disease caused by a combination of genetic and environmental factors, including multiple genes in the HLA complex.

Understanding the genetic basis of disease can help with early detection, prevention, and treatment. For example, genetic testing can identify individuals who are at risk for certain diseases, allowing for earlier intervention and preventive measures. Additionally, understanding the genetic basis of a disease can inform the development of targeted therapies and personalized medicine."


There are several types of thrombophilia, including:

1. Factor V Leiden: This is the most common inherited thrombophilia and is caused by a mutation in the Factor V gene.
2. Prothrombin G20210A: This is another inherited thrombophilia that is caused by a mutation in the Prothrombin gene.
3. Protein C and S deficiency: These are acquired deficiencies of protein C and S, which are important proteins that help to prevent blood clots.
4. Antiphospholipid syndrome: This is an autoimmune disorder that causes the body to produce antibodies against phospholipids, which can lead to blood clots.
5. Cancer-associated thrombophilia: This is a condition where cancer patients are at a higher risk of developing blood clots due to their cancer and its treatment.
6. Hormone-related thrombophilia: This is a condition where hormonal changes, such as those that occur during pregnancy or with the use of hormone replacement therapy, increase the risk of blood clots.
7. Inherited platelet disorders: These are rare conditions that affect the way platelets function and can increase the risk of blood clots.
8. Anti-cardiolipin antibodies: These are autoantibodies that can cause blood clots.
9. Lupus anticoagulant: This is an autoantibody that can cause blood clots.
10. Combined genetic and acquired risk factors: Some people may have a combination of inherited and acquired risk factors for thrombophilia.

Thrombophilia can be diagnosed through various tests, including:

1. Blood tests: These tests measure the levels of certain proteins in the blood that are associated with an increased risk of blood clots.
2. Genetic testing: This can help identify inherited risk factors for thrombophilia.
3. Imaging tests: These tests, such as ultrasound and venography, can help doctors visualize the blood vessels and look for signs of blood clots.
4. Thrombin generation assay: This test measures the body's ability to produce thrombin, a protein that helps form blood clots.
5. Platelet function tests: These tests assess how well platelets work and whether they are contributing to the development of blood clots.

Treatment for thrombophilia usually involves medications to prevent or dissolve blood clots, as well as measures to reduce the risk of developing new clots. These may include:

1. Anticoagulant drugs: These medications, such as warfarin and heparin, are used to prevent blood clots from forming.
2. Thrombolytic drugs: These medications are used to dissolve blood clots that have already formed.
3. Compression stockings: These stockings can help reduce swelling and improve blood flow in the affected limb.
4. Elevating the affected limb: This can help reduce swelling and improve blood flow.
5. Avoiding long periods of immobility: This can help reduce the risk of developing blood clots.

In some cases, surgery may be necessary to remove a blood clot or repair a damaged blood vessel. In addition, people with thrombophilia may need to make lifestyle changes, such as avoiding long periods of immobility and taking regular breaks to move around, to reduce their risk of developing blood clots.

Overall, the prognosis for thrombophilia is generally good if the condition is properly diagnosed and treated. However, if left untreated, thrombophilia can lead to serious complications, such as pulmonary embolism or stroke, which can be life-threatening. It is important for people with thrombophilia to work closely with their healthcare provider to manage the condition and reduce the risk of complications.

1. Anemia: Folic acid plays a critical role in the production of red blood cells, so a deficiency can lead to anemia, which can cause fatigue, weakness, and shortness of breath.
2. Birth defects: Folic acid is crucial for fetal development during pregnancy, and a deficiency can increase the risk of birth defects such as spina bifida and cleft palate.
3. Heart disease: Folic acid helps to regulate homocysteine levels in the blood, which are associated with an increased risk of heart disease and stroke.
4. Neurological problems: Folic acid is important for the health of the nervous system, and a deficiency can lead to neurological problems such as cognitive impairment, mood disturbances, and seizures.
5. Poor wound healing: Folic acid is necessary for the production of collagen, which is important for wound healing. A deficiency can lead to slow or poor wound healing.
6. Increased risk of cancer: Some studies suggest that a folic acid deficiency may increase the risk of certain types of cancer, such as colon cancer.
7. Hair loss: Folic acid is important for hair growth, and a deficiency can lead to hair loss.
8. Skin problems: Folic acid is important for skin health, and a deficiency can lead to skin problems such as dry, flaky skin and mouth sores.
9. Mood changes: Folic acid plays a role in the production of neurotransmitters, which are chemicals that regulate mood. A deficiency can lead to mood changes such as depression and anxiety.
10. Fatigue: Folic acid is important for energy metabolism, and a deficiency can lead to fatigue and weakness.

Folic acid deficiency can be caused by a number of factors, including:

1. Poor diet: A diet that is low in folate-rich foods can lead to a deficiency.
2. Malabsorption: Certain medical conditions such as celiac disease and Crohn's disease can lead to malabsorption of folic acid.
3. Pregnancy and lactation: Women who are pregnant or breastfeeding have a higher need for folic acid, and may be at risk for deficiency if they do not consume enough.
4. Alcoholism: Heavy alcohol consumption can interfere with the absorption of folic acid.
5. Certain medications: Some medications, such as antacids and proton pump inhibitors, can interfere with the absorption of folic acid.

To diagnose a folic acid deficiency, a healthcare provider may perform a physical exam, take a medical history, and order blood tests to measure folic acid levels. Treatment for a folic acid deficiency typically involves dietary changes and supplements. Dietary changes may include consuming more folate-rich foods, such as leafy green vegetables, legumes, and whole grains. Supplements may include folic acid tablets or liquid supplements. In severe cases of deficiency, injections of folic acid may be necessary. It is important to seek medical attention if you suspect a folic acid deficiency, as untreated deficiencies can lead to serious health problems.

Treatment for homocystinuria typically involves a combination of dietary modifications and nutritional supplements to manage the symptoms and prevent long-term complications. In some cases, medication may also be prescribed to reduce the levels of homocysteine in the blood.

The prognosis for individuals with homocystinuria varies depending on the severity of the condition and the effectiveness of treatment. Some individuals with mild forms of the disorder may experience few or no symptoms, while those with more severe forms may have significant developmental delays and disabilities. With appropriate management, however, many individuals with homocystinuria can lead active and fulfilling lives.

There are several types of NTDs, including:

1. Anencephaly: A severe form of NTD where a large portion of the neural tube does not develop, resulting in the absence of a major part of the brain and skull.
2. Spina Bifida: A type of NTD where the spine does not close properly, leading to varying degrees of neurological damage and physical disability.
3. Encephalocele: A type of NTD where the brain or meninges protrude through a opening in the skull.
4. Meningomyelocele: A type of NTD where the spinal cord and meninges protrude through a opening in the back.

Causes and risk factors:

1. Genetic mutations: Some NTDs can be caused by genetic mutations that affect the development of the neural tube.
2. Environmental factors: Exposure to certain chemicals, such as folic acid deficiency, has been linked to an increased risk of NTDs.
3. Maternal health: Women with certain medical conditions, such as diabetes or obesity, are at a higher risk of having a child with NTDs.

Symptoms and diagnosis:

1. Anencephaly: Severely underdeveloped brain, absence of skull, and often death shortly after birth.
2. Spina Bifida: Difficulty walking, weakness or paralysis in the legs, bladder and bowel problems, and intellectual disability.
3. Encephalocele: Protrusion of brain or meninges through a opening in the skull, which can cause developmental delays, seizures, and intellectual disability.
4. Meningomyelocele: Protrusion of spinal cord and meninges through a opening in the back, which can cause weakness or paralysis in the legs, bladder and bowel problems, and intellectual disability.

Treatment and management:

1. Surgery: Depending on the type and severity of the NTD, surgery may be necessary to close the opening in the skull or back, or to release compressed tissue.
2. Physical therapy: To help improve mobility and strength in affected limbs.
3. Occupational therapy: To help with daily activities and fine motor skills.
4. Speech therapy: To help with communication and language development.
5. Medications: To manage seizures, pain, and other symptoms.
6. Nutritional support: To ensure adequate nutrition and growth.
7. Supportive care: To help manage the physical and emotional challenges of living with an NTD.

Prevention:

1. Folic acid supplements: Taking a daily folic acid supplement during pregnancy can help prevent NTDs.
2. Good nutrition: Eating a balanced diet that includes foods rich in folate, such as leafy greens, citrus fruits, and beans, can help prevent NTDs.
3. Avoiding alcohol and tobacco: Both alcohol and tobacco use have been linked to an increased risk of NTDs.
4. Getting regular prenatal care: Regular check-ups with a healthcare provider during pregnancy can help identify potential problems early on and reduce the risk of NTDs.
5. Avoiding infections: Infections such as rubella (German measles) can increase the risk of NTDs, so it's important to avoid exposure to these infections during pregnancy.

It's important to note that not all NTDs can be prevented, and some may be caused by genetic factors or other causes that are not yet fully understood. However, taking steps to maintain good health and getting regular prenatal care can help reduce the risk of NTDs and improve outcomes for babies born with these conditions.

There are several types of spinal dysraphism, including:

1. Spina bifida: This is the most common type of spinal dysraphism, and it occurs when the spine fails to close properly during fetal development. As a result, the spinal cord and meninges (the protective covering of the spinal cord) are exposed and can be damaged.
2. Myelomeningocele: This is a type of spina bifida that occurs when the spinal cord protrudes through an opening in the spine. It is often associated with hydrocephalus (a buildup of fluid in the brain).
3. Meningomyelocele: This is a type of spinal dysraphism that occurs when the meninges protrude through an opening in the spine, but the spinal cord remains within the spine.
4. Diastematomyelia: This is a rare type of spinal dysraphism that occurs when there is a separation or division of the spinal cord.
5. Hemicord syndrome: This is a rare type of spinal dysraphism that occurs when one half of the spinal cord is underdeveloped or absent.

The symptoms of spinal dysraphism can vary depending on the severity and location of the disorder. They may include:

* Muscle weakness or paralysis
* Loss of sensation in the affected limbs
* Bladder and bowel dysfunction
* Hydrocephalus (a buildup of fluid in the brain)
* Neurological problems such as seizures, learning disabilities, and developmental delays.

Treatment for spinal dysraphism depends on the severity of the disorder and may include:

* Surgery to repair or close the opening in the spine
* Shunting procedures to drain excess fluid from the brain
* Physical therapy to improve muscle strength and mobility
* Occupational therapy to help with daily activities and developmental delays.

The long-term outlook for individuals with spinal dysraphism varies depending on the severity of the disorder and the effectiveness of treatment. Some individuals may experience significant improvement with surgery and other treatments, while others may have ongoing neurological problems and developmental delays. It is important for individuals with spinal dysraphism to receive regular medical care and follow-up to monitor their condition and address any complications that may arise.

A condition in which spontaneous abortions occur repeatedly, often due to an underlying cause such as a uterine anomaly or infection. Also called recurrent spontaneous abortion.

Synonym(s): habitual abortion, recurrent abortion, spontaneous abortion.

Antonym(s): multiple pregnancy, retained placenta.

Example Sentence: "The patient had experienced four habitual abortions in the past year and was concerned about her ability to carry a pregnancy to term."

There are several types of inborn errors of amino acid metabolism, including:

1. Phenylketonuria (PKU): This is the most common inborn error of amino acid metabolism and is caused by a deficiency of the enzyme phenylalanine hydroxylase. This enzyme is needed to break down the amino acid phenylalanine, which is found in many protein-containing foods. If phenylalanine is not properly broken down, it can build up in the blood and brain and cause serious health problems.
2. Maple syrup urine disease (MSUD): This is a rare genetic disorder that affects the breakdown of the amino acids leucine, isoleucine, and valine. These amino acids are important for growth and development, but if they are not properly broken down, they can build up in the blood and cause serious health problems.
3. Homocystinuria: This is a rare genetic disorder that affects the breakdown of the amino acid methionine. Methionine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
4. Arginase deficiency: This is a rare genetic disorder that affects the breakdown of the amino acid arginine. Arginine is important for the body's production of nitric oxide, a compound that helps to relax blood vessels and improve blood flow.
5. Citrullinemia: This is a rare genetic disorder that affects the breakdown of the amino acid citrulline. Citrulline is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
6. Tyrosinemia: This is a rare genetic disorder that affects the breakdown of the amino acid tyrosine. Tyrosine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
7. Maple syrup urine disease (MSUD): This is a rare genetic disorder that affects the breakdown of the amino acids leucine, isoleucine, and valine. These amino acids are important for growth and development, but if they are not properly broken down, they can build up in the blood and cause serious health problems.
8. PKU (phenylketonuria): This is a rare genetic disorder that affects the breakdown of the amino acid phenylalanine. Phenylalanine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
9. Methionine adenosyltransferase (MAT) deficiency: This is a rare genetic disorder that affects the breakdown of the amino acid methionine. Methionine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.
10. Homocystinuria: This is a rare genetic disorder that affects the breakdown of the amino acid homocysteine. Homocysteine is important for the body's production of proteins and other compounds, but if it is not properly broken down, it can build up in the blood and cause serious health problems.

It is important to note that these disorders are rare and affect a small percentage of the population. However, they can be serious and potentially life-threatening, so it is important to be aware of them and seek medical attention if symptoms persist or worsen over time.

The causes of colorectal neoplasms are not fully understood, but factors such as age, genetics, diet, and lifestyle have been implicated. Symptoms of colorectal cancer can include changes in bowel habits, blood in the stool, abdominal pain, and weight loss. Screening for colorectal cancer is recommended for adults over the age of 50, as it can help detect early-stage tumors and improve survival rates.

There are several subtypes of colorectal neoplasms, including adenomas (which are precancerous polyps), carcinomas (which are malignant tumors), and lymphomas (which are cancers of the immune system). Treatment options for colorectal cancer depend on the stage and location of the tumor, but may include surgery, chemotherapy, radiation therapy, or a combination of these.

Research into the causes and treatment of colorectal neoplasms is ongoing, and there has been significant progress in recent years. Advances in screening and treatment have improved survival rates for patients with colorectal cancer, and there is hope that continued research will lead to even more effective treatments in the future.

1. Atherosclerosis: A condition in which plaque builds up inside the arteries, causing them to narrow and harden. This can lead to heart disease, heart attack, or stroke.
2. Hypertension: High blood pressure that can damage blood vessels and increase the risk of heart disease, stroke, and other conditions.
3. Peripheral artery disease (PAD): A condition in which the blood vessels in the legs and arms become narrowed or blocked, leading to pain, cramping, and weakness in the affected limbs.
4. Raynaud's phenomenon: A condition that causes blood vessels in the hands and feet to constrict in response to cold temperatures or stress, leading to discoloration, numbness, and tissue damage.
5. Deep vein thrombosis (DVT): A condition in which a blood clot forms in the deep veins of the legs, often caused by immobility or injury.
6. Varicose veins: Enlarged, twisted veins that can cause pain, swelling, and cosmetic concerns.
7. Angioplasty: A medical procedure in which a balloon is used to open up narrowed blood vessels, often performed to treat peripheral artery disease or blockages in the legs.
8. Stenting: A medical procedure in which a small mesh tube is placed inside a blood vessel to keep it open and improve blood flow.
9. Carotid endarterectomy: A surgical procedure to remove plaque from the carotid arteries, which supply blood to the brain, to reduce the risk of stroke.
10. Bypass surgery: A surgical procedure in which a healthy blood vessel is used to bypass a blocked or narrowed blood vessel, often performed to treat coronary artery disease or peripheral artery disease.

Overall, vascular diseases can have a significant impact on quality of life and can increase the risk of serious complications such as stroke, heart attack, and amputation. It is important to seek medical attention if symptoms persist or worsen over time, as early diagnosis and treatment can help to prevent long-term damage and improve outcomes.

"Methylenetetrahydrofolate reductase (MTHFR) 677C>T and methionine synthase reductase (MTRR) 66A>G polymorphisms: association ... FADH2). Flavin mononucleotide binding domain interacts with a coenzyme of flavoprotein oxidoreductase enzymes, FMN. ... It is a member of the ferredoxin-NADP(+) reductase (FNR) family of electron transferases. Methionine synthase reductase (MTRR) ... Methylenetetrahydrofolate reductase act to further the extent of DNA damage. Hypomethylation due to impaired methylation up ...
... methylenetetrahydrofolate reductase (NADPH) * EC 1.5.1.54: methylenetetrahydrofolate reductase (NADH) * *No Wikipedia article ... FADH2) EC 1.14.14.28: long-chain alkane monooxygenase EC 1.14.14.29: 25/26-hydroxycholesterol 7α-hydroxylase EC 1.14.14.30: ... flavin reductase (NADH) EC 1.5.1.37: FAD reductase (NADH) EC 1.5.1.38: FMN reductase (NADPH) EC 1.5.1.39: FMN reductase (NAD(P) ... zeatin reductase EC 1.3.1.70: Δ14-sterol reductase EC 1.3.1.71: Δ24(241)-sterol reductase EC 1.3.1.72: Δ24-sterol reductase EC ...
FADH2) Note dapplication:. Oxidorreductasa dependiente del FAD que se encuentra principalmente en BACTERIAS. Es específica ... Plastoquinol-plastocyanin reductase [D08.811.682.771] Plastoquinol-plastocyanin reductase * Ribonucleotide reductases [D08.811. ... 5,10-Methylenetetrahydrofolate reductase (FADH2) - Concept préféré Concept UI. M0076715. Terme préféré. 5,10- ... 5,10-Metilenotetrahidrofolato Reductasa (FADH2) Espagnol dEspagne Descripteur. 5,10-metilenotetrahidrofolato reductasa (FADH2) ...
FADH2), 9028-69-7. dc.subject.otherChemCAS. Methylenetetrahydrofolate Reductase (NADPH2), EC 1.5.1.20. ... Background: Mutations in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene could reduce the enzyme activity and lead to ... DOI 10.1007-s11010-007-9434-5; Mornet E, 1997, HUM GENET, V100, P512, DOI 10.1007-s004390050544; Mutchinick OM, 1999, MOL GENET ...
Reductase (FADH2). 5,10-Methylenetetrahydrofolate-Reductase (NADH) use Methylenetetrahydrofolate Dehydrogenase (NAD+) ... 7,8-Dihydroxy-9,10-Epoxy-7,8,9,10-Tetrahydrobenzo(a)pyrene use 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide ... 3-Keto-5-alpha-Steroid delta-4-Dehydrogenase use Testosterone 5-alpha-Reductase ... 2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-hexahydro-3-isobutyl-9,10-dimethoxy- ...
entry terms OXIDASES; REDUCTASES, and DEHYDROGENASES are GEN only: see Tree D8 under OXIDOREDUCTASES for all indentions and ... FADH2) [D08.811.682.550] 5,10-Methylenetetrahydrofolate Reductase (FADH2) * NADH, NADPH Oxidoreductases [D08.811.682.608] ... The recommended name will be dehydrogenase, wherever this is possible; as an alternative, reductase can be used. Oxidase is ... The recommended name will be dehydrogenase, wherever this is possible; as an alternative, reductase can be used. Oxidase is ...
FADH2)/genética , Análise de Variância , Apolipoproteínas E/genética , Doenças das Artérias Carótidas/patologia , Genótipo , ... 10. A modified compression model of spinal cord injury in rats: functional assessment and the expression of nitric oxide ... RESULTS: The mean BBB locomotor scores were 10±1.85 and 10±1.85, respectively, on days 1 and 3 in the injury group, and 21 and ... RESULTS: T1 mapping detected an increase in myocardial T1 5 min after an injection of 4 mg/kg LNAME compared with baseline in ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
FADH2) / genetics* Actions. * Search in PubMed * Search in MeSH ... Epub 2009 Mar 10. Mol Psychiatry. 2010. PMID: 19274051 Free PMC ... 2019 May 31;10:1241. doi: 10.3389/fpsyg.2019.01241. eCollection 2019. Front Psychol. 2019. PMID: 31214072 Free PMC article. ... 2018 Apr-Jun;10(2):4-15. Acta Naturae. 2018. PMID: 30116610 Free PMC article. ... Objective: The 5,10-methylenetetrahydrofolate reductase gene (MTHFR) has been linked to unipolar major depressive disorder (MDD ...
In a 3-year-old mentally retarded girl with homocystinuria due to 5,10-methylenetetrahydrofolate reductase deficiency among ... FADH2) Actions. * Search in PubMed * Search in MeSH * Add to Search ... Betaine for treatment of homocystinuria caused by methylenetetrahydrofolate reductase deficiency. Holme E, Kjellman B, Ronge E. ... Survival and psychomotor development with early betaine treatment in patients with severe methylenetetrahydrofolate reductase ...
FADH2) Preferred Concept UI. M0076715. Registry Number. EC 1.5.1.20. Scope Note. An FAD-dependent oxidoreductase found ... Plastoquinol-Plastocyanin Reductase [D08.811.682.771] * Ribonucleotide Reductases [D08.811.682.810] * Succinate Cytochrome c ... FADH2) Preferred Term Term UI T106718. LexicalTag ABX. ThesaurusID NLM (2004). ... FADH2) (NM) 1980-2003. Date Established. 2004/01/01. Date of Entry. 2003/07/09. Revision Date. 2013/07/09. ...
FADH2) Preferred Concept UI. M0076715. Registry Number. EC 1.5.1.20. Scope Note. An FAD-dependent oxidoreductase found ... Plastoquinol-Plastocyanin Reductase [D08.811.682.771] * Ribonucleotide Reductases [D08.811.682.810] * Succinate Cytochrome c ... FADH2) Preferred Term Term UI T106718. LexicalTag ABX. ThesaurusID NLM (2004). ... FADH2) (NM) 1980-2003. Date Established. 2004/01/01. Date of Entry. 2003/07/09. Revision Date. 2013/07/09. ...
N0000167878 Methylenetetrahydrofolate Dehydrogenase (NADP) N0000169060 Methylenetetrahydrofolate Reductase (NADPH2) N0000007462 ... FADH2) N0000166968 5,6-Dihydroxytryptamine N0000166969 5,7-Dihydroxytryptamine N0000168574 5,8,11,14-Eicosatetraynoic Acid ... N0000169057 Nitrate Reductase (NADH) N0000169643 Nitrate Reductase (NADPH) N0000167939 Nitrate Reductases N0000007647 Nitrates ... h N0000178702 Thioredoxin Reductase 1 N0000178714 Thioredoxin Reductase 2 N0000169063 Thioredoxin-Disulfide Reductase ...
FADH2) (NM) 1980-2003 MH - Methylenetetrahydrofolate Reductase (NADPH2) UI - D042965 MN - D8.811.682.107.290 MN - D12.776. ... HN - 2004; use METHYLENETETRAHYDROFOLATE REDUCTASE (NADPH2) (NM) 1986-2003 BX - Methylene-THF Reductase (NADPH) MH - ... AN - do not confuse with METHYLENETETRAHYDROFOLATE DEHYDROGENASE (NADP) HN - 2004; use METHYLENETETRAHYDROFOLATE DEHYDROGENASE ... In most higher eucaryotic organisms this enzyme also includes METHYLENETETRAHYDROFOLATE DEHYDROGENASE (NADP) and FORMATE- ...
Plastoquinol-Plastocyanin Reductase [D08.811.682.771] Plastoquinol-Plastocyanin Reductase * Ribonucleotide Reductases [D08.811. ... FADH2) [D08.811.682.550] 5,10-Methylenetetrahydrofolate Reductase (FADH2) * NADH, NADPH Oxidoreductases [D08.811.682.608] ...
Methylenetetrahydrofolate Dehydrogenase (NADP) [D08.811.682.662.253] * Methylenetetrahydrofolate Reductase (NADPH2) [D08.811. ... FADH2) [D08.811.682.550] * NADH, NADPH Oxidoreductases [D08.811.682.608] * Nitrogenase [D08.811.682.647] ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
Methylenetetrahydrofolate Reductase (NADPH2). Metilenotetrahidrofolato Reductasa (NADPH2). Metilmalonil-CoA Descarboxilase. ... FADH2). 5,10-Metilenotetrahidrofolato Reductasa (FADH2). Acil-CoA Desidrogenase. Acyl-CoA Dehydrogenase. Acil-CoA ... Receptor, Serotonin, 5-HT2C. Receptor de Serotonina 5-HT2C. Receptor A1 de Adenosina. Receptor, Adenosine A1. Receptor de ... Receptors, Serotonin, 5-HT4. Receptores de Serotonina 5-HT4. Receptores Acoplados a Proteína-G. Receptors, G-Protein-Coupled. ...
FADH2)/metabolismo , Proteínas de Escherichia coli/química , Proteínas de Escherichia coli/metabolismo , Escherichia coli/ ... RESULTS: IL-10 AG associated with high secretion in uninfected and infected MDMs (p < 0.05) and was reduced more effectively by ... Costimulatory blockade also induced IL-21R expression in MZP B cells, and IL-21R MZP B cells expressed even more IL-10. B-cell ... Follicles of ≥10 to ≤13 mm diameter (n = 45) were retrospectively categorized into active (n = 18), intermediate (n = 16) and ...

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