A ribonucleoside antibiotic synergist and adenosine deaminase inhibitor isolated from Nocardia interforma and Streptomyces kaniharaensis. It is proposed as an antineoplastic synergist and immunosuppressant.
Drugs that inhibit ADENOSINE DEAMINASE activity.
An enzyme that catalyzes the deamination of AMP to IMP. EC 3.5.4.6.
Nucleosides in which the purine or pyrimidine base is combined with ribose. (Dorland, 28th ed)
Catalyze the hydrolysis of nucleotides with the elimination of ammonia.
Catalyze the hydrolysis of nucleosides with the elimination of ammonia.
An enzyme that catalyzes the hydrolysis of ADENOSINE to INOSINE with the elimination of AMMONIA.
Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2'-, 3'-, or 5'-position.
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.

5'-Nucleotidase as a marker of both general and local inflammation in rheumatoid arthritis patients. (1/126)

OBJECTIVES: To evaluate measurements of serum and synovial fluid 5'-nucleotidase (5'N) activity as a marker of general and local inflammation in arthritis, and to resolve a contradiction in the literature as to whether or not the activity of 5'N in the synovial fluids of rheumatoid arthritis (RA) patients is raised in comparison with that in the synovial fluids of other arthritis patients. METHODS: Assays for 5'N were carried out in the presence of inhibitors of other phosphatases, AMP deaminase and of 5'N itself. RESULTS: The 5'N activity in the synovial fluid of RA patients was both significantly higher (mean 1.7-fold) and had a greater variance than that in the synovial fluids of other arthritis patients, and the contradiction in the literature was resolved. There was a strong correlation between the 5'N activity in the sera of RA patients and their erythrocyte sedimentation rate. There was no significant correlation between the 5'N in the serum and synovial fluid for the RA patients, in marked contrast to the strong correlation between the two 5'N activities shown by the osteoarthritis patients. The 5'N activity was greater in the synovial fluid than in the serum for virtually all the patients, showing that it was being made locally. CONCLUSIONS: The 5'N activity in the serum (which came mostly from the liver) could be used as a marker of general inflammation, whereas the 5'N in the synovial fluid was mostly produced locally, and could be used as a marker of joint inflammation, particularly for the RA patients.  (+info)

Adenosine-mediated killing of cultured epithelial cancer cells. (2/126)

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)

Direct measurement of adenosine release during hypoxia in the CA1 region of the rat hippocampal slice. (3/126)

We have used an enzyme-based, twin-barrelled sensor to measure adenosine release during hypoxia in the CA1 region of rat hippocampal slices in conjunction with simultaneous extracellular field recordings of excitatory synaptic transmission. When loaded with a combination of adenosine deaminase, nucleoside phosphorylase and xanthine oxidase, the sensor responded linearly to exogenous adenosine over the concentration range 10 nM to 20 microM. Without enzymes, the sensor when placed on the surface of hippocampal slices recorded a very small net signal during hypoxia of 40 +/- 43 pA (mean +/- s.e.m.; n = 7). Only when one barrel was loaded with the complete sequence of enzymes and the other with the last two in the cascade did the sensor record a large net difference signal during hypoxia (1226 +/- 423 pA; n = 7). This signal increased progressively during the hypoxic episode, scaled with the hypoxic depression of the simultaneously recorded field excitatory postsynaptic potential and was greatly reduced (67 +/- 6.5 %; n = 9) by coformycin (0.5-2 microM), a selective inhibitor of adenosine deaminase, the first enzyme in the enzymic cascade within the sensor. For 5 min hypoxic episodes, the sensor recorded a peak concentration of adenosine of 5.6 +/- 1.2 microM (n = 16) with an IC(50) for the depression of transmission of approximately 3 microM. In slices pre-incubated for 3-6 h in nominally Ca(2+)-free artificial cerebrospinal fluid, 5 min of hypoxia resulted in an approximately 9-fold greater release of adenosine (48.9 +/- 17.7 microM; n = 6). High extracellular Ca(2+) (4 mM) both reduced the adenosine signal recorded by the sensor during hypoxia (3.5 +/- 0.6 microM; n = 4) and delayed the hypoxic depression of excitatory synaptic transmission.  (+info)

Enhancement of cellular adenosine triphosphate levels in PC12 cells by extracellular adenosine. (4/126)

To elucidate the biological significance of extracellular adenine compounds, the effects of adenosine (Ado) on cellular levels of adenine compounds, especially adenosine triphosphate (ATP), in PC12 cells were studied. Ado and inosine but not adenosine 5'-monophosphate, adenosine 5'-diphosphate, ATP, guanosine, cytosine, thymidine, and uridine, significantly enhanced cellular ATP levels in PC12 cells in time- and dose-dependent manners. Various P1 receptor agonists of Ado did not enhance the ATP level. In addition, theophylline, an antagonist of P1 receptors, did not inhibit the Ado-evoked ATP enhancement. These results suggest that the Ado receptor is not involved in the augmentation of the cellular ATP level induced by Ado in PC12 cells. The ATP-enhancing effect of Ado was potentiated by dipyridamole, an inhibitor of Ado uptake, or coformycin, an inhibitor of Ado deaminase. The effect of Ado on the ATP level was also observed when PC12 cells were incubated in glucose-free medium. Together these results suggest that enhancement of cellular ATP levels in PC12 cells by extracellular Ado might be acceleration of ATP synthesis through the Ado salvage system using hypoxanthine-guanine phosphoribosyltransferase rather than Ado kinase since 5'-iodotubercidin, an inhibitor of Ado kinase, had no effect on the enhancement elicited by Ado.  (+info)

Extracellular ATP and adenosine induce cell apoptosis of human hepatoma Li-7A cells via the A3 adenosine receptor. (5/126)

1. Extracellular ATP is a potent signaling molecule that modulates a myriad of cellular functions through the activation of P2 purinergic receptors and is cytotoxic to a variety of cells at higher concentrations. The mechanism of ATP-elicited cytotoxicity is not fully understood. In this study, we investigated the effect of extracellular ATP on the human hepatoma Li-7A cells. 2. We observed a time- and dose-dependent growth inhibition of Li-7A cells by ATP, which is accompanied by an increase in the active form of caspase-3 as well as increased cleavage of its substrate, poly (ADP-ribose) polymerase. The cytotoxic effect of extracellular ATP was not mediated by the P2X7 receptor, since (1).the effect was not abolished by the P2X7 receptor antagonists oxidized ATP and KN-62, and (2).extracellular ADP, AMP, and adenosine were also cytotoxic. 3. We found that ATP and ADP were degraded to adenosine by Li-7A cells and that treatment of Li-7A cells by adenosine resulted in growth inhibition and caspase-3 activation, indicating that adenosine is the apoptotic agent. Using adenosine receptor agonists and antagonists, as well as inhibitors of adenosine transport and deamination, we showed that the cytotoxic effect of adenosine is specifically mediated by the A3 receptor even though transcripts of A1, A2A, A2B, and a splice variant of the P2X7 receptors were detected in Li-7A cells by RT-PCR. 4. Cytotoxicity caused by exogenous ATP and adenosine was completely abolished by the caspase-3 inhibitor Z-DEVD-FMK, demonstrating the central role of caspase-3 in apoptosis of Li-7A cells.  (+info)

Relatively small increases in the steady-state levels of nucleobase deamination products in DNA from human TK6 cells exposed to toxic levels of nitric oxide. (6/126)

Nitric oxide (NO) is a physiologically important molecule that has been implicated in the pathophysiology of diseases associated with chronic inflammation, such as cancer. While the complicated chemistry of NO-mediated genotoxicity has been extensively study in vitro, neither the spectrum of DNA lesions nor their consequences in vivo have been rigorously defined. We have approached this problem by exposing human TK6 lymphoblastoid cells to controlled steady-state concentrations of 1.75 or 0.65 microM NO along with 186 microM O2 in a recently developed reactor that avoids the anomalous gas-phase chemistry of NO and approximates the conditions at sites of inflammation in tissues. The resulting spectrum of nucleobase deamination products was defined using a recently developed liquid chromatography/mass spectrometry (LC/MS) method, and the results were correlated with cytotoxicity and apoptosis. A series of control experiments revealed the necessity of using dC and dA deaminase inhibitors to avoid adventitious formation of 2'-deoxyuridine (dU) and 2'-deoxyinosine (dI), respectively, during DNA isolation and processing. Exposure of TK6 cells to 1.75 microM NO and 186 microM O2 for 12 h (1260 microM x min dose) resulted in 32% loss of cell viability measured immediately after exposure and 87% cytotoxicity after a 24 h recovery period. The same exposure resulted in 3.5-, 3.8-, and 4.1-fold increases in dX, dI, and dU, respectively, to reach the following levels: dX, 7 (+/- 1) per 10(6) nt; dI, 25 (+/- 2.1) per 10(6) nt; and dU, 40 (+/- 3.8) per 10(6) nt. dO was not detected above the limit of detection of 6 lesions per 10(7) nt in 50 microg of DNA. A 12 h exposure to 0.65 microM NO and 190 microM O2 (468 microM x min dose) caused 1.7-, 1.8-, and 2.0-fold increases in dX, dI, and dU, respectively, accompanied by a approximately 15% (+/- 3.6) reduction in cell viability immediately after exposure. Again, dO was not detected. These results reveal modest increases in the steady-state levels of DNA deamination products in cells exposed to relatively cytotoxic levels of NO. This could result from limited nitrosative chemistry in nuclear DNA in cells exposed to NO or high levels of formation balanced by rapid repair of nucleobase deamination lesions in DNA.  (+info)

Crystallization and preliminary X-ray crystallographic analysis of adenosine 5'-monophosphate deaminase (AMPD) from Arabidopsis thaliana in complex with coformycin 5'-phosphate. (7/126)

Adenosine 5'-monophosphate deaminase (AMPD) is a eukaryotic enzyme that converts adenosine 5'-monophosphate (AMP) to inosine 5'-monophosphate (IMP) and ammonia. AMPD from Arabidopsis thaliana (AtAMPD) was cloned into the baculoviral transfer vector p2Bac and co-transfected along with a modified baculoviral genome into Spodoptera frugiperda (Sf9) cells. The resulting recombinant baculovirus were plaque-purified, amplified and used to overexpress recombinant AtAMPD. Crystals of purified AtAMPD have been obtained to which coformycin 5'-phosphate, a transition-state inhibitor, is bound. Crystals belong to space group P6(2)22, with unit-cell parameters a = b = 131.325, c = 208.254 A, alpha = beta = 90, gamma = 120 degrees. Diffraction data were collected to 3.34 A resolution from a crystal in complex with coformycin 5'-phosphate and to 4.05 A resolution from a crystal of a mercury derivative.  (+info)

AMP-activated protein kinase-independent inhibition of hepatic mitochondrial oxidative phosphorylation by AICA riboside. (8/126)

AICA riboside (5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside) has been extensively used in cells to activate the AMPK (AMP-activated protein kinase), a metabolic sensor involved in cell energy homoeostasis. In the present study, we investigated the effects of AICA riboside on mitochondrial oxidative; phosphorylation. AICA riboside was found to dose-dependently inhibit the oligomycin-sensitive JO2 (oxygen consumption rate) of isolated rat hepatocytes. A decrease in P(i) (inorganic phosphate), ATP, AMP and total adenine nucleotide contents was also observed with AICA riboside concentrations >0.1 mM. Interestingly, in hepatocytes from mice lacking both alpha1 and alpha2 AMPK catalytic subunits, basal JO2 and expression of several mitochondrial proteins were significantly reduced compared with wild-type mice, suggesting that mitochondrial biogenesis was perturbed. However, inhibition of JO2 by AICA riboside was still present in the mutant mice and thus was clearly not mediated by AMPK. In permeabilized hepatocytes, this inhibition was no longer evident, suggesting that it could be due to intracellular accumulation of Z nucleotides and/or loss of adenine nucleotides and P(i). ZMP did indeed inhibit respiration in isolated rat mitochondria through a direct effect on the respiratory-chain complex I. In addition, inhibition of JO2 by AICA riboside was also potentiated in cells incubated with fructose to deplete adenine nucleotides and P(i). We conclude that AICA riboside inhibits cellular respiration by an AMPK-independent mechanism that likely results from the combined intracellular P(i) depletion and ZMP accumulation. Our data also demonstrate that the cellular effects of AICA riboside are not necessarily caused by AMPK activation and that their interpretation should be taken with caution.  (+info)

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.

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.

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.

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.

Nucleotide deaminases are a group of enzymes that catalyze the removal of an amino group (-NH2) from nucleotides, which are the building blocks of DNA and RNA. Specifically, these enzymes convert cytidine or adenosine to uridine or inosine, respectively, by removing an amino group from the corresponding nitrogenous base (cytosine or adenine).

There are several types of nucleotide deaminases that differ in their substrate specificity and cellular localization. For example, some enzymes deaminate DNA or RNA directly, while others act on free nucleotides or nucleosides. Nucleotide deaminases play important roles in various biological processes, including the regulation of gene expression, immune response, and DNA repair.

Abnormal activity or mutations in nucleotide deaminases have been associated with several human diseases, such as cancer, autoimmune disorders, and viral infections. Therefore, understanding the function and regulation of these enzymes is crucial for developing new therapeutic strategies to treat these conditions.

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 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.

Adenosine monophosphate (AMP) is a nucleotide that is the monophosphate ester of adenosine, consisting of the nitrogenous base adenine attached to the 1' carbon atom of ribose via a β-N9-glycosidic bond, which in turn is esterified to a phosphate group. It is an important molecule in biological systems as it plays a key role in cellular energy transfer and storage, serving as a precursor to other nucleotides such as ADP and ATP. AMP is also involved in various signaling pathways and can act as a neurotransmitter in the central nervous system.

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.

Coformycin is a naturally occurring antibiotic. Malki, Yohan; Martinez, Jean; Masurier, Nicolas (July 2021). "1,3-Diazepine: A ...
In enzymology, a 8-oxocoformycin reductase (EC 1.1.1.235) is an enzyme that catalyzes the chemical reaction coformycin + NADP+ ... The systematic name of this enzyme class is coformycin:NADP+ 8-oxidoreductase. This enzyme is also called 8-ketodeoxycoformycin ... deoxycoformycin and coformycin". Biochemistry. 27 (15): 5790-5. doi:10.1021/bi00415a059. PMID 3052586. Portal: Biology v t e ( ... displaystyle \rightleftharpoons } 8-oxocoformycin + NADPH + H+ Thus, the two substrates of this enzyme are coformycin and NADP+ ...
... coformycin MeSH D13.570.800.453 - guanosine MeSH D13.570.800.453.500 - nucleoside q MeSH D13.570.800.573 - inosine MeSH D13.570 ... coformycin MeSH D13.570.685.350.200.700 - pentostatin MeSH D13.570.685.705 - thymidine MeSH D13.570.685.705.875 - stavudine ...
Coformycin is a naturally occurring antibiotic. Malki, Yohan; Martinez, Jean; Masurier, Nicolas (July 2021). "1,3-Diazepine: A ...
Examples Coformycin. Substance. CAS Registry & name. Categories. Source. Drugs* 5-. deazaformycin A 0 *Formycins. J Org Chem ...
Coformycin. 21. + 40. Silicone Oils. 20. + 41. Phenylephrine. 20. + 42. Antigens, CD56. 20. + ...
coformycin(1+) cresyl violet + Cu(I)-S-Mo(IV)(=O)O-NBIC Cluster ...
... oligemia hear yourselves Saarinen coformycin around mine mulatta. Blighties unadjustably periled somebody green-belt Basics ... oligemia hear yourselves Saarinen Check Out Your Url coformycin around mine mulatta. Untenantable does cheap repaglinide work ...
Herbicides such anisomycin, bialaphos, coformycin, hydantocidin, phthoxazolin, homoalanosin, etc. are made by several ...
7lkk (Fe: 4) - Crystal Structure of Helicobacter Pylori Aminofutalosine Deaminase (Aflda) in Complex with Methylthio-Coformycin ...
Because the specific AMP deaminase inhibitor coformycin (10 microM) blocks the formation of IMP from ATP and causes a ...
Active site of ADA2 with and without coformycin (stereo views). A, ligand-free active site. B, ADA2 complexed with coformycin. ... 2,Fo, − ,Fc,, αc) density for water molecules in A and coformycin in B is shown as a gray mesh at a contour level of 1 σ. ... The coformycin molecule in the ADA2 catalytic site is shown as spheres. B, superposition of active site residues in human ADA2 ... Carbon atoms in ADA2, ADA1, coformycin, and HDPR are shown in pink, yellow, cyan, and green, respectively. Atoms of oxygen and ...
The presence of coformycin phosphate is unlikely to alter the AMPD 3D structure since coformycin phosphate, a well-known AMPD ... proximity (K173, Y174, D444, D445) to coformycin -phosphate as determined by PyMol [28], and was calculated in all models by ... Phe170 and Tyr174 displace the ribose ring of coformycin -phosphate, and Lys169, Lys173, Arg182, Asp444 and Glu448 are able to ... The catalytic zinc is represented by a yellow sphere, the coformycin -phosphate and phosphate ion are depicted as stick models ...
Coformycin / analogs & derivatives Actions. * Search in PubMed * Search in MeSH * Add to Search ...
Coformycin,N0000007670, Propanolamines,N0000007669, Interferon-beta,N0000007668, Atropine Derivatives,N0000007667, Coenzymes, ...
All buffers were supplemented with the deaminase inhibitors coformycin (5 µg/mL) (National Cancer Institute, Bethesda, MD) and ...
When protected from deamination by either deoxycoformycin or coformycin, both of which are adenosine deaminase inhibitors, ...
Coformycin Preferred Term Term UI T008901. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1979). ... Coformycin. Tree Number(s). D03.383.742.680.350.200. D13.570.685.350.200. D13.570.800.410.200. Unique ID. D003070. RDF Unique ... Coformycin Preferred Concept UI. M0004720. Registry Number. 11033-22-0. Scope Note. A ribonucleoside antibiotic synergist and ...
Coformycin Preferred Term Term UI T008901. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1979). ... Coformycin. Tree Number(s). D03.383.742.680.350.200. D13.570.685.350.200. D13.570.800.410.200. Unique ID. D003070. RDF Unique ... Coformycin Preferred Concept UI. M0004720. Registry Number. 11033-22-0. Scope Note. A ribonucleoside antibiotic synergist and ...
... coformycin,noun,E0301062,formycin,noun,E0400065,yes co,cofounder,noun,E0508664,founder,noun,E0028671,yes co,cofractionate,verb, ...
Coformycin - Preferred Concept UI. M0004720. Scope note. A ribonucleoside antibiotic synergist and adenosine deaminase ...
A knowledge graph of biological entities such as genes, gene functions, diseases, phenotypes and chemicals. Embeddings are generated with Walking RDF and OWL method ...
Crystal Structure Of Adenosine Deaminase From Pseudomonas Aeruginosa Pao1 with bound Zn and methylthio-coformycin _struct.pdbx ...
Coordinated Biosynthesis of the Purine Nucleoside Antibiotics Aristeromycin and Coformycin in Actinomycetes. ... and coformycin (COF) in Micromonospora haikouensis DSM 45626 (a new producer for ARM and COF) and Streptomyces citricolor NBRC ...
D3.438.759.646.138.382 Coformycin D3.383.742.680.350.200 Coke D20.345.108.110 Colestipol J1.637.51.720.200 Colistin D12.644. ...
... coformycin,noun,E0301062,no deoxy,deoxycorticosteroid,noun,E0532192,corticosteroid,noun,E0019219,no deoxy, ...
Coformycin (1967) inhibiting adenosine deaminase, 8- Lactamase inhibitor (1974). 1) 2) 3) 4) A Bibliography of H. Umezawas ... e yn HO 0 OH OH Coformycin inhibiting adenosine deaminase ...
Treatment of murine or human B cells with combinations of coformycin, an inhibitor of adenosine deaminase, homocysteine, and ...
Of special groups, by name of group in ethics number where available ...

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