G7637
鸟苷 5′-[β-硫代]二磷酸 三锂盐
≥85% (HPLC), G-protein inhibitor, powder
别名:
GDPβS 三锂盐, GDP-β-S, GDP-β-S-Li3
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关于此项目
经验公式（希尔记法）:
C10H12Li3N5O10P2S
化学文摘社编号:
分子量:
477.07
Beilstein:
8181243
MDL编号:
UNSPSC代码:
41106305
PubChem化学物质编号:
NACRES:
NA.77
产品名称
鸟苷 5′-[β-硫代]二磷酸 三锂盐, ≥85% (HPLC), powder
方案
≥85% (HPLC)
表单
powder
颜色
white
溶解性
H2O: 20 mg/mL (Solutions are very unstable; prepare immediately prior to use.)
运输
dry ice
储存温度
−20°C
SMILES字符串
[Li+].[Li+].[Li+].NC1=Nc2c(ncn2[C@@H]3O[C@H](COP([O-])(=O)OP([O-])([O-])=S)[C@@H](O)[C@H]3O)C(=O)N1
InChI
1S/C10H15N5O10P2S.3Li/c11-10-13-7-4(8(18)14-10)12-2-15(7)9-6(17)5(16)3(24-9)1-23-26(19,20)25-27(21,22)28;;;/h2-3,5-6,9,16-17H,1H2,(H,19,20)(H2,21,22,28)(H3,11,13,14,18);;;/q;3*+1/p-3/t3-,5-,6-,9-;;;/m1.../s1
InChI key
LMCWQGPJYZRMKU-CYCLDIHTSA-K
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相关类别
应用
鸟苷5′-[β-硫代]二磷酸三锂盐已作为G蛋白激活抑制剂，用于研究其对袋细胞神经元中的乙酰胆碱电流的影响。它还用于研究其对胆碱能依赖性平台期电位的影响。
生化/生理作用
鸟苷5′-[β-硫代]二磷酸是鸟苷的不可水解类似物，可用作G蛋白激活抑制剂。
特点和优势
这种化合物是环核苷酸研究的特色产品。点击此处发现更多特色环核苷酸产品。在sigma.com/discover-bsm可了解更多关于生物活性小分子的其他研究领域。
其他说明
不可水解的 GDP 类似物
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
E Y Moon et al.
Life sciences, 86(17-18), 683-690 (2010-03-03)
We evaluated Gi-protein inhibitor, guanosine 5'-O-(2-thiodiphosphate)(GOT)-induced senescence-associated(SA)-beta-galactosidase(Gal) positive cell formation to determine if it occurred through phosphorylation of cyclic AMP-dependent response element binding protein (CREB). IMR-90 human lung fibroblast cells were used. SA-beta-Gal positive cells and senescence-associated heterochromatic foci (SAHF)
G L Kucera et al.
Biochemical and biophysical research communications, 153(1), 417-421 (1988-05-31)
The inhibition by guanosine 5'-[beta-thio]diphosphate (GDP beta S) of phospholipase C was compared in intact and saponin-permeabilized human platelets in order to assess whether effects of GDP beta S on phospholipase C activation unrelated to guanine nucleotide binding function were
D D Fraser et al.
Journal of neurophysiology, 85(3), 1197-1205 (2001-03-15)
We previously identified cholinergic-dependent plateau potentials (PPs) in CA1 pyramidal neurons that were intrinsically generated by interplay between voltage-gated calcium entry and a Ca(2+)-activated nonselective cation conductance. In the present study, we examined both the second-messenger pathway and the role
Evan D Vickers et al.
Neuron, 99(4), 720-735 (2018-08-07)
Parvalbumin (PV)-expressing interneurons mediate fast inhibition of principal neurons in many brain areas; however, long-term plasticity at PV-interneuron output synapses has been less well studied. In the auditory cortex, thalamic inputs drive reliably timed action potentials (APs) in principal neurons
Ruth Goldberg et al.
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 21(5), 703-713 (2006-06-01)
The etiology of skeletal growth retardation accompanying metabolic acidosis is not clear. Using ex vivo models for endochondral ossification, we showed that the cAMP/PKA pathway, probably triggered by proton sensitive G-protein-coupled receptors, is responsible for impaired skeletal growth in acidosis.
商品
Cyclic nucleotides like cAMP modulate cell function via PKA activation and ion channels.
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