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Anaspec/Beta - Amyloid (1 - 42), <i>Human</i>/1 mg/AS-20276
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Anaspec/Beta - Amyloid (1 - 42), Human/1 mg/AS-20276
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AS-20276
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DescriptionSequence(One-Letter Code)
Product NameBeta - Amyloid (1 - 42), HumanDAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA
Size1 mg
Catalog #AS-20276
US$$295
Purity% Peak Area By HPLC ≥ 95%

Aß (1-42), a major component of amyloid plaques, accumulates in neurons of Alzheimer’s disease brains. Biochemical analysis of the amyloid peptides isolated from Alzheimer’s disease brain indicates that Aß (1-42) is the principal species associated with senile plaque amyloids, while Aß (1-40) is more abundant in cerebrovascular amyloid deposit.

Solvent Information

Detailed InformationDatasheet
Material Safety Data Sheets (MSDS)
Storage-20°C
ReferencesRef: Nagele, R. et al. Neurosci. 110, 199 (2002); Garzon-Rodriguez, W. et al. J. Biol. Chem. 272, 21037 (1997).
Molecular Weight4514.1
DAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA
Sequence(Three-Letter Code)H - Asp - Ala - Glu - Phe - Arg - His - Asp - Ser - Gly - Tyr - Glu - Val - His - His - Gln - Lys - Leu - Val - Phe - Phe - Ala - Glu - Asp - Val - Gly - Ser - Asn - Lys - Gly - Ala - Ile - Ile - Gly - Leu - Met - Val - Gly - Gly - Val - Val - Ile - Ala - OH
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Arriagada, C. et al. (2009). Apoptosis is directly related to intracellular amyloid accumulation in a cell line derived from the cerebral cortex of a trisomy 16 mouse, an animal model of Down syndrome. Neuro Lett 470, 81. doi:10.1016/j.neulet.2009.12.062.
Giliberto, L. et al. (2009). Mutant presenilin 1 increases the expression and activity of BACE1. J Biol Chem 284, 9027. doi: 10.1074/jbc.M805685200.Gu, Z. et al. (2009). β-Amyloid impairs AMPA receptor trafficking and function by reducing CA2+/calmodulin-dependent protein kinase II synaptic distribution. J Biol Chem 284, 10639. doi: 10.1074/jbc.M806508200.Guix, FX. et al. (2009). Amyloid-dependent triosphosphate isomerase nitrotyrosination induces glycation and tau fibrillation. Brain 132, 1335. doi: 10.1093/brain/awp023.Li, M. et al. (2009). Amyloid Aβ interaction with receptor for advanced glycation end products up-regulates brain endothelial CCR5 expression and promotes T cells crossing the blood-brain barrier. J Immunol 182, 5778. doi: 10.4049/​jimmunol.0803013Zhao, L. et al. (2009). Macrophage-mediated degradation of Aβ-amyloid via an apolipoprotein E isoform-dependent mechanism. J Neurosci 29, 3603. doi: 10.1523/JNEUROSCI.5302-08.2009.Jimenez, S. et al. (2008). Inflammatory response in the hippocampus of PS1M146L/APP751SL mouse model of Alzheimer"s Disease: age-dependent switch in the microglial phenotype from alternative to classic. J Neurosci 28, 11650. doi: 10.1523/JNEUROSCI.3024-08.2008.Gevorkian, G. et al. (2008). Amyloid-β peptide binds to microtubule-associated protein 1B (MAP1B). Neurochem Int 52, 1030. doi:10.1016/j.neuint.2007.10.020.Solorzano-Vargas, RS. et al. (2008). Epitope mapping and neuroprotective properties of a human single chain FV antibody that binds an internal epitope of amyloid-beta 1-42. Mol Immunol 45, 881. doi: doi:10.1016/j.molimm.2007.08.008.Watanabe, T. et al. (2008). Spatial memory impairment without apoptosis induced by the combination of beta-amyloid oligomers and cerebral ischemia is related to decreased acetylcholine release in rats. J Pharmacol Sci 106, 84.Chafekar, SM. et al. (2007). Aβ 1-42 induces mild endoplasmic reticulum stress in an aggregation state-dependent manner. Antioxid Redox Signaling 9, 2245.Nelson, TJ. & DL. Alkon (2007). Protection against beta-amyloid induced apoptosis by peptides interacting with beta-amyloid. J Biol Chem 282, 31238. doi: 10.1074/jbc.M705558200.Bales, KR. et al. (2006). Cholinergic dysfunction in a mouse model of Alzheimer disease is reversed by an anti-Aβ antibody. J Clin Invest 116, 825. doi:10.1172/JCI27120.Guo, J-P. et al. (2006). Aβ and tau form soluble complexes that may promote self aggregation of both into the insoluble forms observed in Alzheimer"s disease. PNAS 103, 1953.Shaked, GM. et al. (2006). Aβ induces cell death by direct interaction with its cognate extracellular domain on APP (APP597-624). FASEB J 20, 1254.doi: 10.1096/fj.05-5032fje.Osada, Y. et al. (2005). CLAC binds to amyloid β peptides through the positively charged amino acid cluster within the collagenous domain 1 and inhibits formation of amyloid fibrils. J Biol Chem 280, 8596. doi: 10.1074/jbc.M413340200.Piccini, A. et al. (2005). β-amyloid is different in normal aging and in Alzheimer disease. J Biol Chem 280, 34186.Seidler, N. & TJ. Squire (2005). Aβ-polyacrolein aggregates: Novel mechanism of plastic formation in senile plaques. Biochem Biophys Res Communications 335, 501.Boyd-Kimball, D. et al. (2004). Role of phenylalanine 20 in Alzheimer"s amyloid β-peptide (1-42)-induced oxidative stress and neurotoxicity. Chem Res Toxicol 17, 1743.Legleiter, J. et al. (2004). Effect of different anti-Aβ antibodies on Aβ fibrillogenesis as assessed by atomic force microscopy. J Mol Biol 335, 997. doi:10.1016/j.jmb.2003.11.019.Bard, F. et al. (2003). Epitope and isotope specificities of antibodies to β-amyloid peptide for protection against Alzheimer"s disease-like neuropathology. PNAS 100, 2023. doi:10.1073/pnas.0436286100.Takata, K. et al. (2003). Role of high mobility group protein-1 (HMG1) in amyloid-β homeostasis. Biochem Biophys Res Commun 301, 699. doi:10.1016/S0006-291X(03)00024-X.Uryu, S. et al. (2003). β-amyloid-specific upregulation of stearoyl coenzyme A desaturase-1 in macrophages. Biochem Biophys Res Commun 303, 302. doi:10.1016/S0006-291X(03)00334-6.Arispe, N. & M. Doh (2002). Plasma membrane cholesterol controls the cytotoxicity of Alzheimer"s disease AβP (1-40) and (1-42) peptides. FASEB J 16, 1526. doi: 10.1096/fj.02-0829com.Kanski, J. et al. (2002). The hydrophobic environment of Met35 of Alzheimer"s Aβ(1-42) is important for the neurotoxic and oxidative properties of the peptides. Neurotox Res 10.1080/10298420290023945.Barger, SW. & AS. Basile (2001). Activation of microglia by secreted amyloid precursor protein evokes release of glutamate by cystine exchange and attenuates synaptic function. J Neurochem 76, 846. doi: 10.1046/j.1471-4159.2001.00075.x.Yao, Z-X. et al. (2001). The Ginkgo biloba extract EGb 761 rescues the PC12 neuronal cells from β-amyloid-induced cel death by inhibiting the formation of β-derived diffusible neurotoxic ligands. Brain Res 889, 181. doi: 10.1016/S0006-8993(00)03131-0.Yatin, SM. et al. (2000). Vitamin E prevents Alzheimer"s amyloid β-peptide (1-42)-induced neuronal protein oxidation and reactive oxygen species production. J Alzheimer"s Dis 2, 123.Yao, Z-X. et al. (1999). Free radicals and lipid peroxidation do not mediate β-amyloid-induced neuronal cell death. Brain Res 847, 203. doi: doi:10.1016/S0006-8993(99)02047-8.Yatin, SM. 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. doi: 10.1016/S0304-3940(99)00101-9.Bradt, BM. et al. (1998). Complement-dependent proinflammatory properties of the Alzheimer"s disease β-peptide. J Exp Med 188, 431. doi: 10.1084/jem.188.3.431.
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北京雷根生物技术有限公司在发布的pH计电极保护液供应信息,浏览与pH计电极保护液相关的产品或在搜索更多与pH计电极保护液相关的内容。 查看更多>
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测量范围:pH:-2.000到19.999;温度:-5到105;℃mV:-1999到+1999mV 分辨率:pH:0.1/0.01/0.001可选;温度:0.1;mV:0.1 相对精度:pH:±0.001pH;温度:±;0.1℃mV:±0.1mV和0.05% 校正点:5点自动标定,US、NIST和用户自定义,校正完成自动显示电极斜率 温度范围:5到45 相对湿度:5到85% 电源:4×AA电池 查看更多>
任何东西在使用的时候,不单单只要了解使用方法,还要懂得它的保养及存放方法。当然不例外的,使用PH计与酸度计的同时更需要我们了解。 查看更多>
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实验室pH计操作规程.doc123
怪兽89012002021-08-11
看测量的溶液成分,温度,实验室使用台式PH计会比较合适。
什么是PH计缓冲液123
玲随风忆2021-07-22
就是校准pH计的溶液。通常都是一组,如4.01,7.00,9.18的。
我流动相pH为7.0,校正pH计时用6.86的先定位,然后再用4.00还是9.18的调斜率呢,冬天配完缓冲盐pH为8.18,夏天才7.8左右,温度也是按实际温度来校正的,怎么会有如此大的差异
pH计进行3点校正时,会得到一条校正曲线。请问其斜率应在什么范围内?对截距有没有要求呢?
PH计哪个牌子性价比高,国产的就可以,精度0.01,希望各位推荐一下,谢谢!
工作原理是基于电位分析法的原理测量氢离子浓度。电位分析法是根据测量化学原电池的电极电位E,用能斯特方程求得溶液中待测氢离子的浓度。所谓化学原电池是一种借助氧化还原反应将化学能转变为电能的装置,由正负两个电极组成,中间由KCl盐桥沟通电路,当用导线将原电池的两级连接起来时,便产生了电流,再通过测量两电极之间的电极电位,代入能斯特方程式,即可求得溶液中氢离子浓度。

现代酸度计具有:结构简单,操作方便,测量准确和自动化程度高的优点。

对pH值准确度要求高的小伙伴们要记得定期校正pH计哦,新一代ÄKTA纯化系统可以在线校正啦:

我们公司粉针车间调节pH时,使用pH计均是从外面借用,用完再还出去,据说以前曾购买过pH计,但用的时间不长就不准了,有人估计是每天臭氧灭菌对pH电极产生影响,不知各位同仁是怎样做的?
MSDS_for_PEDOTPSS_AI4083_123
自黑达人爱自黑2017-10-23
转换成电压,需要你的PH计有电压模拟量输出功能才可以。
甘汞电极。由于复合电极使用比较广泛,以下主要讨论复合电极。
实验室使用的复合电极主要有全封闭型和非封闭型两种,全封闭型比较少,主要是以国外企业生产为主。复合电极使用前首先检查玻璃球泡是否有裂痕、破碎,如果没有,用pH缓冲溶液进行两点标定时,定位与斜率按钮均可调节到对应的pH值时,一般认为可以使用,否则可按使用说明书进行电极活化处理。活化方法是在4%氟化氢溶液中浸3~5 s左右,取出用蒸馏水进行冲洗,然后在0.1mol/L的盐酸溶液中浸泡数小时后,用蒸馏水冲洗干净,再进行标定,即用pH值为6.86(25℃)的缓冲溶液进行定位,调节好后任意选择另一种pH缓冲溶液进行斜率调节,如无法调节到,则需更换电极。非封闭型复合电极,里面要加外参比溶液即3 mol/L氯化钾溶液,所以必须检查电极里的氯化钾溶液是否在1/3以上,如果不到,需添加3 mol/L氯化钾溶液。如果氯化钾溶液超出小孔位置,则把多余的氯化钾溶液甩掉,使溶液位于小孔下面,并检查溶液中是否有气泡,如有气泡要轻弹电极,把气泡完全赶出。
在使用过程中应把电极上面的橡皮剥下,使小孔露在外面,否则在进行分析时,会产生负压,导致氯化钾溶液不能顺利通过玻璃球泡与被测溶液进行离子交换,会使测量数据不准确。测量完成后应把橡皮复原,封住小孔。电极经蒸馏水清洗后,应浸泡在3 mol/L氯化钾溶液中,以保持电极球泡的湿润,如果电极使用前发现保护液已流失,则应在3 mol/L氯化钾溶液中浸泡数小时,以使电极达到最好的测量状态。在实际使用时,发现有的分析人员把复合电极当作玻璃电极来处理,放在蒸馏水中长时间浸泡,这是不正确的,这会使复合电极内的氯化钾溶液浓度大大降低,导致在测量时电极反应不灵敏,最终导致测量数据不准确,因此不应把复合电极长时间浸泡在蒸馏水中。
电极使用
1、玻璃电极插座应保持干燥、清洁,严禁接触酸雾、盐雾等有害气体,严禁沾上水溶液,保证仪器的高输入阻抗。
2、 不进行测量时,应将输入短路,以免损坏仪器。
3、 新电极或久置不用的电极在使用前,必须在蒸馏水中浸泡数小时。使电极不对称电位降低达到稳定,降低电极内阻。
4、 测量时,电极球泡应全部浸入被测溶液中。
5、 使用时,应使内参比电极浸在内参比溶液中,不要让内参比溶液倒向电极帽一端,使内参比悬空。
6、 使用时,应拔去参比电极电解液加液口的橡皮塞,以使参比电解液(盐桥)借重力作用维持一定流速渗透并与被测溶液相通。否则,会造成读数漂移。
7、 氯化钾溶液中应该没有气泡,以免使测量回路断开。
8、 应该经常添加氯化钾盐桥溶液,保持液面高于银/氯化银丝。
上海阔思电子温馨提醒:没那么复杂,PH传感器就是PH电极,他是PH计的核心组成部分。
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