| ZLN005transcriptional regulator of PGC-1α |
Sample solution is provided at 25 µL, 10mM.
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- Purity = 98.00%
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Chemical structure
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| Cas No. | 49671-76-3 | SDF | Download SDF |
| Chemical Name | 2-(4-tert-butylphenyl)-1H-benzimidazole | ||
| Canonical SMILES | CC(C)(C)C1=CC=C(C=C1)C2=NC3=CC=CC=C3N2 | ||
| Formula | C17H18N2 | M.Wt | 250.34 |
| Solubility | ≥23.3mg/mL in DMSO | Storage | Store at -20°C |
| Physical Appearance | A solid | Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. | ||
ZLN005 is a novel transcriptional regulator of PGC-1α [1].
Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is an inducible coregulator that regulates energy metabolism. PGC-1α regulates glucose and fatty acid metabolism, mitochondrial biogenesis and so on. Dysregulation of PGC-1α is correlated with insulin resistance and type 2 diabetes mellitus [1].
ZLN005 is a novel PGC-1α transcriptional regulator. In the PGC-1α promoter reporter assay, ZLN005 potently inhibited luciferases. In L6 myotubes, ZLN005 dose-dependently increased PGC-1α mRNA levels. ZLN005 (10 μM) increased the mRNA levels of cytochrome c oxidase 5b (cox5b), acyl-CoA oxidase, strogen-related receptor α (ERRα), NRF1 and GLUT4. ZLN005 (20 μM) increased glucose uptake and oxidation of palmitic acid by 1.8-fold and 1.28-fold respectively in a dose dependent way. In L6 myotubes transfected with PGC-1α siRNA, ZLN005-stimulated oxidation of palmitic acid and expression of the PGC-1α gene was blocked. In L6 myotubes, ZLN005 increased the phosphorylation of AMPK and acetyl-CoA carboxylase (ACC) [1].
In db/db mice, ZLN005 reduced RER, suggesting a shift to fatty acid use. ZLN005 significantly reduced fasting blood glucose and random blood glucose levels. Also, ZLN005 improved glucose clearance and pyruvate tolerance and reduced insulin resistance [1].
Reference:[1]. Zhang LN, Zhou HY, Fu YY, et al. Novel Small-Molecule PGC-1a Transcriptional Regulator With Beneficial Effects on Diabetic db/db Mice. Diabetes, 2013, 62(4): 1297-1307.
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利用NheI和HindIII双酶切插入目的片段，为什么双酶切有目的片段和切开的质粒，测序却没有？
并且测序后在NheI位点后的序列变成了-GGCTAGGTAC-Kpn位点（CGTTTAAACTTAAGCTTG消失。之前和之后的序列都相符），之间的怎么都没了？
请教高人，这样的问题怎么解决？
多谢
你所说的“测序酶”在一般情况下就是“聚合酶”。
因为目前的的测序方法主要就是借助聚合反应。
当然，有些测序方法（比如曾经的SOLiD系统）是利用连接反应，那么它用的“测序酶”肯定是连接酶。
估计，也就是这个原因有人把它。
两个基因大小分别230kb和450kb，酶切后，450kb的有目的条带，但很弱，230kb的质粒条带亮，其下方有一很微弱条带，用的酶分别是：Ncol和Spel体系是（Takara，两个酶切体系不同，用的官网推荐体系）：
NcoI1μl
Spel1μl
10×KBuffer2μl
0.1%BSA2μl
DNA3ul
灭菌水upto20μl37℃4h电泳1h
期待着高手们的指点，谢谢。
【之前构建的4个重组质粒里也有两个出现这样的问题（aagtcc变成agtcc），但是酶切能切出插入的片段】
目前问测序公司得到的答复是样品可能不是单克隆，测序结果是不准确的，建议重新挑取单克隆测序。
不知道还有没有别的方法？
●应用酶水解多肽不会破坏氨基酸，也不会发生消旋化。水解的产物为较小的肽段。向左转|向右转
