Guanosine, self-association

Dependence of tt complex binding constants upon nucleoside ionization potentials for ( ) uridine, ( ) thymidine, (A) cytidine, (o) adenosine, (O) guanosine, and (A) N,N,-dimethyladenosine. Panel A shows association constants for the binding of nucleosides to riboflavin. Panel B shows association constants for the self association of nucleosides. (Reproduced from Ref. 82. Copyright 1981, American Chemical Society.)... 

Furthermore, 13C NMR data allow one to determine the self-association of nucleotides, as was reported for disodium guanosine 5 -monophosphate (5 -GMP) With increasing concentration of 5 -GMP all purine carbon signals shift upfield, which is interpreted in terms of stack formation [753, 762]. 

The self-association of guanosine (G), cytidine (C), and adenosine (A) and the base pairing between guanosine, cytidine, adenosine, and uridine in dimethylsulfoxide have... 

The pathogenesis of the neuro-behavioral abnormalities associated with the Lesch-Nyhan syndrome remains obscure despite recent reports of neurotransmitter abnormalities in these patients. Many attempts to correct the characteristic manifestations of spasticity, mental retardation, choreoathetosis, and compulsive self-mutilation have been reported but none have reported sustained clinical efficacy. Many pathogenic mechanisms have been proposed over the past two decades to explain the relationship between the known aberration in purine metabolism and the observed neurologic dysfunction. One of these proposed mechanisms is that the absence of the purine salvage pathway in the central nervous system (CNS) results in (1) the accumulation of oxy-purines in the spinal fluid which then may act as toxic endogenous mediators and (2) the depletion of guanine and adenine nucleotides that are important to normal CNS function. Supplementation of purine intermediates with dietary adenine, guanosine, inosine, and GMP have not altered the clinical course of the disease. 

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