guanosine 5'diphosphate

Guanosine 5'-diphosphate (GDP) 是核苷二磷酸，是潜在的铁动员剂，能够阻断铁调素-铁转运蛋白相互作用并调节白细胞介素-6 (IL-6) stat-3 途径。

Guanosine 5’-diphosphate (GDP) is a purine nucleotide and biosynthetic precursor of guanosine 5’-triphosphate .1It has been used to study the conformations of GTPases.2GDP (100 μM) activates sulfonylurea receptor 2B (SUR2B) linked to the inward-rectifier potassium channel 6.1 (Kir6.1) in HEK293T cells in a patch-clamp assay.3 1.Berg, J.M., Tymoczko, J.L., and Stryer, L.Biochemistry(2002) 2.Vetter, I.R., and Wittinghofer, A.The guanine nucleotide-binding switch in three dimensionsScience294(5545)1299-1304(2001) 3.Yamada, M., Isomoto, S., Matsumoto, S., et al.Sulphonylurea receptor 2B and Kir6.1 form a sulphonylurea-sensitive but ATP-insensitive K+ channelJ. Physiol.499(Pt 3)715-720(1997)

Guanosine 5'-diphosphate ditromethamine（GDP ditromethamine）作为一种核苷二磷酸，能够激活5'-三磷酸腺苷敏感的K+通道。此外，此化合物是一种有效的铁动员剂，其通过阻断铁调素-铁转运蛋白（hepcidin-ferroportin）相互作用，并可调节IL-6 stat-3通路，进而在炎症性贫血（AI）等炎症研究中发挥重要作用。

Guanosine 5'-diphosphate (GDP) sodium 是一种核苷二磷酸，可激活 5'-三磷酸腺苷敏感的 K+通道。Guanosine 5'-diphosphate sodium 是一种潜在的铁动员剂，可阻断铁调素-铁转运蛋白 (hepcidin-ferroportin) 相互作用并调节 IL-6 stat-3通路。Guanosine 5'-diphosphate sodium 可用于炎症研究，如炎症性贫血 (AI)。

Guanosine 5'-diphosphate disodium salt (5'-GDP-Na2) 是一种核苷二磷酸。它是一种潜在的铁动员剂，能够阻断铁调素-铁转运蛋白相互作用，也可以调节白 IL-6 stat-3 途径。

7-Methylguanosine 5’-diphosphate (7-Methyl-GDP) sodium, a cap analog, can be used in the synthesis of mRNA cap analogues[1]. 7-Methylguanosine 5’-diphosphate sodium inhibits binding of eukaryotic initiation factors to reovirus capped mRNA and complex formation involving uncapped mRNA or 18 S rRNA[1].T. brucei mRNA decapping enzyme (TbDcp2) that cleaves 7-Methylguanosine 5’-diphosphate sodium from capped RNA to generate pRNA, a substrate for TbCe1[2]. [1]. Sonenberg N, et al. Nonspecific effect of m7GMP on protein-RNA interactions. J Biol Chem. 1978;253(19):6630-6632.[2]. Ignatochkina AV, et al. The messenger RNA decapping and recapping pathway in Trypanosoma. Proc Natl Acad Sci U S A. 2015;112(22):6967-6972.