Sak K, Kelve M, Uri A, Järv J
Institute of Chemical Physics, Tartu University, Estonia.
FEBS Lett. 1998 Nov 13;439(1-2):107-9. doi: 10.1016/s0014-5793(98)01348-9.
Regulation of inositol phospholipid hydrolysis by UTP and UDP in neuroblastoma x glioma hybrid cell line NG108-15 was potentiated in the presence of ATP. The effect of ATP was dose dependent and shifted the EC50 value for these uracil nucleotides up to three powers of magnitude, having no influence on the maximal value of the response. Adenine nucleotides (ADP, AMP, adenosine 5'-O-(3-thiotriphosphate) (ATPgammaS), beta,gamma-methyleneadenosine 5'-triphosphate (betagammaMeATP), 3'-O-(4-benzoyl)benzoyl ATP (BzATP) and 3'-deoxyadenosine 5'-O-(1-thio)triphosphate (dATPalphaS)) as well as adenosine, had no influence on the pyrimidinoceptor response. The potentiation effect was abolished by excess of EDTA. The results were in agreement with the hypothesis of pyrimidinoceptor affinity regulation via extracellular phosphorylation of the receptor protein, initiated by ATP. This mechanism may have physiological implication for functioning of uracil nucleotides as endogenous signaling molecules.
在神经母细胞瘤×胶质瘤杂交细胞系NG108 - 15中，UTP和UDP对肌醇磷脂水解的调节作用在ATP存在时增强。ATP的作用呈剂量依赖性，使这些尿嘧啶核苷酸的EC50值上移达三个数量级，而对反应的最大值无影响。腺嘌呤核苷酸（ADP、AMP、腺苷5'-O-(3-硫代三磷酸)（ATPγS）、β,γ-亚甲基腺苷5'-三磷酸（βγMeATP）、3'-O-(4-苯甲酰)苯甲酰ATP（BzATP）和3'-脱氧腺苷5'-O-(1-硫代)三磷酸（dATPαS））以及腺苷，对嘧啶受体反应均无影响。过量的EDTA可消除这种增强作用。这些结果与通过ATP引发的受体蛋白细胞外磷酸化来调节嘧啶受体亲和力的假说相符。这种机制可能对尿嘧啶核苷酸作为内源性信号分子的功能具有生理意义。
