¥1,081.44
预计发货时间2025年5月19日详情
推荐产品
生物来源
synthetic (organic)
质量水平
方案
≥99% (HPLC)
表单
powder
mp
~300 °C (dec.) (lit.)
溶解性
DMF: 9.80-10.20 mg/mL, clear, colorless to light yellow
SMILES字符串
Cn1cnc(N)c2ncnc12
InChI
1S/C6H7N5/c1-11-3-10-5(7)4-6(11)9-2-8-4/h2-3H,7H2,1H3
InChI key
FSASIHFSFGAIJM-UHFFFAOYSA-N
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此商品 | 70050 | PHL89252 | M6760 |
|---|---|---|---|
| form solid | form powder | form solid | form crystalline |
| Quality Level 100 | Quality Level 200 | Quality Level - | Quality Level 100 |
| manufacturer/tradename Calbiochem® | manufacturer/tradename - | manufacturer/tradename PhytoLab | manufacturer/tradename - |
| storage temp. 2-8°C | storage temp. - | storage temp. - | storage temp. - |
| storage condition OK to freeze, protect from light | storage condition - | storage condition - | storage condition - |
应用
3-甲基腺嘌呤作为自噬抑制剂已用于：
- 使用转染人骨髓间充质干细胞(BM-MSC)检测自噬相关基因（Beclin 1，轻链3(LC3)和p62）的表达[1]
- 协同顺铂(cisplatin)研究A2780cp细胞的自噬抑制会否影响顺铂诱导的细胞凋亡[2]
- 研究多黏菌素(colistin)诱导的自噬和凋亡之间的相互作用[3]
3-甲基腺嘌呤（3-MA）用于抑制和研究多种条件下自噬（溶酶体自我降解）和细胞凋亡的机制。3-MA可通过抑制III型磷脂酰肌醇3-激酶（PI-3K）阻断自噬体的形成来对自噬进行抑制。 3-MA通常以5 mM的浓度用作自噬抑制剂。
在癌症生成过程中核酸甲基化检测的标准品。
生化/生理作用
3-甲基腺嘌呤（3-MA）用于抑制和研究多种条件下自噬（溶酶体自我降解）和细胞凋亡的机制。3-MA可通过抑制III型磷脂酰肌醇3-激酶（PI-3K）阻断自噬体的形成来对自噬进行抑制。[4]
制备说明
该产品可溶于DMF（10 mg/mL；可能需要温和受热）。 受热情况下，其可以30 mg/ml的浓度溶于水、95％乙醇或1 N NaOH，但在冷却后会从溶液中析出。 可在DMSO中配制100 mM的3-MA溶液。
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
Heng Wang et al.
Journal of dairy science, 102(9), 8264-8272 (2019-07-01)
Staphylococcus aureus is an important pathogen causing chronic and subclinical mastitis of cows. Autophagy is an important regulatory mechanism that participates in the elimination of invading pathogenic organisms. Here, we hypothesize that autophagy is involved in the process of Staph.
Jingyuan Chen et al.
Shock (Augusta, Ga.), 52(1), 111-121 (2018-10-05)
Sepsis-induced myopathy is a heavy burden for patients during respiratory failure as well as after discharge, which could be characterized with qualitative changes to nAChR in a rat model of sepsis, regulated by NRG-1. Autophagy is an innate immune defense
Feng-Xia Guo et al.
Cell death and differentiation, 26(9), 1670-1687 (2019-01-27)
Atherosclerosis is a progressive, chronic inflammation in arterial walls. Long noncoding RNAs (lncRNAs) participate in inflammation, but the exact mechanism in atherosclerosis is unclear. Our microarray analyses revealed that the levels of lncRNA-FA2H-2 were significantly decreased by oxidized low-density lipoprotein
Do Eun Rim et al.
Journal of biochemical and molecular toxicology, 33(8), e22348-e22348 (2019-05-09)
Golgi S-nitro-N-acetylpenicillamine receptor complex 1 (GS28) has been implicated in Golgi vesicle transport. We examined the role of GS28 and its molecular mechanisms in sodium nitroprusside (SNP)-induced cell death using GS28 siRNA (siGS28)-transfected HeLa cells. Significant inhibition of cytotoxicity was
Halima Alsamri et al.
Frontiers in oncology, 9, 743-743 (2019-08-29)
We have previously demonstrated that carnosol, a naturally occurring diterpene, inhibited in vitro cell viability and colony growth, as well as induced cell cycle arrest, autophagy and apoptosis in human triple negative breast cancer (TNBC) cells. In the present study
商品
We presents an article on Autophagy in Cancer Promotes Therapeutic Resistance
High titer lentiviral particles for LC3 variants used for live cell analysis of cellular autophagy.
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