Drugs that inhibit ADENOSINE DEAMINASE activity.
A ribonucleoside antibiotic synergist and adenosine deaminase inhibitor isolated from Nocardia interforma and Streptomyces kaniharaensis. It is proposed as an antineoplastic synergist and immunosuppressant.
A potent inhibitor of ADENOSINE DEAMINASE. The drug induces APOPTOSIS of LYMPHOCYTES, and is used in the treatment of many lymphoproliferative malignancies, particularly HAIRY CELL LEUKEMIA. It is also synergistic with some other antineoplastic agents and has immunosuppressive activity.
An enzyme that catalyzes the hydrolysis of ADENOSINE to INOSINE with the elimination of AMMONIA.
Catalyze the hydrolysis of nucleosides with the elimination of ammonia.
A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.
Nucleosides in which the purine or pyrimidine base is combined with ribose. (Dorland, 28th ed)
Adenosine molecules which can be substituted in any position, but are lacking one hydroxyl group in the ribose part of the molecule.
An enzyme that catalyzes the formation of ADP plus AMP from adenosine plus ATP. It can serve as a salvage mechanism for returning adenosine to nucleic acids. EC 2.7.1.20.
A purine base and a fundamental unit of ADENINE NUCLEOTIDES.
A purine nucleoside that has hypoxanthine linked by the N9 nitrogen to the C1 carbon of ribose. It is an intermediate in the degradation of purines and purine nucleosides to uric acid and in pathways of purine salvage. It also occurs in the anticodon of certain transfer RNA molecules. (Dorland, 28th ed)
An antibiotic purine ribonucleoside that readily substitutes for adenosine in the biological system, but its incorporation into DNA and RNA has an inhibitory effect on the metabolism of these nucleic acids.
An inhibitor of nucleotide metabolism.
A nucleoside antibiotic isolated from Streptomyces antibioticus. It has some antineoplastic properties and has broad spectrum activity against DNA viruses in cell cultures and significant antiviral activity against infections caused by a variety of viruses such as the herpes viruses, the VACCINIA VIRUS and varicella zoster virus.
An enzyme which catalyzes the catabolism of S-ADENOSYLHOMOCYSTEINE to ADENOSINE and HOMOCYSTEINE. It may play a role in regulating the concentration of intracellular adenosylhomocysteine.
A class of cell surface receptors that prefer ADENOSINE to other endogenous PURINES. Purinergic P1 receptors are widespread in the body including the cardiovascular, respiratory, immune, and nervous systems. There are at least two pharmacologically distinguishable types (A1 and A2, or Ri and Ra).
An enzyme that catalyzes the deamination of AMP to IMP. EC 3.5.4.6.
The removal of an amino group (NH2) from a chemical compound.
A subclass of adenosine A2 receptors found in LEUKOCYTES, the SPLEEN, the THYMUS and a variety of other tissues. It is generally considered to be a receptor for ADENOSINE that couples to the GS, STIMULATORY G-PROTEIN.
A subtype of ADENOSINE RECEPTOR that is found expressed in a variety of tissues including the BRAIN and DORSAL HORN NEURONS. The receptor is generally considered to be coupled to the GI, INHIBITORY G-PROTEIN which causes down regulation of CYCLIC AMP.
An enzyme that catalyzes the deamination of cytidine, forming uridine. EC 3.5.4.5.
A subtype of ADENOSINE RECEPTOR that is found expressed in a variety of locations including the BRAIN and endocrine tissues. The receptor is generally considered to be coupled to the GI, INHIBITORY G-PROTEIN which causes down regulation of CYCLIC AMP.
An enzyme which catalyzes the deamination of CYTOSINE resulting in the formation of URACIL. It can also act on 5-methylcytosine to form THYMIDINE.
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.
An enzyme that catalyzes the hydrolytic deamination of deoxycytidylic acid to deoxyuridylic acid and ammonia. It plays an important role in the regulation of the pool of deoxynucleotides in higher organisms. The enzyme also acts on some 5-substituted deoxycytidylic acids. EC 3.5.4.12.
A subclass of adenosine A2 receptors found in the CECUM, the COLON, the BLADDER, and a variety of other tissues. It is generally considered to be a low affinity receptor for ADENOSINE that couples to the GS, STIMULATORY G-PROTEIN.
An enzyme that catalyzes the deamination of guanine to form xanthine. EC 3.5.4.3.
A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes SMOOTH MUSCLE, stimulates CARDIAC MUSCLE, stimulates DIURESIS, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide PHOSPHODIESTERASES, antagonism of ADENOSINE RECEPTORS, and modulation of intracellular calcium handling.
Elements of limited time intervals, contributing to particular results or situations.
A loosely defined grouping of drugs that have effects on psychological function. Here the psychotropic agents include the antidepressive agents, hallucinogens, and tranquilizing agents (including the antipsychotics and anti-anxiety agents).
Disorders related to substance abuse.
A loosely defined group of drugs that tend to increase behavioral alertness, agitation, or excitation. They work by a variety of mechanisms, but usually not by direct excitation of neurons. The many drugs that have such actions as side effects to their main therapeutic use are not included here.
Drugs obtained and often manufactured illegally for the subjective effects they are said to produce. They are often distributed in urban areas, but are also available in suburban and rural areas, and tend to be grossly impure and may cause unexpected toxicity.
A behavioral response manifested by leaving home in order to escape from threatening situations. Children or adolescents leaving home without permission is usually implied.

The extracellular versus intracellular mechanisms of inhibition of TCR-triggered activation in thymocytes by adenosine under conditions of inhibited adenosine deaminase. (1/193)

The absence or low levels of adenosine deaminase (ADA) in humans result in severe combined immunodeficiency (SCID), which is characterized by hypoplastic thymus, T lymphocyte depletion and autoimmunity. Deficiency of ADA causes increased levels of both intracellular and extracellular adenosine, although only the intracellular lymphotoxicity of accumulated adenosine is considered in the pathogenesis of ADA SCID. It is shown that extracellular but not intracellular adenosine selectively inhibits TCR-triggered up-regulation of activation markers and apoptotic events in thymocytes under conditions of ADA deficiency. The effects of intracellular adenosine are dissociated from effects of extracellular adenosine in experiments using an adenosine transporter blocker. We found that prevention of toxicity of intracellular adenosine led to survival of TCR-cross-linked thymocytes in long-term (4 days) assays, but it was not sufficient for normal T cell differentiation under conditions of inhibited ADA. Surviving TCR-cross-linked thymocytes had a non-activated phenotype due to extracellular adenosine-mediated, TCR-antagonizing signaling. Taken together the data suggest that both intracellular toxicity and signaling by extracellular adenosine may contribute to pathogenesis of ADA SCID. Accordingly, extracellular adenosine may act on thymocytes, which survived intracellular toxicity of adenosine during ADA deficiency by counteracting TCR signaling. This, in turn, could lead to failure of positive and negative selection of thymocytes, and to additional elimination of thymocytes or autoimmunity of surviving T cells.  (+info)

Nucleotide pool imbalance and adenosine deaminase deficiency induce alterations of N-region insertions during V(D)J recombination. (2/193)

Template-independent nucleotide additions (N regions) generated at sites of V(D)J recombination by terminal deoxynucleotidyl transferase (TdT) increase the diversity of antigen receptors. Two inborn errors of purine metabolism, deficiencies of adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP), result in defective lymphoid development and aberrant pools of 2'-deoxynucleotides that are substrates for TdT in lymphoid precursors. We have asked whether selective increases in dATP or dGTP pools result in altered N regions in an extrachromosomal substrate transfected into T-cell or pre-B-cell lines. Exposure of the transfected cells to 2'-deoxyadenosine and an ADA inhibitor increased the dATP pool and resulted in a marked increase in A-T insertions at recombination junctions, with an overall decreased frequency of V(D)J recombination. Sequence analysis of VH-DH-JH junctions from the IgM locus in B-cell lines from ADA-deficient patients demonstrated an increase in A-T insertions equivalent to that found in the transfected cells. In contrast, elevation of dGTP pools, as would occur in PNP deficiency, did not alter the already rich G-C content of N regions. We conclude that the frequency of V(D)J recombination and the composition of N-insertions are influenced by increases in dATP levels, potentially leading to alterations in antigen receptors and aberrant lymphoid development. Alterations in N-region insertions may contribute to the B-cell dysfunction associated with ADA deficiency.  (+info)

Quantification of extracellular and intracellular adenosine production: understanding the transmembranous concentration gradient. (3/193)

BACKGROUND: Inhibitors of adenosine membrane transport cause vasodilation and enhance the plasma adenosine concentration. However, it is unclear why the plasma adenosine concentration rises rather than falls when membrane transport is inhibited. We tested the hypothesis that the cytosolic adenosine concentration exceeds the interstitial concentration under well-oxygenated conditions. METHODS AND RESULTS: In isolated, isovolumically working guinea pig hearts (n=50), the release rate of adenosine and accumulation of S-adenosylhomocysteine (after 20 minutes of 200 micromol/L homocysteine), a measure of the free cytosolic adenosine concentration, were determined in the absence and presence of specific and powerful blockers of adenosine membrane transport (nitrobenzylthioinosine 1 micromol/L), adenosine deaminase (erythro-9-hydroxy-nonyl-adenine 5 micromol/L), and adenosine kinase (iodotubericidine 10 micromol/L). Data analysis with a distributed multicompartment model revealed a total cardiac adenosine production rate of 2294 pmol. min-1. g-1, of which 8% was produced in the extracellular region. Because of a high rate of intracellular metabolism, however, 70.3% of extracellularly produced adenosine was taken up into cellular regions, an effect that was effectively eliminated by membrane transport block. The resulting approximately 2.8-fold increase of the interstitial adenosine concentration evoked near-maximal coronary dilation. CONCLUSIONS: We rejected the hypothesis that the cytosolic adenosine concentration exceeds the interstitial. Rather, there is significant extracellular production, and the parenchymal cell represents a sink, not a source, for adenosine under well-oxygenated conditions.  (+info)

Diinosine pentaphosphate (IP5I) is a potent antagonist at recombinant rat P2X1 receptors. (4/193)

1. The antagonist activity of a series of diinosine polyphosphates (IpnI, where n=3, 4, 5) was assessed against ATP-activated inward currents at rat P2X(1-4) receptors expressed in Xenopus oocytes and studied under voltage-clamp conditions. 2. Diinosine polyphosphates were prepared by the enzymatic degradation of their corresponding diadenosine polyphosphates (e.g., Ap5A into Ip5I) using 5'-adenylic deaminase, and purified using reverse-phase chromatography. 3. Against ATP-responses at rP2X1 receptors, the potency order for antagonism was (pIC50): Ip5I (8.5)>Ip4I (6.3)>Ip3I (>4.5). Ip5I (10-100 nM) caused a concentration-dependent rightwards displacement of the ATP concentration-response curve without reducing the maximum ATP effect. However, the Schild plot was non-linear which indicated Ip5I is not a competitive antagonist. Blockade by micromolar concentrations of Ip5I was not surmountable. Ip4I also behaved as a non-surmountable antagonist. 4. Against ATP-responses at rP2X3 receptors, the potency order for antagonism was (pIC50): Ip4I (6. 0)>Ip5I (5.6)>Ip3I (>4.5). Blockade by Ip4I (pA2, 6.75) and Ip5I (pA2, 6.27) was surmountable at micromolar concentrations. 5. Diinosine polyphosphates failed to inhibit ATP-responses at rP2X2 receptors, whereas agonist responses at rP2X4 were reversibly potentiated by Ip4I and Ip5I. None of the parent diadenosine polyphosphates behave as antagonists at rP2X1 - 4 receptors. 6. Thus, Ip5I acted as a potent and relatively-selective antagonist at the rP2X1 receptor. This dinucleotide pentaphosphate represents a high-affinity antagonist for the P2X1 receptor, at which it acts in a competitive manner at low (100 nM) concentrations.  (+info)

The anticonvulsant BW534U87 depresses epileptiform activity in rat hippocampal slices by an adenosine-dependent mechanism and through inhibition of voltage-gated Na+ channels. (5/193)

1. The cellular and molecular actions of BW534U87 were studied using intracellular and extracellular recordings from the CA1 region of rat hippocampal slices and whole-cell voltage-clamp recordings of recombinant human brain type IIA Na+ channels expressed in Chinese hamster ovary (CHO) cells. 2. Normal excitatory and inhibitory postsynaptic potentials evoked in hippocampal slices were unaffected by BW534U87 or the adenosine deaminase inhibitor EHNA. However, epileptiform activity was depressed by BW534U87 (50 micronM) and this inhibition was reversed by the adenosine receptor antagonist 8-phenyl theophylline (8-PT, 30 micronM). EHNA (10 micronM) mimicked the effects of BW534U87. Furthermore, BW534U87 enhanced the inhibitory effects of exogenous adenosine on evoked synaptic potentials. BW534U87 (50 micronM) also voltage- and use-dependently inhibited action potentials elicited by current injection, independent of the adenosine system, since it was not affected by 8-PT. 3. In CHO cells expressing the recombinant human brain Na+ channel, BW534U87 produced a concentration- and voltage-dependent inhibition of Na+ currents with a half-maximal inhibitory concentration of 10 micronM at a Vh of -60 mV. Use-dependent inhibition was evident at high-frequencies (20x20 ms pulse train at 10 Hz). 4 In conclusion, BW534U87 blocks hippocampal epileptiform activity by a dual mechanism. The first action is similar to that produced by EHNA and is dependent on endogenous adenosine probably by inhibition of adenosine deaminase. Secondly, BW534U87 directly inhibits voltage-gated Na+ channels in a voltage- and frequency-dependent manner. Both actions of BW534U87 are activity-dependent and may synergistically contribute to its overall anticonvulsant effects in animal models of epilepsy.  (+info)

A normal level of adenosine deaminase activity in the red cell lysates of carriers and patients with severe combined immunodeficiency disease. (6/193)

The red cell lysates of two children with severe combined immunodeficiency disease (SCID) exhibited a virtually total absence of adenosine deaminase (adenosine aminohydrolase, EC 3.5.4.4) when standard volumes were assayed. Under these conditions the parents exhibited depressed specific activity except for one mother, whose lysate showed a normal value for activity. Upon storage of the lysate at 4 degrees, a significant amount of activity appeared in one of the SCID children, and the activity of the heterozygous carriers was stimulated. With the use of a sensitive spectrophotometric assay based on conversion of inosine to uric acid, it was shown that the specific enzymatic activity in each of the SCID patients increased progressively as the volume of lysate assayed was lowered. With the smallest amount of lysate this specific activity was in the normal range. Similarly, the specific activity of each of the parents' lysates increased to the level of normal (or, in one case, about twice normal) as smaller volumes were assayed. The activity in the SCID patient was inhibitable by 2-fluoroadenosine and N6-methyladenosine, known competitive inhibitors of human red cell adenosine deaminase. The lysate from the SCID patient was also shown to inhibit adenosine deaminase partially purified from a normal individual. The results are interpreted in terms of a genetically programmed production of an adenosine deaminase inhibitor in at least one variant of the severe combined immunodeficiency disease.  (+info)

Age-related changes in A(1)-adenosine receptor-mediated bradycardia. (7/193)

The impact of age on functional sensitivity to A(1)-adenosine receptor activation was studied in Langendorff-perfused hearts from young (1-2 mo) and old (12-18 mo) male Wistar rats. Adenosine mediated bradycardia in young and old hearts, with sensitivity enhanced approximately 10-fold in old [negative logarithm of EC(50) (pEC(50)) = 4.56 +/- 0.11] versus young hearts (pEC(50) = 3.70 +/- 0. 09). Alternatively, the nonmetabolized A(1) agonists N(6)-cyclohexyladenosine and (R)-N(6)-phenylisopropyladenosine were equipotent in young (pEC(50) = 7.43 +/- 0.12 and 6.61 +/- 0.19, respectively) and old hearts (pEC(50) = 7.07 +/- 0.10 and 6.80 +/- 0. 11, respectively), suggesting a role for uptake and/or catabolism in age-related changes in adenosine sensitivity. In support of this suggestion, [(3)H]-adenosine uptake was approximately twofold greater in young than in old hearts (from 3-100 microM adenosine). However, although inhibition of adenosine deaminase and adenosine transport with 10 microM erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride and 10 microM S-(4-nitrobenzyl)-6-thioinosine increased adenosine sensitivity three- to fourfold, it failed to abolish the sensitivity difference in old (pEC(50) = 4.95 +/- 0.08) versus young (pEC(50) = 4.29 +/- 0.13) hearts. Data indicate that 1) age increases functional A(1) receptor sensitivity to adenosine without altering the sensitivity of the A(1) receptor itself, and 2) age impairs adenosine transport and/or catabolism, but this does not explain differing functional sensitivity to adenosine. This increased functional sensitivity to adenosine may have physiological significance in the older heart.  (+info)

Adenosine-mediated killing of cultured epithelial cancer cells. (8/193)

Because micromolar concentrations of adenosine (Ado) have been documented recently in the interstitial fluid of carcinomas growing in animals, we examined the effects of low concentrations of Ado on the growth of cultured human carcinoma cells. Ado alone had little effect upon cell growth. In the presence of one of a number of Ado deaminase (ADA) inhibitors, Ado led to significant growth inhibition of all cell lines tested. Similar effects were found when ATP, ADP, or AMP was substituted for Ado. Surprisingly, the ADA inhibitor coformycin (CF) had a much greater potentiating effect than did 2'-deoxycoformycin (DCF), although DCF is a more potent ADA inhibitor. The growth inhibition of the Ado/CF combination was not abrogated by pyrimidines or caffeine, a nonspecific Ado receptor blocker. Toxicity was prevented by the addition of the Ado transport inhibitor dipyridamole or the Ado kinase inhibitor 5'-amino 5'-deoxyadenosine. S-Adenosylhomocysteine hydrolase is not involved because neither homocysteine thiolactone nor an S-adenosylhomocysteine hydrolase inhibitor (adenosine dialdehyde) potentiated toxicity of the Ado/CF combination. Unexpectedly, substitution of 2'-deoxyadenosine (the toxic moiety in congenital ADA deficiency) for Ado, did not lead to equivalent toxicity. The Ado/CF combination inhibited DNA synthesis and brought about morphological changes consistent with apoptosis. Together, these findings indicate that the Ado-mediated killing proceeds via an intracellular route that requires the action of Ado kinase. The enhanced cofactor activity of CF may be attributable to its being a more potent inhibitor of AMP deaminase than is DCF.  (+info)

Adenosine deaminase inhibitors are a class of medications that work by blocking the action of the enzyme adenosine deaminase. This enzyme is responsible for breaking down adenosine, a chemical in the body that helps regulate the immune system and is involved in the inflammatory response.

By inhibiting the activity of adenosine deaminase, these medications can increase the levels of adenosine in the body. This can be useful in certain medical conditions where reducing inflammation is important. For example, adenosine deaminase inhibitors are sometimes used to treat rheumatoid arthritis, a chronic autoimmune disease characterized by inflammation and damage to the joints.

One common adenosine deaminase inhibitor is called deoxycoformycin (also known as pentostatin). This medication is typically given intravenously and is used to treat hairy cell leukemia, a rare type of cancer that affects white blood cells.

It's important to note that adenosine deaminase inhibitors can have serious side effects, including suppression of the immune system, which can make people more susceptible to infections. They should only be used under the close supervision of a healthcare provider.

Coformycin is an antimetabolite antibiotic, which means it interferes with the growth of bacteria by inhibiting the synthesis of nucleic acids, the genetic material of bacteria. It is derived from Streptomyces coelicolor and is used primarily in research to study bacterial metabolism.

Coformycin is a potent inhibitor of bacterial enzyme adenosine deaminase, which is involved in purine biosynthesis. By inhibiting this enzyme, Coformycin prevents the bacteria from synthesizing the building blocks needed to make DNA and RNA, thereby inhibiting their growth.

Coformycin has not been approved for use as a therapeutic drug in humans or animals due to its narrow spectrum of activity and potential toxicity. However, it is still used in research settings to study bacterial metabolism and the mechanisms of antibiotic resistance.

Pentostatin is a medication used in the treatment of certain types of cancer, including hairy cell leukemia and certain T-cell lymphomas. It is a type of drug called a purine nucleoside analog, which works by interfering with the production of DNA and RNA, the genetic material found in cells. This can help to stop the growth and multiplication of cancer cells.

Pentostatin is given intravenously (through an IV) in a healthcare setting, such as a hospital or clinic. It is usually administered on a schedule of every other week. Common side effects of pentostatin include nausea, vomiting, diarrhea, and loss of appetite. It can also cause more serious side effects, such as low blood cell counts, infections, and liver problems.

It's important to note that this is a medical definition of the drug and its use, and it should not be used as a substitute for professional medical advice. If you have any questions about pentostatin or your treatment, it is best to speak with your healthcare provider.

Adenosine Deaminase (ADA) is an enzyme that plays a crucial role in the immune system by helping to regulate the levels of certain chemicals called purines within cells. Specifically, ADA helps to break down adenosine, a type of purine, into another compound called inosine. This enzyme is found in all tissues of the body, but it is especially active in the immune system's white blood cells, where it helps to support their growth, development, and function.

ADA deficiency is a rare genetic disorder that can lead to severe combined immunodeficiency (SCID), a condition in which babies are born with little or no functional immune system. This makes them extremely vulnerable to infections, which can be life-threatening. ADA deficiency can be treated with enzyme replacement therapy, bone marrow transplantation, or gene therapy.

Nucleoside deaminases are a group of enzymes that catalyze the removal of an amino group (-NH2) from nucleosides, converting them to nucleosides with a modified base. This modification process is called deamination. Specifically, these enzymes convert cytidine and adenosine to uridine and inosine, respectively. Nucleoside deaminases play crucial roles in various biological processes, including the regulation of gene expression, immune response, and nucleic acid metabolism. Some nucleoside deaminases are also involved in the development of certain diseases and are considered as targets for drug design and discovery.

Adenosine is a purine nucleoside that is composed of a sugar (ribose) and the base adenine. It plays several important roles in the body, including serving as a precursor for the synthesis of other molecules such as ATP, NAD+, and RNA.

In the medical context, adenosine is perhaps best known for its use as a pharmaceutical agent to treat certain cardiac arrhythmias. When administered intravenously, it can help restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardia (PSVT) by slowing conduction through the atrioventricular node and interrupting the reentry circuit responsible for the arrhythmia.

Adenosine can also be used as a diagnostic tool to help differentiate between narrow-complex tachycardias of supraventricular origin and those that originate from below the ventricles (such as ventricular tachycardia). This is because adenosine will typically terminate PSVT but not affect the rhythm of VT.

It's worth noting that adenosine has a very short half-life, lasting only a few seconds in the bloodstream. This means that its effects are rapidly reversible and generally well-tolerated, although some patients may experience transient symptoms such as flushing, chest pain, or shortness of breath.

Ribonucleosides are organic compounds that consist of a nucleoside bound to a ribose sugar. Nucleosides are formed when a nitrogenous base (such as adenine, guanine, uracil, cytosine, or thymine) is attached to a sugar molecule (either ribose or deoxyribose) via a beta-glycosidic bond. In the case of ribonucleosides, the sugar component is D-ribose. Ribonucleosides play important roles in various biological processes, particularly in the storage, transfer, and expression of genetic information within cells. When ribonucleosides are phosphorylated, they become the building blocks of RNA (ribonucleic acid), a crucial biomolecule involved in protein synthesis and other cellular functions. Examples of ribonucleosides include adenosine, guanosine, uridine, cytidine, and inosine.

Deoxyadenosine is a chemical compound that is a component of DNA, one of the nucleic acids that make up the genetic material of living organisms. Specifically, deoxyadenosine is a nucleoside, which is a molecule consisting of a sugar (in this case, deoxyribose) bonded to a nitrogenous base (in this case, adenine).

Deoxyribonucleosides like deoxyadenosine are the building blocks of DNA, along with phosphate groups. In DNA, deoxyadenosine pairs with thymidine via hydrogen bonds to form one of the four rungs in the twisted ladder structure of the double helix.

It is important to note that there is a similar compound called adenosine, which contains an extra oxygen atom on the sugar molecule (making it a ribonucleoside) and is a component of RNA, another nucleic acid involved in protein synthesis and other cellular processes.

Adenosine kinase (ADK) is an enzyme that plays a crucial role in the regulation of adenosine levels in cells. The medical definition of adenosine kinase is:

"An enzyme (EC 2.7.1.20) that catalyzes the phosphorylation of adenosine to form adenosine monophosphate (AMP) using ATP as the phosphate donor. This reaction helps maintain the balance between adenosine and its corresponding nucleotides in cells, and it plays a significant role in purine metabolism, cell signaling, and energy homeostasis."

Adenosine kinase is widely distributed in various tissues, including the brain, heart, liver, and muscles. Dysregulation of adenosine kinase activity has been implicated in several pathological conditions, such as ischemia-reperfusion injury, neurodegenerative disorders, and cancer. Therefore, modulating adenosine kinase activity has emerged as a potential therapeutic strategy for treating these diseases.

Adenine is a purine nucleotide base that is a fundamental component of DNA and RNA, the genetic material of living organisms. In DNA, adenine pairs with thymine via double hydrogen bonds, while in RNA, it pairs with uracil. Adenine is essential for the structure and function of nucleic acids, as well as for energy transfer reactions in cells through its role in the formation of adenosine triphosphate (ATP), the primary energy currency of the cell.

Inosine is not a medical condition but a naturally occurring compound called a nucleoside, which is formed from the combination of hypoxanthine and ribose. It is an intermediate in the metabolic pathways of purine nucleotides, which are essential components of DNA and RNA. Inosine has been studied for its potential therapeutic benefits in various medical conditions, including neurodegenerative disorders, cardiovascular diseases, and cancer. However, more research is needed to fully understand its mechanisms and clinical applications.

Tubercidin is not a medical term itself, but it is a type of antibiotic that belongs to the class of compounds known as nucleoside antibiotics. Specifically, tubercidin is a naturally occurring adenine analogue that is produced by several species of Streptomyces bacteria.

Tubercidin has been found to have antimicrobial and antitumor activities. It works by inhibiting the enzyme adenosine deaminase, which plays a crucial role in the metabolism of nucleotides in cells. By inhibiting this enzyme, tubercidin can interfere with DNA and RNA synthesis, leading to cell death.

While tubercidin has shown promise as an anticancer agent in preclinical studies, its clinical use is limited due to its toxicity and potential for causing mutations in normal cells. Therefore, it is primarily used for research purposes to study the mechanisms of nucleotide metabolism and the effects of nucleoside analogues on cell growth and differentiation.

Tetrahydrouridine (THU) is not a medication itself, but rather a metabolic inhibitor. It is a derivative of the nucleoside uridine and has been studied in the context of its ability to inhibit the enzyme cytidine deaminase. This enzyme is responsible for the breakdown of certain antiviral medications, such as zidovudine (AZT) and stavudine (d4T), which are used in the treatment of HIV infection.

By inhibiting cytidine deaminase, THU can help to increase the levels and effectiveness of these antiviral drugs, while also reducing some of their side effects. However, it is important to note that THU is not currently approved for use as a medication by itself and is typically used in research or experimental settings in combination with other antiretroviral therapies.

Vidarabine is an antiviral medication used to treat herpes simplex infections, particularly severe cases such as herpes encephalitis (inflammation of the brain caused by the herpes simplex virus). It works by interfering with the DNA replication of the virus.

In medical terms, vidarabine is a nucleoside analogue that is phosphorylated intracellularly to the active form, vidarabine triphosphate. This compound inhibits viral DNA polymerase and incorporates into viral DNA, causing termination of viral DNA synthesis.

Vidarabine was previously used as an injectable medication but has largely been replaced by more modern antiviral drugs such as acyclovir due to its greater efficacy and lower toxicity.

Adenosylhomocysteinase is an enzyme that plays a crucial role in the methionine cycle, which is a biochemical pathway involved in the synthesis and metabolism of various essential molecules in the body. The formal medical definition of adenosylhomocysteinase is:

"An enzyme that catalyzes the reversible conversion of S-adenosylhomocysteine to homocysteine and adenosine. This reaction is the first step in the recycling of methionine, a sulfur-containing amino acid that is essential for various metabolic processes, including the synthesis of proteins, neurotransmitters, and phospholipids."

In simpler terms, adenosylhomocysteinase helps break down S-adenosylhomocysteine, a byproduct of methylation reactions in the body, into its component parts: homocysteine and adenosine. This breakdown is essential for the proper functioning of the methionine cycle and the maintenance of normal levels of homocysteine, which can be toxic at high concentrations.

Deficiencies or mutations in the adenosylhomocysteinase gene can lead to an accumulation of S-adenosylhomocysteine and homocysteine, which can contribute to various health issues, including neurological disorders, cardiovascular disease, and developmental abnormalities.

Purinergic P1 receptors are a type of G-protein coupled receptor that bind to nucleotides such as adenosine. These receptors are involved in a variety of physiological processes, including modulation of neurotransmitter release, cardiovascular function, and immune response. There are four subtypes of P1 receptors (A1, A2A, A2B, and A3) that have different signaling pathways and functions. Activation of these receptors can lead to a variety of cellular responses, including inhibition or stimulation of adenylyl cyclase activity, changes in intracellular calcium levels, and activation of various protein kinases. They play important roles in the central nervous system, cardiovascular system, respiratory system, gastrointestinal system, and immune system.

AMP deaminase is an enzyme that is responsible for the conversion of adenosine monophosphate (AMP) to inosine monophosphate (IMP), which is a part of the purine nucleotide cycle. This enzyme plays a crucial role in energy metabolism, particularly in muscles during exercise. A deficiency in AMP deaminase has been linked to muscle fatigue and weakness.

Deamination is a biochemical process that refers to the removal of an amino group (-NH2) from a molecule, especially from an amino acid. This process typically results in the formation of a new functional group and the release of ammonia (NH3). Deamination plays a crucial role in the metabolism of amino acids, as it helps to convert them into forms that can be excreted or used for energy production. In some cases, deamination can also lead to the formation of toxic byproducts, which must be efficiently eliminated from the body to prevent harm.

Adenosine A2A receptor is a type of G protein-coupled receptor that binds to the endogenous purine nucleoside, adenosine. It is a subtype of the A2 receptor along with the A2B receptor and is widely distributed throughout the body, particularly in the brain, heart, and immune system.

The A2A receptor plays an essential role in various physiological processes, including modulation of neurotransmission, cardiovascular function, and immune response. In the brain, activation of A2A receptors can have both excitatory and inhibitory effects on neuronal activity, depending on the location and context.

In the heart, A2A receptor activation has a negative chronotropic effect, reducing heart rate, and a negative inotropic effect, decreasing contractility. In the immune system, A2A receptors are involved in regulating inflammation and immune cell function.

Pharmacologically, A2A receptor agonists have been investigated for their potential therapeutic benefits in various conditions, including Parkinson's disease, chronic pain, ischemia-reperfusion injury, and cancer. Conversely, A2A receptor antagonists have also been studied as a potential treatment for neurodegenerative disorders, such as Alzheimer's disease, and addiction.

Adenosine A1 receptor is a type of G protein-coupled receptor that binds to the endogenous purine nucleoside adenosine. When activated, it inhibits the production of cyclic AMP (cAMP) in the cell by inhibiting adenylyl cyclase activity. This results in various physiological effects, such as decreased heart rate and reduced force of heart contractions, increased potassium conductance, and decreased calcium currents. The Adenosine A1 receptor is widely distributed throughout the body, including the brain, heart, kidneys, and other organs. It plays a crucial role in various biological processes, including cardiovascular function, neuroprotection, and inflammation.

Cytidine deaminase is an enzyme that catalyzes the removal of an amino group from cytidine, converting it to uridine. This reaction is part of the process of RNA degradation and also plays a role in the immune response to viral infections.

Cytidine deaminase can be found in various organisms, including bacteria, humans, and other mammals. In humans, cytidine deaminase is encoded by the APOBEC3 gene family, which consists of several different enzymes that have distinct functions and expression patterns. Some members of this gene family are involved in the restriction of retroviruses, such as HIV-1, while others play a role in the regulation of endogenous retroelements and the modification of cellular RNA.

Mutations in cytidine deaminase genes have been associated with various diseases, including cancer and autoimmune disorders. For example, mutations in the APOBEC3B gene have been linked to an increased risk of breast cancer, while mutations in other members of the APOBEC3 family have been implicated in the development of lymphoma and other malignancies. Additionally, aberrant expression of cytidine deaminase enzymes has been observed in some autoimmune diseases, such as rheumatoid arthritis and systemic lupus erythematosus, suggesting a potential role for these enzymes in the pathogenesis of these conditions.

Adenosine A3 receptor (A3R) is a type of G-protein coupled receptor that binds to adenosine, a purine nucleoside, and plays a role in various physiological processes. The activation of A3R leads to the inhibition of adenylate cyclase activity, which results in decreased levels of intracellular cAMP. This, in turn, modulates several downstream signaling pathways that are involved in anti-inflammatory and neuroprotective effects.

A3R is widely expressed in various tissues, including the brain, heart, lungs, liver, kidneys, and immune cells. In the central nervous system, A3R activation has been shown to have neuroprotective effects, such as reducing glutamate release, protecting against excitotoxicity, and modulating neuroinflammation. Additionally, A3R agonists have been investigated for their potential therapeutic benefits in various pathological conditions, including pain management, ischemia-reperfusion injury, and neurodegenerative diseases.

Overall, the Adenosine A3 receptor is an important target for drug development due to its role in modulating inflammation and cellular responses in various tissues and diseases.

Cytosine deaminase is an enzyme that catalyzes the hydrolytic deamination of cytosine residues in DNA or deoxycytidine residues in RNA, converting them to uracil or uridine, respectively. This enzyme plays a role in the regulation of gene expression and is also involved in the defense against viral infections in some organisms. In humans, cytosine deamination in DNA can lead to mutations and has been implicated in the development of certain diseases, including cancer.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

DCMP deaminase is an enzyme that catalyzes the deamination of deoxycytidine monophosphate (dCMP) to deoxyuridine monophosphate (dUMP). This reaction is a part of the pyrimidine nucleotide biosynthesis pathway. The enzyme's systematic name is "deoxycytidine monophosphate deaminase." It plays a crucial role in DNA synthesis and maintenance by providing the necessary precursor (dUMP) for thymidylate synthesis, which is essential for the production of thymidine triphosphate (dTTP), one of the four building blocks of DNA.

Adenosine A2B receptor (A2BAR) is a type of G protein-coupled receptor that binds the endogenous purine nucleoside adenosine. It is a subtype of the A2 class of adenosine receptors, which also includes A2A receptor.

The A2BAR is widely expressed in various tissues and cells, including vascular smooth muscle cells, endothelial cells, fibroblasts, immune cells, and epithelial cells. Activation of the A2BAR by adenosine leads to a variety of cellular responses, such as relaxation of vascular smooth muscle, inhibition of platelet aggregation, modulation of inflammatory responses, and stimulation of fibroblast proliferation and collagen production.

The A2BAR has been implicated in several physiological and pathophysiological processes, such as cardiovascular function, pain perception, neuroprotection, tumor growth and metastasis, and pulmonary fibrosis. Therefore, the development of selective A2BAR agonists or antagonists has been an area of active research for therapeutic interventions in these conditions.

Guanine Deaminase is an enzyme that catalyzes the chemical reaction in which guanine, one of the four nucleotides that make up DNA and RNA, is deaminated to form xanthine. This reaction is part of the purine catabolism pathway, which is the breakdown of purines to produce energy and eliminate nitrogenous waste. The gene that encodes this enzyme in humans is located on chromosome 2 and is called GDA. Deficiency in guanine deaminase has been associated with Lesch-Nyhan syndrome, a rare genetic disorder characterized by mental retardation, self-mutilation, spasticity, and uric acid overproduction.

Caffeine is a central nervous system stimulant that occurs naturally in the leaves, seeds, or fruits of some plants. It can also be produced artificially and added to various products, such as food, drinks, and medications. Caffeine has a number of effects on the body, including increasing alertness, improving mood, and boosting energy levels.

In small doses, caffeine is generally considered safe for most people. However, consuming large amounts of caffeine can lead to negative side effects, such as restlessness, insomnia, rapid heart rate, and increased blood pressure. It is also possible to become dependent on caffeine, and withdrawal symptoms can occur if consumption is suddenly stopped.

Caffeine is found in a variety of products, including coffee, tea, chocolate, energy drinks, and some medications. The amount of caffeine in these products can vary widely, so it is important to pay attention to serving sizes and labels to avoid consuming too much.

In the field of medicine, "time factors" refer to the duration of symptoms or time elapsed since the onset of a medical condition, which can have significant implications for diagnosis and treatment. Understanding time factors is crucial in determining the progression of a disease, evaluating the effectiveness of treatments, and making critical decisions regarding patient care.

For example, in stroke management, "time is brain," meaning that rapid intervention within a specific time frame (usually within 4.5 hours) is essential to administering tissue plasminogen activator (tPA), a clot-busting drug that can minimize brain damage and improve patient outcomes. Similarly, in trauma care, the "golden hour" concept emphasizes the importance of providing definitive care within the first 60 minutes after injury to increase survival rates and reduce morbidity.

Time factors also play a role in monitoring the progression of chronic conditions like diabetes or heart disease, where regular follow-ups and assessments help determine appropriate treatment adjustments and prevent complications. In infectious diseases, time factors are crucial for initiating antibiotic therapy and identifying potential outbreaks to control their spread.

Overall, "time factors" encompass the significance of recognizing and acting promptly in various medical scenarios to optimize patient outcomes and provide effective care.

Psychotropic drugs, also known as psychoactive drugs, are a class of medications that affect the function of the central nervous system, leading to changes in consciousness, perception, mood, cognition, or behavior. These drugs work by altering the chemical neurotransmitters in the brain, such as dopamine, serotonin, and norepinephrine, which are involved in regulating mood, thought, and behavior.

Psychotropic drugs can be classified into several categories based on their primary therapeutic effects, including:

1. Antipsychotic drugs: These medications are used to treat psychosis, schizophrenia, and other related disorders. They work by blocking dopamine receptors in the brain, which helps reduce hallucinations, delusions, and disordered thinking.
2. Antidepressant drugs: These medications are used to treat depression, anxiety disorders, and some chronic pain conditions. They work by increasing the availability of neurotransmitters such as serotonin, norepinephrine, or dopamine in the brain, which helps improve mood and reduce anxiety.
3. Mood stabilizers: These medications are used to treat bipolar disorder and other mood disorders. They help regulate the ups and downs of mood swings and can also be used as adjunctive treatment for depression and anxiety.
4. Anxiolytic drugs: Also known as anti-anxiety medications, these drugs are used to treat anxiety disorders, panic attacks, and insomnia. They work by reducing the activity of neurotransmitters such as GABA, which can help reduce anxiety and promote relaxation.
5. Stimulant drugs: These medications are used to treat attention deficit hyperactivity disorder (ADHD) and narcolepsy. They work by increasing the availability of dopamine and norepinephrine in the brain, which helps improve focus, concentration, and alertness.

It is important to note that psychotropic drugs can have significant side effects and should only be used under the close supervision of a qualified healthcare provider.

Substance-related disorders, as defined in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), refer to a group of conditions caused by the use of substances such as alcohol, drugs, or medicines. These disorders are characterized by a problematic pattern of using a substance that leads to clinically significant impairment or distress. They can be divided into two main categories: substance use disorders and substance-induced disorders. Substance use disorders involve a pattern of compulsive use despite negative consequences, while substance-induced disorders include conditions such as intoxication, withdrawal, and substance/medication-induced mental disorders. The specific diagnosis depends on the type of substance involved, the patterns of use, and the presence or absence of physiological dependence.

Central nervous system (CNS) stimulants are a class of drugs that increase alertness, attention, energy, and/or mood by directly acting on the brain. They can be prescribed to treat medical conditions such as narcolepsy, attention deficit hyperactivity disorder (ADHD), and depression that has not responded to other treatments.

Examples of CNS stimulants include amphetamine (Adderall), methylphenidate (Ritalin, Concerta), and modafinil (Provigil). These medications work by increasing the levels of certain neurotransmitters, such as dopamine and norepinephrine, in the brain.

In addition to their therapeutic uses, CNS stimulants are also sometimes misused for non-medical reasons, such as to enhance cognitive performance or to get high. However, it's important to note that misusing these drugs can lead to serious health consequences, including addiction, cardiovascular problems, and mental health issues.

"Street drugs" is a colloquial term rather than medical jargon, but it generally refers to illegal substances or medications that are used without a prescription. These can include a wide variety of drugs such as marijuana, cocaine, heroin, methamphetamines, ecstasy, LSD, and many others. They are called "street drugs" because they are often bought and sold on the street or in clandestine settings, rather than through legitimate pharmacies or medical professionals. It's important to note that these substances can be highly dangerous and addictive, with serious short-term and long-term health consequences.

Runaway behavior is not a formally recognized medical term, but it is often used in the context of psychiatry and psychology to describe a pattern of behavior where an individual, usually a teenager or adolescent, leaves home without permission or runs away from their living situation with the intent of avoiding responsibility, authority figures, or difficult situations. This behavior can be associated with various mental health conditions such as conduct disorder, oppositional defiant disorder, depression, anxiety, or trauma-related disorders. It's important to note that running away can pose significant risks to the individual's safety and well-being, and professional help should be sought if runaway behavior is a concern.

No data available that match "adenosine deaminase inhibitors"


Careful postmarketing surveillance for adverse effects, especially among the DPP4 inhibitors, and continue … ... Adenosine Deaminase Inhibitors* * Diabetes Mellitus, Type 2 / drug therapy* * Dipeptidyl Peptidase 4 ... Careful postmarketing surveillance for adverse effects, especially among the DPP4 inhibitors, and continued evaluation in ... Dipeptidyl peptidase 4 inhibitors had an increased risk of infection (risk ratio, 1.2 [95% CI, 1.0-1.4] for nasopharyngitis and ...
"Adenosine deaminase: functional implications and different classes of inhibitors". Medicinal Research Reviews. 21 (2): 105-128 ... their mechanism of action is inhibition of adenosine deaminase. Adenosine deaminase deficiency GRCh38: Ensembl release 89: ... Adenosine deaminase (also known as adenosine aminohydrolase, or ADA) is an enzyme (EC 3.5.4.4) involved in purine metabolism. ... Adenosine deaminase deficiency leads to pulmonary fibrosis, suggesting that chronic exposure to high levels of adenosine can ...
Be sure to mention adenosine deaminase inhibitors such as pentostatin (Nipent). Your doctor may need to change the doses of ...
View and buy high purity products active at Deaminases from Tocris Bioscience. ... ADAR1 (adenosine deaminases acting on double-stranded RNA) inhibitor; inhibits leukemia stem cell self-renewal. ... Adenosine deaminases (ADA) irreversibly convert adenosine into inosine by the removal of an amino group and they are necessary ... two well known members of this group are adenosine deaminase and cytidine deaminase. ...
... and the adenosine-deaminase inhibitor, erythro-9,2-hydroxyl-3-nonyl-adenine (EHNA), in the incubation medium. Epithelium ... intact trachealis to adenosine was increased significantly in the presence of the adenosine uptake and degradation inhibitors. ... and adenosine response curves were obtained with and without the adenosine uptake blocker, dipyridamole, ... Adenosine effects were comparable in intact and epithelium stripped preparations in the absence of dipyridamole and EHNA. ...
Ada ?=? adenosine deaminase, Adk ?=? adenosine kinase, ALI ?=? acute lung injury, Alp ?=? alkaline phosphatase, Cx43 ?=? ... The caspase-3 inhibitor Ac-DEVD-CHO, however, only partially inhibited the high-dose SNP-induced cell death, indicating that ... Adenosine is produced by T cells at a sophisticated price from ATP however, not from NAD and as well as upregulated A2a ... CD4+ T cells from wounded lung rapidly metabolized extracellular ATP to adenosine and AMP however, not NAD or cAMP. These ...
Categorized as Adenosine Deaminase Post navigation. Previous post. Glioblastoma the most frequent primary malignant brain tumor ... an EGF receptor tyrosine kinase inhibitor) provide minimal palliation for individuals with advanced pancreatic cancers; latest ...
adenosine deaminase inhibitor (Pentostatin). halogenated/ribonucleotide reductase inhibitors (Cladribine, Clofarabine, ... Enzyme inhibitors. FI (Tipifarnib) • CDK inhibitors (Alvocidib, Seliciclib) • PrI (Bortezomib) • PhI (Anagrelide) • IMPDI ( ... thymidylate synthase inhibitor (Fluorouracil, Capecitabine, Tegafur, Carmofur, Floxuridine). DNA polymerase inhibitor ( ... dihydrofolate reductase inhibitor (Aminopterin, Methotrexate, Pemetrexed, Pralatrexate) • thymidylate synthase inhibitor ( ...
Pentostatin is a specific adenosine deaminase (ADA) inhibitor. The enzyme ADA is essential for the development of T- and B- ... Another option to overcome BRAF inhibitor resistance is the combination with MEK inhibitors [41, 43]. In an open-label phase II ... 6.1.1.2.4BRAF inhibitors. The detection of the BRAF V600E mutation in almost all patients with classic HCL offers a new target ... A prerequisite for the use of BRAF inhibitors is the detection of the BRAF V600E mutation. The analysis can be performed in ...
GluR2 RNA editing can be completed by an RNA-dependent adenosine deaminase (ADAR2). Lack of GluR2 editing qualified prospects ... Interestingly ADAR2 cleavage was not blocked by any of the caspase inhibitors examined suggesting that ADAR2 was not cleaved by ... could be sufficient to hamper the activity of the cleaved C terminal fragment which only contains the DRBM1 and the deaminase ... DRBM1 in ADAR2 contributes primarily to ADAR2 dimerization and RNA binding and that DRBM2 mainly contributes to the deaminase ...
Adenosine by deaminase is converted to inosine and then to uric acid. All these molecules remain high in DS patients. H2S is a ... Recently, RAR and RXR have been shown to upregulate plasminogen activator inhibitor-1 (PAI-1), a major player involved in ECM ... Thus, it is important to determine whether SIRT3 (inhibitor of HDAC3) can decrease the trans-sulfuration activity in DS ... We treated mouse mesangial cells with or without H2S donor, GYY4137 and FOXO1 inhibitor, AS1842856 in HHcy condition and ...
Adenosine deaminase inhibitors: synthesis and structure-activity relationships of 2-hydroxy-3-nonyl derivatives of azoles.. ... Adenosine Deaminase: Functional Implications and Different Classes of Inhibitors. 2001 Cristalli, G.; Costanzi, S.; Lambertucci ... Adenosine Deaminase: Functional Implications and Different Classes of Inhibitors 2001 Cristalli, G.; Costanzi, S.; Lambertucci ... Adenosine deaminase inhibitors: synthesis and structure-activity relationships of 2-hydroxy-3-nonyl derivatives of azoles. 1994 ...
Class/mechanism: Purine (adenosine) analog, inhibitor of adenosine deaminase (ADA), causes elevated intracellular levels of ...
... removing ambient adenosine (by adding adenosine deaminase) can reproduce the actions of methylxanthines. Plasma concentrations ... 14] Caffeine is an inhibitor of the adenosine A2 receptor and was shown to improves motor deficits in a mouse model of ... Interaction between adenosine A2a receptors and dopamine D2 receptors in the striatum might underlie some of the behavioral ... Thus, adenosine receptor blockade appears to be the predominant mode of action. Methylxanthines act as competitive antagonists ...
... manifest non-immunologic symptoms including pulmonary dysfunction likely attributable to elevated systemic adenosine levels. ... Adenosine deaminase-deficient severe combined immunodeficiency (ADA-SCID) is characterized by impaired T-, B- and NK-cell ... may benefit from therapies that target peripheral airway inflammation like inhaled corticosteroids and leukotriene inhibitors [ ... Adenosine-dependent pulmonary fibrosis in adenosine deaminase-deficient mice. J Immunol. 2005;175(3):1937-46. ...
Double-strand RNA-dependent adenosine deaminases (ADARs) are another type of host enzymes that edit viral genomes by ... and analysis of population sequences has shown that resistance to protease inhibitors and non-nucleoside polymerase inhibitors ... predicted RNA secondary structures as substrates for adenosine deaminases that act on RNA. J Gen Virol 83:1445-1455 ... Cao Y, Bao Y, Xia W, Wu H, Wei F, Zhang Y, Zhang R, Xu X (2016) Resistance-associated mutations to HCV protease inhibitors ...
Adenosine Deaminase Inhibitors [D27.505.519.389.092] Adenosine Deaminase Inhibitors * Adenylyl Cyclase Inhibitors [D27.505. ... Acetylcholinesterase Inhibitors Entry term(s). Acetylcholinesterase Inhibitor Inhibitor, Acetylcholinesterase Inhibitors, ... Inhibitors, Acetylcholinesterase. Inhibitors, Cholinesterase. Inhibitors, Irreversible Cholinesterase. Inhibitors, Reversible ... Inhibitors, Reversible Cholinesterase Reversible Cholinesterase Inhibitors Acetylcholinesterase Inhibitors - Narrower Concept ...
ADAR, RNA-specific adenosine deaminase; IRF, IFN-regulatory factor; JAK, Janus kinase; Mx, myxovirus-resistance proteins; OAS, ... SARSCoV-2 cell entry depends on ace2 and tmprss2 and is blocked by a clinically proven protease inhibitor. Ou X, Liu Y, Lei X, ... A recently discovered IFN-induced gene is the RNA-specific adenosine deaminase ADAR 23although its potential antiviral function ... USA 99 , - Patterson, J. Mechanism of interferon action: double-stranded RNA-specific adenosine deaminase from human cells is ...
Adenosine Deaminase Inhibitors [D27.505.519.389.092] Adenosine Deaminase Inhibitors * Adenylyl Cyclase Inhibitors [D27.505. ... Inhibitor, RNA Synthesis Inhibitors, RNA Synthesis RNA Synthesis Inhibitor Synthesis Inhibitor, RNA Synthesis Inhibitors, RNA ... DNA Synthesis Inhibitor Inhibitor, DNA Synthesis Inhibitors, DNA Synthesis Synthesis Inhibitor, DNA Synthesis Inhibitors, DNA ... DNA Polymerase Inhibitor Inhibitor, DNA Polymerase Inhibitors, DNA Polymerase Polymerase Inhibitor, DNA Polymerase Inhibitors, ...
LIN28 inhibitor LI71 is a potent and cell-permeable LIN28 inhibitor, which abolishes LIN28-mediated oligouridylation with an ... Adenosine Deaminase. *Serine/threonine kinase. *FAAH. *15-PGDH. *CETP. *Ferroptosis. *HMG-CoA Reductase ... Keywords: buy LIN28 inhibitor LI71 , LIN28 inhibitor LI71 Supplier , purchase LIN28 inhibitor LI71 , LIN28 inhibitor LI71 cost ... LIN28 inhibitor LI71 manufacturer , order LIN28 inhibitor LI71 , LIN28 inhibitor LI71 distributor , buy 1357248-83-9 , 1357248- ...
Dipeptidyl peptidase-4 (DPP4 or DPPIV), also known as adenosine deaminase complexing protein 2 or CD26 (cluster of ... The MEROPS online database for peptidases and their inhibitors: S09.003. *Dipeptidyl-Peptidase+IV at the U.S. National Library ... Kameoka J, Tanaka T, Nojima Y, Schlossman SF, Morimoto C (July 1993). "Direct association of adenosine deaminase with a T cell ... DPP-4 also binds the enzyme adenosine deaminase specifically and with high affinity. The significance of this interaction has ...
Adenosine Deaminase. *Aldose Reductase. *Apoptosis Inducer. *COMT. *Enolase. *Endogenous Metabolite. *Glucokinase. *PAI-1 ...
Adenosine Deaminase *Adenylyl Cyclase *AMY Receptors *ATPase *AXOR12 Receptor *Ca2+ Ionophore *Cannabinoid, Other ...
Adenosine Deaminase. 1. 2004. 239. 0.050. Why? Amyloidogenic Proteins. 1. 2022. 151. 0.050. Why? ... Protein Synthesis Inhibitors. 1. 2003. 192. 0.060. Why? Injections, Intraventricular. 1. 2003. 232. 0.060. Why? ...
Adenosine Deaminase Inhibitors. *Adenylyl Cyclase Inhibitors. *Aromatic Amino Acid Decarboxylase Inhibitors. *beta-Lactamase ... "Cyclooxygenase Inhibitors" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical ... This graph shows the total number of publications written about "Cyclooxygenase Inhibitors" by people in this website by year, ... Below are the most recent publications written about "Cyclooxygenase Inhibitors" by people in Profiles. ...
Adenosine deaminase inhibitor (Pentostatin). *Halogenated/ribonucleotide reductase inhibitors (Cladribine. *Clofarabine. * ...
"Adenosine/AMP deaminase domain [Interproscan].","protein_coding" "PTI_15G03740.1","No alias","Phaeodactylum tricornutum"," ... ","Proteinase inhibitor I13, potato inhibitor I [Interproscan].","protein_coding" "Sro19_g013570.1","Contig446.g6021"," ... "Adenosine/AMP deaminase domain [Interproscan].","protein_coding" "TP07G02030.1","No alias","Thalassiosira pseudonana"," ... ","Septum formation inhibitor MinC, C-terminal; EF-hand domain; Sodium/calcium exchanger membrane region [Interproscan]."," ...
Author researchensembleCategories Adenosine DeaminaseTags Rabbit Polyclonal to ZNF691., Rilpivirine Post navigation. Previous ...
Adenosine deaminase severe combined immunodeficiency (ADA-SCID) is an autosomal recessive disorder in which a lack of ADA ... Adding an inhibitor, erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA), has been previously reported to minimize enzyme activity, ... Development of dried blood spot quality control materials for adenosine deaminase severe combined immunodeficiency and an LC-MS ... We describe an alternative method using unnatural L-enantiomer nucleosides (L-adenosine and L-2-deoxyadenosine) which ...
Identification of ADAR1 adenosine deaminase dependency in a subset of cancer cells. Nat Commun. 2018 12 21; 9(1):5450. View in: ... Oncogenic transformation by inhibitor-sensitive and -resistant EGFR mutants. PLoS Med. 2005 Nov; 2(11):e313. View in: Pubmed ... Author Correction: Identification of ADAR1 adenosine deaminase dependency in a subset of cancer cells. Nat Commun. 2022 Apr 01 ... Resistance to CDK2 inhibitors is associated with selection of polyploid cells in CCNE1-amplified ovarian cancer. Clin Cancer ...
  • It is needed for the breakdown of adenosine from food and for the turnover of nucleic acids in tissues. (wikipedia.org)
  • Adenosine deaminases (ADA) irreversibly convert adenosine into inosine by the removal of an amino group and they are necessary for the breakdown of food and turnover of nucleic acids. (tocris.com)
  • It has also been proposed that ADA, in addition to adenosine breakdown, stimulates release of excitatory amino acids and is necessary to the coupling of A1 adenosine receptors and heterotrimeric G proteins. (wikipedia.org)
  • 2-Alkenyl and 2-alkyl derivatives of adenosine and adenosine-5'-N-ethyluronamide: different affinity and selectivity of E- and Z-diastereomers at A2A adenosine receptors. (unipg.it)
  • ADA irreversibly deaminates adenosine, converting it to the related nucleoside inosine by the substitution of the amino group by a keto group. (wikipedia.org)
  • Competitive inhibition has been observed for ADA, where the product inosine acts at the competitive inhibitor to enzymatic activity. (wikipedia.org)
  • Adenosine by deaminase is converted to inosine and then to uric acid. (bvsalud.org)
  • Adenosine deaminase deficiency leads to pulmonary fibrosis, suggesting that chronic exposure to high levels of adenosine can exacerbate inflammation responses rather than suppressing them. (wikipedia.org)
  • Adenosine deaminase (ADA) deficiency is among the most severe forms of PIDs, leading to severe combined immunodeficiency (SCID) and susceptibility to severe and recurrent opportunistic infections. (biomedcentral.com)
  • Adenosine deaminase (also known as adenosine aminohydrolase, or ADA) is an enzyme (EC 3.5.4.4) involved in purine metabolism. (wikipedia.org)
  • Class/mechanism: Purine (adenosine) analog, inhibitor of adenosine deaminase (ADA), causes elevated intracellular levels of dATP, and inhibits ribonucleotide reductase, which interferes with DNA synthesis. (hemonc.org)
  • Be sure to mention adenosine deaminase inhibitors such as pentostatin (Nipent). (medlineplus.gov)
  • two well known members of this group are adenosine deaminase and cytidine deaminase. (tocris.com)
  • They are usually named after their substrate and two well known members of this group are adenosine deaminase (E.C. 3.5.4.4) and cytidine deaminase (E.C. 3.5.4.5). (tocris.com)
  • Cytidine deaminases convert cytosine and deoxycytosine to uridine and deoxyuridine respectively, and are involved in maintaining the cellular pyrimidine pool. (tocris.com)
  • Additionally, massive numbers of mutations can be introduced by some virus-encoded diversity-generating elements, as well as by host-encoded cytidine/adenine deaminases. (springer.com)
  • Adenosine deaminase inhibitors: synthesis and structure-activity relationships of 2-hydroxy-3-nonyl derivatives of azoles. (unipg.it)
  • Adenosine deaminase inhibitors: synthesis, diastereoisomeric resolution and biological activity of 1-(2-hydroxy-3-nonyl)-1,2,4-triazole-3-carboxamide. (unipg.it)
  • We searched MEDLINE (1966-May 20, 2007) and the Cochrane Central Register of Controlled Trials (second quarter, 2007) for English-language randomized controlled trials involving an incretin mimetic (glucagonlike peptide 1 [GLP-1] analogue) or enhancer (dipeptidyl peptidase 4 [DPP4] inhibitor). (nih.gov)
  • Dipeptidyl peptidase-4 ( DPP4 or DPPIV ), also known as adenosine deaminase complexing protein 2 or CD26 ( cluster of differentiation 26) is a protein that, in humans, is encoded by the DPP4 gene . (wikizero.com)
  • A class of oral hypoglycemics called dipeptidyl peptidase-4 inhibitors works by inhibiting the action of this enzyme, thereby prolonging incretin effect in vivo . (wikizero.com)
  • Incretins lowered hemoglobin A(1c) compared with placebo (weighted mean difference, -0.97% [95% confidence interval {CI}, -1.13% to -0.81%] for GLP-1 analogues and -0.74% [95% CI, -0.85% to -0.62%] for DPP4 inhibitors) and were noninferior to other hypoglycemic agents. (nih.gov)
  • Glucagonlike peptide 1 analogues resulted in weight loss (1.4 kg and 4.8 kg vs placebo and insulin, respectively) while DPP4 inhibitors were weight neutral. (nih.gov)
  • Careful postmarketing surveillance for adverse effects, especially among the DPP4 inhibitors, and continued evaluation in longer-term studies and in clinical practice are required to determine the role of this new class among current pharmacotherapies for type 2 diabetes. (nih.gov)
  • It has also been recognized that AMP deaminase protein and activity is upregulated in mouse hearts that overexpress HIF-1α, which in part explains the attenuated levels of adenosine in HIF-1α expressing hearts during ischemic stress. (wikipedia.org)
  • Affected children, in addition to early onset of infections, manifest non-immunologic symptoms including pulmonary dysfunction likely attributable to elevated systemic adenosine levels. (biomedcentral.com)
  • 2-Alkynyl derivatives of adenosine-5'-N-ethyluronamide: selective A2 adenosine receptor agonists with potent inhibitory activity on platelet aggregation. (unipg.it)
  • 2-Aralkynyl and 2-heteroalkynyl derivatives of adenosine-5'-N-ethyluronamide as selective A2a adenosine receptor agonists. (unipg.it)
  • The effects of the selective ITK inhibitor BI 10N on cell lines and mouse models were also decided. (hdac-pathway.com)
  • Some mutations in the gene for adenosine deaminase cause it not to be expressed. (wikipedia.org)
  • H2S is a potent inhibitor of mitochondrial complexes I-IV, and regulated by UCP1. (bvsalud.org)
  • The substrate, adenosine, is stabilized and bound to the active site by nine hydrogen bonds. (wikipedia.org)
  • 2006 have shown that DRBM1 in ADAR2 contributes primarily to ADAR2 dimerization and RNA binding and that DRBM2 mainly contributes to the deaminase activity. (biotech-angels.com)
  • Loss of dimerization and RNA binding could be sufficient to hamper the activity of the cleaved C terminal fragment which only contains the DRBM1 and the deaminase domain. (biotech-angels.com)
  • Deaminases are enzymes that catalyze the hydrolysis of C-NH 2 bonds in amino compounds, producing ammonia. (tocris.com)
  • DPP-4 also binds the enzyme adenosine deaminase specifically and with high affinity. (wikizero.com)
  • Adenosine deaminase-deficient severe combined immunodeficiency (ADA-SCID) is characterized by impaired T-, B- and NK-cell function. (biomedcentral.com)
  • The X-ray structures of murine adenosine deaminase with bound potent inhibitors (Ki values approximately 10(-13) M) (8R)-hydroxyl-2'-deoxycoformycin (pentostatin), a transition state analogue, and (6S)-hydroxyl-1,6-dihydropurine riboside, a reaction coordinate analogue, have been determined and refined to resolutions of 2.6 and 1.95 A, respectively. (nih.gov)
  • Be sure to mention adenosine deaminase inhibitors such as pentostatin (Nipent). (medlineplus.gov)
  • Pentostatin is a potent transition state inhibitor of the enzyme adenosine deaminase (ADA). (nih.gov)
  • Pentostatin inhibition of ADA, particularly in the presence of adenosine or deoxyadenosine, leads to cytotoxicity, and this is believed to be due to elevated intracellular levels of dATP which can block DNA synthesis through inhibition of ribonucleotide reductase. (nih.gov)
  • In man, following a single-dose of 4 mg/m 2 of pentostatin infused over 5 minutes, the distribution half-life was 11 minutes, the mean terminal half-life was 5.7 hours, the mean plasma clearance was 68 mL/min/m 2 , and approximately 90% of the dose was excreted in the urine as unchanged pentostatin and/or metabolites as measured by adenosine deaminase inhibitory activity. (nih.gov)
  • Comment: Pentostatin is a potent inhibitor of adenosine deaminase (pegademase). (medscape.com)
  • Deoxyadenosine at low concentrations and in the presence of an inhibitor of adenosine deaminase (adenosine aminohydrolase, EC 3.5.4.4) is markedly toxic to lymphoblast cell lines of T cell origin but does not impair growth of B cell lines. (stanfordhealthcare.org)
  • Adenosine deaminase, which catalyzes the irreversible hydrolytic deamination of adenosine nucleosides to inosine nucleosides and ammonia, is a key enzyme in purine metabolism and lymphoid development. (nih.gov)
  • Cytidine Deaminase (3.5.4.5) is a homotetramer enzyme that catalyzes the irreversible deamination of cytidine to produce uridine, thus maintaining the intracellular pyrimidine pool of uridine. (abcam.com)
  • AN - traumatic kidney injury: index KIDNEY/ inj HN - 2011 MH - Adenosine A1 Receptor Agonists UI - D058907 MN - D27.505.519.625.725.200.100.100 MN - D27.505.696.577.725.200.100.100 MS - Compounds that bind to and stimulate ADENOSINE A1 RECEPTORS. (nih.gov)
  • Another option is 5-α-reductase inhibitors , which can reduce prostate size and increase urine flow. (mederinutricion.com)
  • 5. Treatment of acute lymphoblastic leukemia with 2'-deoxycoformycin: clinical and biochemical consequences of adenosine deaminase inhibition. (nih.gov)
  • 10. Inhibition of adenosine deaminase to increase the antitumor activity of adenine nucleoside analogues. (nih.gov)
  • 12. In vivo inhibition of adenosine deaminase by 2'-deoxycoformycin in mouse blood and leukemia L1210 cells. (nih.gov)
  • 14. Biochemical consequences of adenosine deaminase inhibition in vivo. (nih.gov)
  • ARRANON is a nucleoside metabolic inhibitor indicated for the treatment of patients with T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL) in adult and pediatric patients age 1 year and older whose disease has not responded to or has relapsed following treatment with at least two chemotherapy regimens. (nih.gov)
  • 19. Biochemical changes induced in hairy-cell leukemia following treatment with the adenosine deaminase inhibitor 2'-deoxycoformycin. (nih.gov)
  • and adenosine response curves were obtained with and without the adenosine uptake blocker, dipyridamole, and the adenosine-deaminase inhibitor, erythro-9,2-hydroxyl-3-nonyl-adenine (EHNA), in the incubation medium. (cdc.gov)
  • Adenosine effects were comparable in intact and epithelium stripped preparations in the absence of dipyridamole and EHNA. (cdc.gov)
  • HN - 2011 MH - 5-Lipoxygenase-Activating Protein Inhibitors UI - D058946 MN - D27.505.519.389.86 MS - Compounds that bind to and inhibit the action of 5-LIPOXYGENASE-ACTIVATING PROTEINS. (nih.gov)
  • Identifying Potential Inhibitors of Biofilm-Antagonistic Proteins to Promote Biofilm Formation: A Virtual Screening and Molecular Dynamics Simulations approach. (edu.in)
  • Drugs that inhibit ADENOSINE DEAMINASE activity. (bvsalud.org)
  • 2. Remission induction with adenosine-deaminase inhibitor 2'-deoxycoformycin in Thy-lymphoblastic leukaemia. (nih.gov)
  • Cytidine Deaminase Assay Kit (ab239723) uses Cytidine Deaminase (CDA) to convert cytidine to uridine and NH 3 , as intermediates. (abcam.com)
  • This product is manufactured by BioVision, an Abcam company and was previously called K451 Cytidine Deaminase Activity Assay Kit (Fluorometric). (abcam.com)
  • Polymorphisms in STAT4, PTPN2, PSORS1C1 and TRAF3IP2 Genes Are Associated with the Response to TNF Inhibitors in Patients with Rheumatoid Arthritis. (cdc.gov)
  • The sensitivity of denuded lung trachealis compared to intact trachealis to adenosine was increased significantly in the presence of the adenosine uptake and degradation inhibitors. (cdc.gov)
  • Adenosine Deaminase Gene Polymorphism and Baseline Serum Level of Adenosine Deaminase as a Biomarker of Response to Methotrexate in Rheumatoid Arthritis. (cdc.gov)
  • 4. Purinogenic lymphocytotoxicity: clues to a wider chemotherapeutic potential for the adenosine deaminase inhibitors. (nih.gov)
  • 2022). Adenosine Deaminase and Cytokines Associated with Infectious Diseases as Risk Factors for Inflammatory Arthritis and Methotrexate as a Potential Prophylactic Agent. (edu.in)
  • Further confirmed by increase in the tumor marker enzymes (Aryl hydrocarbon hydroxylase, γ-glutamyl transpeptidase, 5 -Nucleotidase, lactate dehydrogenase and Adenosine deaminase). (scialert.net)
  • 8/9/2010) TOTAL 2011 NEW DESCRIPTORS = 573 MH - 14-alpha Demethylase Inhibitors UI - D058888 MN - D27.505.519.389.49 MS - Compounds that specifically inhibit STEROL 14-DEMETHYLASE. (nih.gov)
  • 1. Treatment of acute lymphoblastic leukemia with the adenosine deaminase inhibitor 2'-deoxycoformycin. (nih.gov)