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Peptides  >  Amyloid Peptides  >  Beta-Amyloid Peptide Fragments  >>  Beta-Amyloid (25-35), Human, mouse/rat
Product Name Beta - Amyloid (25 - 35), Human, mouse/rat
Size 5 mg
Catalog # 24228
US$ $193
Purity % Peak Area By HPLC ≥ 95%
Description

Aß (25-35) is the main factor responsible for Aß neurotoxic effects.
Detailed Information Datasheet
Material Safety Data Sheets (MSDS)
Storage -20°C
References Ref: Carvalho, K. et al. Braz. J. Med. Biol. Res. 3, 1153 (1997).
Molecular Weight 1060.3
Sequence
(One-Letter Code)		 GSNKGAIIGLM
Sequence
(Three-Letter Code)		 H - Gly - Ser - Asn - Lys - Gly - Ala - Ile - Ile - Gly - Leu - Met - OH
Product Citations Qu, J. et al. (2011) S-Nitrosylation activates Cdk5 and contributes to synaptic spine loss induced by β-amyloid peptide. PNAS 108, 14330 (2011). doi: 10.1073/pnas.1105172108
Morte, B. et al. (2011). Monocyte-mediated regulation of genes by the amyloid and prion peptides in SH-SY5Y neuroblastoma cells. Neurochem Int doi:10.1016/j.neuint.2011.01.019.
Ravindran, C. et al. (2010). CpG-ODNs induces up-regulated expression of chemokine CCL9 in mouse macrophages and microglia. Cell Immunol 260, 113.
Huang, W-C. et al. (2009). Enlargement of Aβ aggregates through chemokine-dependent microglial clustering. Neurosci. Res. 63, 280.
Wang, HY. et al. (2009). Dissociating β-amyloid from α7 nicotinic acetylcholine receptor by a novel therapeutic agent, S 24795, normalizes α7 nicotinic acetylcholine and NMDA receptor function in Alzheimer's Disease brain. J Neurosci 29, 10961.
Seyb, K. et al. (2008). Identification of small molecule inhibitors of β-amyloid cytotoxicity through a cell-based high-throughput screening platform. J Biomol Screen 13, 870.
Sun, K. et al. (2008). Novel Genetic Tools Reveal Cdk5’s Major Role in Golgi Fragmentation in Alzheimer’s Disease. Mol Biol Cell 19, 3052.
Tateno, M. et al. (2008). Neuroprotective effects of Yi-Gan San against beta amyloid-induced cytotoxicity on rat cortical neurons. Pro Neuro-Pyschopharmacol Biol Pysch 32, 1704.
Hashioka, S. et al. (2007). Phosphatidylserine and phosphatidylcholine-containing liposomes inhibit amyloid β and interferon-γ-induced microglial activation. Free Radical Bio. Med. 42, 945.
Martínez, T. and A. Pascual (2007). Gene expression profile in β-amyloid-treated SH-SY5Y neuroblastoma cells. Brain Res. Bull. 72, 225.
Nelson, TJ. and DL. Alkon (2007). Protection against β-Amyloid-induced Apoptosis by Peptides Interacting with β-Amyloid. J. Biol. Chem. 282, 31238.
Pu, F. et al. (2005). Differential effects of buckwheat and kudingcha extract on neuronal damage in cultured hippocampal neurons and spatial memory impairment induced by scopolamine in an eight-arm radial maze. J. Health Sci. 51, 636.
Egashira, N. et al. (2002). Hypoxia enhances β-amyloid-induced apoptosis in rat cultured hippocampal neurons. Japanese J. Pharmacol. 90, 321.
Kawahara, M. and Y. Kuroda (2001). Intracellular Calcium Changes in Neuronal Cells Induced by Alzheimer's ß-Amyloid Protein Are Blocked by Estradiol and Cholesterol. Cell. Mol. Neurobio. 21, 1.
Yatin, S. et al. (1999). Alzheimer's amyloid β-peptide associated free radicals increase rat embryonic neuronal polyamine uptake and ornithine decarboxylase activity: protective effect of vitamin E. Neurosci Lett 263, 17.
Yatin, SM. et al. (1998). Temporal relations among amyloid β-peptide-induced free-radical oxidative stress, neuronal toxicity, and neuronal defensive responses. J. Mol. Neurosci. 11, 183.
     
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