(S)-TXNIP-IN-1
(Synonyms: (2S)-2-(1,3-二氧代-1,3-二氢-2H-吡咯并[3,4-C]吡啶-2-基)-3-甲基丁酸) 目录号 : GC60422
(S)-TXNIP-IN-1是TXNIP-IN-1的S-对映体。TXNIP-IN-1是一种TXNIP-TRX复合物抑制剂，可用于TXNIP-TRX复合物相关代谢紊乱(糖尿病)、心血管疾病或炎症疾病的研究。
Cas No.:1212421-96-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
(S)-TXNIP-IN-1 is the S-enantiomer of TXNIP-IN-1 . TXNIP-IN-1 is a TXNIP-TRX complex inhibitor which can be used in the research of TXNIP-TRX complex associated metabolic disorder (diabetes), cardiovascular disease, or inflammatory disease[1]
[1]. Rama Natarajan, et al. Txnip-trx complex inhibitors and methods of using the same. US20200085800A1.
| Cas No. | 1212421-96-9 | SDF | |
| 别名 | (2S)-2-(1,3-二氧代-1,3-二氢-2H-吡咯并[3,4-C]吡啶-2-基)-3-甲基丁酸 | ||
| Canonical SMILES | O=C(O)[C@H](C(C)C)N(C1=O)C(C2=C1C=CN=C2)=O | ||
| 分子式 | C12H12N2O4 | 分子量 | 248.23 |
| 溶解度 | DMSO : 100 mg/mL (402.85 mM; Need ultrasonic) | 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。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.0285 mL | 20.1426 mL | 40.2852 mL |
| 5 mM | 0.8057 mL | 4.0285 mL | 8.057 mL |
| 10 mM | 0.4029 mL | 2.0143 mL | 4.0285 mL |
| 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。
Finkelstein'S Test Is Superior to Eichhoff'S Test in the Investigation of de Quervain'S Disease
J Hand Microsurg 2018 Aug;10(2):116-118.PMID:30154628DOI:10.1055/s-0038-1626690.
Introduction de Quervain'S tenosynovitis is a common pathologic condition of the hand. Finkelstein'S test has long been considered to be a pathognomonic sign of this diagnosis, yet most clinicians and instruction manuals erroneously describe what is in fact the Eichhoff'S test, which is thought to produce similar pain by tendon stretching in a normal wrist. The purpose of this study was to compare Finkelstein'S test with Eichhoff'S test in asymptomatic individuals. Materials and Methods Thirty-six asymptomatic participants (72 wrists) were examined using both Finkelstein'S and Eichhoff'S tests with a minimum interval of 24 hours between the tests. Results The results showed that Finkelstein'S test was more accurate than Eichhoff'S test. It demonstrated higher specificity, produced significantly fewer numbers of false-positive results, and also caused significantly less discomfort to patients. Conclusion This study recommends Finkelstein'S test as the clinical examination of choice for the diagnosis of de Quervain'S disease.
Craniometrics and Ventricular Access: A Review of Kocher'S, Kaufman'S, Paine'S, Menovksy'S, Tubbs', Keen'S, Frazier'S, Dandy'S, and Sanchez'S Points
Oper Neurosurg (Hagerstown) 2020 May 1;18(5):461-469.PMID:31420653DOI:10.1093/ons/opz194.
Intraventricular access is frequently required during neurosurgery, and when neuronavigation is unavailable, the neurosurgeon must rely upon craniometrics to achieve successful ventricular cannulation. In this historical review, we summarize the most well-described ventricular access points: Kocher'S, Kaufman'S, Paine'S, Menovksy'S, Tubbs', Keen'S, Frazier'S, Dandy'S, and Sanchez'S. Additionally, we provide multiview, 3-dimensional illustrations that provide the reader with a novel understanding of the craniometrics associated with each point.
Algorithmic approach to find S -consistency in Common-Edge signed graph
MethodsX 2022 Jul 21;9:101783.PMID:35942208DOI:10.1016/j.mex.2022.101783.
Common-Edge signed graph C E ( S ) of a signed graph S is a signed graph whose vertex-set is the pairs of adjacent edges in S and two vertices are adjacent if the corresponding pairs of adjacent edges of S have exactly one edge in common, with the sign same as that of Common-Edge. S -Marked signed graph T is a signed graph which receives the marking μ due to the signed graph S called marker. Further, T is S -consistent if a marker S is defined and if S -marking μ of T with respect to which marked signed graph T μ is consistent. In this paper, we give an algorithm to detect if C E ( S ) is S -consistent or not and determine its complexity. • Algorithm to detect if C E ( S ) is S -consistent or not. • Determination of algorithm'S complexity.
Molecular mechanism of the S-RNase-based gametophytic self-incompatibility in fruit trees of Rosaceae
Breed Sci 2016 Jan;66(1):116-21.PMID:27069396DOI:10.1270/jsbbs.66.116.
Self-incompatibility (SI) is a major obstacle for stable fruit production in fruit trees of Rosaceae. SI of Rosaceae is controlled by the S locus on which at least two genes, pistil S and pollen S, are located. The product of the pistil S gene is a polymorphic and extracellular ribonuclease, called S-RNase, while that of the pollen S gene is a protein containing the F-box motif, SFB (S haplotype-specific F-box protein)/SFBB (S locus F-box brothers). Recent studies suggested that SI of Rosaceae includes two different systems, i.e., Prunus of tribe Amygdaleae exhibits a self-recognition system in which its SFB recognizes self-S-RNase, while tribe Pyreae (Pyrus and Malus) shows a non-self-recognition system in which many SFBB proteins are involved in SI, each recognizing subset of non-self-S-RNases. Further biochemical and biological characterization of the S locus genes, as well as other genes required for SI not located at the S locus, will help our understanding of the molecular mechanisms, origin, and evolution of SI of Rosaceae, and may provide the basis for breeding of self-compatible fruit tree cultivars.
Anti-U-like as an alloantibody in S-s-U- and S-s-U+(var) black people
Transfusion 2012 Mar;52(3):622-8.PMID:21880045DOI:10.1111/j.1537-2995.2011.03318.x.
Background: S, S, and U antigens belong to the MNS system. They are carried by glycophorin B (GPB), encoded by GYPB. Black people with the low-prevalence S-s- phenotype, either U- or U+(var), can make a clinically significant anti-U. Anti-U-like, a cold immunoglobulin G autoantibody quite commonly observed in S-s+U+ black persons, was previously described to be nonreactive with ficin-, α-chymotrypsin-, and pronase-treated red blood cells (RBCs); nonreactive or weakly reactive with papain-treated RBCs; and reactive with trypsin-treated RBCs. Here we describe, in S-s- people from different molecular backgrounds, an alloantibody to a high-prevalence GPB antigen, which presents the same pattern of reactivity with proteases as autoanti-U-like. Study design and methods: Four S-s- patients with an alloantibody to a high-prevalence GPB antigen were investigated by serologic and molecular methods. Results: An alloantibody was observed in two S-s-U-/Del GYPB, one S-s-U+(var)/GYPB(P2), and one S-s-U+(var)/GYPB(NY) patients. As this alloantibody showed the same pattern of reactivity with proteases as autoanti-U-like, we decided to name it "anti-U-like." Anti-U-like made by the two S-s-U- patients was reactive with the S-s-U+(var) RBCs of the two other patients. Conclusion: S-s-U-/Del GYPB, S-s-U+(var)/GYPB(P2), and S-s-U+(var)/GYPB(NY) patients can make an alloanti-U-like. Anti-U-like made by S-s-U- people appears reactive with GYPB(P2) and GYPB(NY) RBCs, which both express a weak and partial U-like reactivity. We recommend transfusing S-s-U- RBCs in S-s-U- patients showing alloanti-U-like. Our study contributes to a better understanding of alloimmunization to GPB in black people and confirms importance of genotyping in S-s- patients, especially those with sickle cell disease to be frequently transfused.