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N6-Ethyladenosine Sale

(Synonyms: NSC 516603) 目录号 : GC34921

An adenosine A1 and A3 receptor agonist

N6-Ethyladenosine Chemical Structure

Cas No.:14357-08-5

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10mM (in 1mL DMSO)
¥1,485.00
现货
10mg
¥1,350.00
现货
50mg
¥4,050.00
现货

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Sample solution is provided at 25 µL, 10mM.

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产品描述

N6-Ethyladenosine is an adenosine A1 and A3 receptor agonist.1 It binds selectively to rat adenosine A1 and human adenosine A3 receptors over rat adenosine A2A and A3 receptors (Kis = 4.9, 4.7, 8,900 and 1,050 nM, respectively, for the recombinant receptors in CHO cells). N6-Ethyladenosine completely inhibits forskolin-induced cAMP accumulation in CHO cells expressing the human recombinant adenosine A3 receptor when used at a concentration of 10 ?M.

1.Gao, Z.-G., Blaustein, J.B., Gross, A.S., et al.N6-Substituted adenosine derivatives: Selectivity, efficacy, and species differences at A3 adenosine receptorsBiochem. Pharmacol.65(10)1675-1684(2003)

Chemical Properties

Cas No. 14357-08-5 SDF
别名 NSC 516603
Canonical SMILES OC[C@@H]1[C@H]([C@H]([C@H](N2C=NC3=C2N=CN=C3NCC)O1)O)O
分子式 C12H17N5O4 分子量 295.29
溶解度 DMSO : ≥ 83.33 mg/mL (282.20 mM) 储存条件 Store at -20°C
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1 mM 3.3865 mL 16.9325 mL 33.865 mL
5 mM 0.6773 mL 3.3865 mL 6.773 mL
10 mM 0.3387 mL 1.6933 mL 3.3865 mL
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Research Update

Regulators of proteostasis are translationally repressed in fibroblasts from patients with sporadic and LRRK2-G2019S Parkinson's disease

NPJ Parkinsons Dis 2023 Feb 6;9(1):20.PMID:36746972DOI:PMC9902458

Deficits in protein synthesis are associated with Parkinson's disease (PD). However, it is not known which proteins are affected or if there are synthesis differences between patients with sporadic and Leucine-Rich Repeat Kinase 2 (LRRK2) G2019S PD, the most common monogenic form. Here we used bio-orthogonal non-canonical amino acid tagging for global analysis of newly translated proteins in fibroblasts from sporadic and LRKK2-G2019S patients. Quantitative proteomic analysis revealed that several nascent proteins were reduced in PD samples compared to healthy without any significant change in mRNA levels. Using targeted proteomics, we validated which of these proteins remained dysregulated at the static proteome level and found that regulators of endo-lysosomal sorting, mRNA processing and components of the translation machinery remained low. These proteins included autophagy-related protein 9A (ATG9A) and translational stability regulator YTH N6-Ethyladenosine RNA binding protein 3 (YTHDF3). Notably, 77% of the affected proteins in sporadic patients were also repressed in LRRK2-G2019S patients (False discovery rate (FDR) < 0.05) in both sporadic and LRRK2-G2019S samples. This analysis of nascent proteomes from PD patient skin cells reveals that regulators of proteostasis are repressed in both sporadic and LRRK2-G2019S PD.