Adenosine deaminase
(Synonyms: 腺苷脫氨酶) 目录号 : GC35250
腺苷脱氨酶是一种酶，可催化腺苷和 2'-脱氧腺苷不可逆地分别脱氨为肌苷和 2'-脱氧肌苷。
Cas No.:9026-93-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Adenosine deaminase is an enzyme that catalyzes the irreversible deamination of adenosine and 2’-deoxyadenosine to inosine and 2’-deoxyinosine, respectively.
Adenosine deaminase (ADA; EC 3.5.4.4) catalyzes the irreversible deamination of adenosine and 2′-deoxyadenosine to inosine and 2′-deoxyinosine, respectively. Adenosine deaminase is implicated in purine metabolism and distributed in most mammalian tissues. Genetic Adenosine deaminase deficiency results in lymphopenia and severe combined immunodeficiency disease by decreasing the differentiation and maturation of lymphoid cells[1]. Adenosine deaminase is a signaling molecule related to the activation of T lympho-cytes, making it a useful inflammation marker, especially for menin-gitis and tuberculous pleuritis[2].
腺苷脱氨酶是一种催化腺苷和 2'-脱氧腺苷不可逆地分别脱氨为肌苷和 2'-脱氧肌苷的酶。
腺苷脱氨酶 (ADA; EC 3.5.4.4) 催化腺苷和 2'-脱氧腺苷分别不可逆地脱氨为肌苷和 2'-脱氧肌苷。腺苷脱氨酶参与嘌呤代谢并分布在大多数哺乳动物组织中。遗传性腺苷脱氨酶缺乏症会降低淋巴样细胞的分化和成熟，从而导致淋巴细胞减少和严重的联合免疫缺陷病 [1]。腺苷脱氨酶是一种与 T 淋巴细胞活化相关的信号分子，使其成为一种有用的炎症标志物，尤其是脑膜炎和结核性胸膜炎[2]。
[1]. Tian X, et al. Probing inhibition mechanisms of adenosine deaminase by using molecular dynamics simulations. PLoS One. 2018 Nov 16;13(11):e0207234.
[2]. Silva Dalsasso Joaquim L, et al. Analytical validation of an in-house method for adenosine deaminase determination. J Clin Lab Anal. 2018 Nov 29:e22823.
| Cas No. | 9026-93-1 | SDF | |
| 别名 | 腺苷脫氨酶 | ||
| Canonical SMILES | [Adenosine deaminase] | ||
| 分子式 | 分子量 | ~33 kDa (SDS-PAGE) | |
| 溶解度 | Buffered aqueous glycerol solution | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
The roles of Adenosine deaminase in autoimmune diseases
Autoimmun Rev 2021 Jan;20(1):102709.PMID:33197575DOI:10.1016/j.autrev.2020.102709.
Autoimmune diseases patients are characterized by the autoimmune disorders, whose immune system can't distinguish between auto- and foreign- antigens. Thus, Immune homeostasis disorder is the key factor for autoimmune diseases development. Adenosine deaminase (ADA) is the degrading enzyme for an immunosuppressive signal - adenosine, and play an important role in immune homeostasis regulation. Increasing evidences have shown that ADA is involved in various autoimmune diseases. ADA activity were changed in multiple autoimmune diseases patients and could be served as a biomarker for clinical diagnosis. In this study, we analyze the change of ADA activity in patients with autoimmune diseases, and we underline its potential diagnostic value for autoimmune diseases patients.
Adenosine deaminase (ADA)-Deficient Severe Combined Immune Deficiency (SCID): Molecular Pathogenesis and Clinical Manifestations
J Clin Immunol 2017 Oct;37(7):626-637.PMID:28842866DOI:10.1007/s10875-017-0433-3.
Deficiency of Adenosine deaminase (ADA, EC3.5.4.4), a housekeeping enzyme of purine metabolism encoded by the Ada gene, is a cause of human severe combined immune deficiency (SCID). Numerous deleterious mutations occurring in the ADA gene have been found in patients with profound lymphopenia (T- B- NK-), thus underscoring the importance of functional purine metabolism for the development of the immune defense. While untreated ADA SCID is a fatal disorder, there are multiple life-saving therapeutic modalities to restore ADA activity and reconstitute protective immunity, including enzyme replacement therapy (ERT), allogeneic hematopoietic stem cell transplantation (HSCT) and gene therapy (GT) with autologous gene-corrected hematopoietic stem cells (HSC). We review the pathogenic mechanisms and clinical manifestations of ADA SCID.
Moonlighting Adenosine deaminase: a target protein for drug development
Med Res Rev 2015 Jan;35(1):85-125.PMID:24933472DOI:10.1002/med.21324.
Interest in Adenosine deaminase (ADA) in the context of medicine has mainly focused on its enzymatic activity. This is justified by the importance of the reaction catalyzed by ADA not only for the intracellular purine metabolism, but also for the extracellular purine metabolism as well, because of its capacity as a regulator of the concentration of extracellular adenosine that is able to activate adenosine receptors (ARs). In recent years, other important roles have been described for ADA. One of these, with special relevance in immunology, is the capacity of ADA to act as a costimulator, promoting T-cell proliferation and differentiation mainly by interacting with the differentiation cluster CD26. Another role is the ability of ADA to act as an allosteric modulator of ARs. These receptors have very general physiological implications, particularly in the neurological system where they play an important role. Thus, ADA, being a single chain protein, performs more than one function, consistent with the definition of a moonlighting protein. Although ADA has never been associated with moonlighting proteins, here we consider ADA as an example of this family of multifunctional proteins. In this review, we discuss the different roles of ADA and their pathological implications. We propose a mechanism by which some of their moonlighting functions can be coordinated. We also suggest that drugs modulating ADA properties may act as modulators of the moonlighting functions of ADA, giving them additional potential medical interest.
Consensus approach for the management of severe combined immune deficiency caused by Adenosine deaminase deficiency
J Allergy Clin Immunol 2019 Mar;143(3):852-863.PMID:30194989DOI:10.1016/j.jaci.2018.08.024.
Inherited defects in Adenosine deaminase (ADA) cause a subtype of severe combined immunodeficiency (SCID) known as severe combined immune deficiency caused by Adenosine deaminase defects (ADA-SCID). Most affected infants can receive a diagnosis while still asymptomatic by using an SCID newborn screening test, allowing early initiation of therapy. We review the evidence currently available and propose a consensus management strategy. In addition to treatment of the immune deficiency seen in patients with ADA-SCID, patients should be followed for specific noninfectious respiratory, neurological, and biochemical complications associated with ADA deficiency. All patients should initially receive enzyme replacement therapy (ERT), followed by definitive treatment with either of 2 equal first-line options. If an HLA-matched sibling donor or HLA-matched family donor is available, allogeneic hematopoietic stem cell transplantation (HSCT) should be pursued. The excellent safety and efficacy observed in more than 100 patients with ADA-SCID who received gammaretrovirus- or lentivirus-mediated autologous hematopoietic stem cell gene therapy (HSC-GT) since 2000 now positions HSC-GT as an equal alternative. If HLA-matched sibling donor/HLA-matched family donor HSCT or HSC-GT are not available or have failed, ERT can be continued or reinstituted, and HSCT with alternative donors should be considered. The outcomes of novel HSCT, ERT, and HSC-GT strategies should be evaluated prospectively in "real-life" conditions to further inform these management guidelines.
Does the Adenosine deaminase (ADA) gene confer risk of sleepwalking?
J Sleep Res 2022 Aug;31(4):e13537.PMID:34913218DOI:10.1111/jsr.13537.
Sleepwalking is a common non-rapid eye movement (NREM) parasomnia and a significant cause of sleep-related injuries. While evidence suggest that the occurrence of this condition is partly determined by genetic factors, its pattern of inheritance remains unclear, and few molecular studies have been conducted. One promising candidate is the Adenosine deaminase (ADA) gene. Adenosine and the ADA enzyme play an important role in the homeostatic regulation of NREM sleep. In a single sleepwalking family, genome-wide analysis identified a locus on chromosome 20, where ADA lies. In this study, we examined if variants in the ADA gene were associated with sleepwalking. In total, 251 sleepwalking patients were clinically assessed, and DNA samples were compared to those from 94 unaffected controls. Next-generation sequencing of the whole ADA gene was performed. Bio-informatic analysis enabled the identification of variants and assessed variants enrichment in our cohort compared to controls. We detected 25 different coding and non-coding variants, of which 22 were found among sleepwalkers. None were enriched in the sleepwalking population. However, many missense variants were predicted as likely pathogenic by at least two in silico prediction algorithms. This study involves the largest sleepwalking cohort in which the role of a susceptibility gene was investigated. Our results did not reveal an association between ADA gene and sleepwalking, thus ruling out the possibility of ADA as a major genetic factor for this condition. Future work is needed to identify susceptibility genes.