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Drug-Target Interaction

Drug

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PubChem ID:6029
Structure:
Synonyms:
1-.beta.-D-Ribofuranosyluracil
1-beta-D-ribofuranosylpyrimidine-2,4(1H,3H)-dione
1-beta-D-Ribofuranosyluracil
1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]pyrimidine-2,4
12693-39-9
1af2
21231-59-4
58-96-8
68184-15-6
69010-88-4
6B6FA3F8-70A2-44EA-B99C-D35D0A9237AA
AC1L1LN9
AC1Q1I4E
AC1Q77T8
AI3-52690
AIDS-185903
AIDS185903
AR-1L8071
araU
Bio-0197
bmse000158
C00299
C9H12N2O6
CHEBI:16704
CHEMBL100259
EINECS 200-407-5
FT-0082887
HMS2230P13
LS-158705
MLS000069625
MolPort-001-792-520
NCGC00017312-02
NCGC00142368-01
nchembio.186-comp37
NSC 20256
NSC20256
SBB000838
SMP1_000029
SMR000058222
ST023512
TL8003766
U0020
U3003_SIGMA
U3750_SIGMA
U6381_SIGMA
Uracil riboside
Uracil, 1-beta-D-ribofuranosyl-
Uracil-1-beta-D-ribofuranoside
Urd
URI
Uridin
URIDINE
Uridine, labeled with tritium
ZINC02583633

Target

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Uniprot ID:ADA_HUMAN
Synonyms:
Adenosine aminohydrolase
Adenosine deaminase
EC-Numbers:3.5.4.4
Organism:Homo sapiens
Human
PDB IDs:1M7M 3IAR
Structure:
3IAR

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

176177
Effect of adenosine deaminase inhibition upon human lymphocyte blastogenesis.. D A Carson; J E Seegmiller (1976) The Journal of clinical investigation display abstract
The biochemical mechanisms by which a genetically determined deficiency of adenosine deaminase leads to immunodeficiency are still poorly understood and prompted this study. We have examined the effects of the adenosine deaminase inhibitor erythro-9-(2-hydroxy-3-nonyl) adenine hydrochloride (EHNA) upon the response of human peripheral blood mononuclear cells to the mitogen concanavalin A (Con A). Cells isolated from normal volunteers were incubated in microtiter plates in the presence of various inhibitors, and the incorporation of tritrated thymidine or leucine into macromolecular material was measured after 64 h. EHNA at a concentration of 0.3 muM, which inhibited 90% of the adenosine deaminase (ADA) activity in a mononuclear preparation, impaired the incorporation of tritrated leucine into protein; 100 muM EHNA was the minimal concentration that inhibited thymidine uptake. The addition of 15 muM adenosine or 10 muM cyclic AMP to Con A-stimulated lymphocytes inhibited leucine uptake, while millimolar concentrations were required to inhibit thymidine uptake. Lower doses of adenosine and cyclic AMP stimulated thymidine incorporation. The inhibition of thymidine uptake observed with millimolar concentrations of adenosine was independent of the type of mitogen (pokeweed or Con A), the concentration of mitogen, or the medium used, but could be increased if the cells were cultured in a serum with reduced levels of adenosine deaminase. Washout experiments failed to demonstrate a critical period early in immune induction during which adenosine exerted its inhibitory effects. Noninhibitory doses of EHNA potentiated the effects of adenosine and cyclic AMP on leucine and thymidine uptake. EHNA at a concentration of 50 muM also potentiated the inhibitory effects on thymidine uptake of dibutyryl cyclic AMP, butyric acid, norepinephrine, and isoproterenol, but not theophylline. When mitogenesis was assayed by leucine incorporations, no synergy between EHNA and these compounds was apparent. Uridine relieved to some extent the inhibition of blastogenesis produced by adenosine and cyclic AMP, but not by dibutyryl cyclic AMP, norepinephreine, isoproterenol, or theophylline. Neither uridine alone nor uridine plus adenosine protected lymphocytes from the inhibitory effects of EHNA.