For research use only. Not for therapeutic Use.
β-Amyloid (31-35) is the shortest sequence of native Amyloid-β peptide that retains neurotoxic activity.
β-Amyloid (31-35) is a functional cytotoxic domain of Aβ peptide. β-Amyloid (31-35) increases the phosphorylation of biotinylated Aβ(1-40), enhances CDK-1 activity, and also inhibits binding of Aβ to cyclin B1. β-Amyloid (31-35) is cytotoxic, and such an effect can be inhibited by olomoucine in differentiated human teratocarcinoma cell line, Ntera 2/cl-D1 (NT-2) neurons[1].
β-Amyloid Aggregation Guidelines (Following is our recommended protocol. This protocol only provides a guideline, and should be modified according to your specific needs).
1. Solid Aβ peptide was dissolved in cold hexafluoro-2-propanol (HFIP). The peptide was incubated at room temperature for at least 1h to establish monomerization and randomization of structure.
2. The HFIP was removed by evaporation, and the resulting peptide was stored as a film at -20 or -80 °C.
3. The resulting film was dissolved in anhydrous DMSO at 5 mM and then diluted into the appropriate concentration and buffer (serum- and phenol red-free culture medium) with vortexing.
4. Next, the solution was age 48h at 4-8 °C. The sample was then centrifuged at 14000g for 10 min at 4-8 °C; the soluble oligomers were in the supernatant. The supernatant was diluted 10-200-fold for experiments.
Methods vary depends on the downstream applications.
| Catalog Number | M092090 |
| CAS Number | 149385-65-9 |
| Synonyms | (2S)-2-[[(2S)-2-[[2-[[(2S,3S)-2-[[(2S,3S)-2-amino-3-methylpentanoyl]amino]-3-methylpentanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]-4-methylsulfanylbutanoic acid |
| Molecular Formula | C25H47N5O6S |
| Purity | ≥95% |
| InChI | InChI=1S/C25H47N5O6S/c1-8-15(5)20(26)23(33)30-21(16(6)9-2)24(34)27-13-19(31)28-18(12-14(3)4)22(32)29-17(25(35)36)10-11-37-7/h14-18,20-21H,8-13,26H2,1-7H3,(H,27,34)(H,28,31)(H,29,32)(H,30,33)(H,35,36)/t15-,16-,17-,18-,20-,21-/m0/s1 |
| InChIKey | ZMDGLWRNBGRYQB-ZKHIMWLXSA-N |
| SMILES | CCC(C)C(C(=O)NC(C(C)CC)C(=O)NCC(=O)NC(CC(C)C)C(=O)NC(CCSC)C(=O)O)N |
| Reference | [1]. Milton NG, et al. The amyloid-beta peptide binds to cyclin B1 and increases human cyclin-dependent kinase-1 activity. Neurosci Lett. 2002 Apr 5;322(2):131-3. [2]. Misiti F, et al. Fragment 31-35 of beta-amyloid peptide induces neurodegeneration in rat cerebellar granule cells via bax gene expression and caspase-3 activation. A crucial role for the redox state of methionine-35 residue. Neurochem Int. 2006 Oct;49(5): [3]. M Jesús Pérez de Vega, et al. Synthesis and biological properties of beta-turned Abeta(31-35) constrained analogues. Bioorg Med Chem Lett. 2008 Mar 15;18(6):2078-82. |
