Beta-Amyloid (1-42), TFA

Name: Beta-Amyloid (1-42), TFA
SKU: A-1002-1
Price: 175.00 USD
Availability: InStock

Beta-amyloid (A-beta) has been long reported as the major constituent of amyloid plaques in the brains of Alzheimer’s patients, and is believed by many to be the cause of Alzheimer’s Disease (AD). AD is the most common neurodegenerative disease and afflicts more than 10% of the population over 65. Recombinantly expressed and sourced from E. coli, rPeptide’s high quality beta-amyloid products offer batch-to-batch consistency and ultrapure starting material for your research needs. The TFA (trifluoro-acetic acid) counter-ion is a peptide which was lyophilized in a final solution containing TFA and is a popular choice for researchers wishing to build on previous studies using this same product.

Catalog ID: A-1002-1

$175.00

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Product Details
- Size: 0.5 mg
- Physical State: White lyophilized powder
- Temperature Storage: -20°C
- Temperature Shipping: Ambient
- Sequence:
  D A E F R H D S G Y E V H H Q K L V F F A E D V G S N K G A I I G L M V G G V V I A
- Source: Recombinant. A DNA sequence encoding the human beta-amyloid (1-42) sequence was expressed in E. coli
- Purity: >97% by Mass Spec.
- Molecular Mass: 4,514 Da theoretical
References

1. Yankner, B., et al., (1990) Science, 250 : 279-282
2. Stine, W., et al., (2003) J. Biol. Chem, 278 : 11612-11622
3. Frank, R., et al., (2003) Neurobiology of Aging, 24 : 521-536
4. Gericke, C., et al., (2020) Front. Immunol., 11 : 1029
Publications

Comparison of ELISA- and SIMOA-based quantification of plasma Aβ ratios for early detection of cerebral amyloidosis.
Alzheimer's Research & Therapy; doi.org/10.1186/s13195-020-00728-w.
Meyer, S., Schaeverbeke,J., Verbek, I., Gille, B., Schaepdryver, M., Luckett, E., Gabel, S., Bruffaerts, R., Mauroo, K., Thijssen, E., Stoops, E., Vanderstichele, H., Teunissen, C., Vandenberghe, R., Poesen, K.

A human induced pluripotent stem cell‐derived cortical neuron human‐on‐a chip system to study Aβ42 and tau‐induced pathophysiological effects on long‐term potentiation.
Alzheimer's & Dementia; doi: 10.1002/trc2.12029.
Caneus,J., Akanda, N., Rumsey,J.,Guo, X., Jackson, M., Long, C., Sommerhage, F., Georgieva, S., Kanaan, N., Morgan, D., Hickman, J.

Plasma metabolomics of presymptomatic PSEN1-H163Y mutation carriers: A pilot study.
bioRxiv; doi: doi.org/10.1101/2020.05.16.093559..
Natarajan, K., Ullgren, A., Khoshnood, B., Johansson, C., Laffita-Mesa, J., Pannee, J., Zetterberg, H., Blennow, K., Graff, C.

Iron chelators inhibit amyloid-β-induced production of lipocalin 2 in cultured astrocytes ..
Neurochemistry International; doi.org/10.1016/j.neuint.2019.104607.
Dekens, D., Deyn, P., Sap, F., Eisel, U., Naude, P.,

Increased levels of Stress-inducible phosphoprotein-1 accelerates amyloid-β deposition in a mouse model of Alzheimer’s disease.
Acta Neuropathologica Communications; doi.org/10.1186/s40478-020-01013-5.
Lackie,R., Marques-Lopes,J., Ostapchenko,V., Good,S., Choy,W., Oosten-Hawle, P., Pasternak,S., Prado,V., Prado,M.

Detection of Active Caspase-3 in Mouse Models of Stroke and Alzheimer’s Disease with a Novel Dual Positron Emission Tomography/Fluorescent Tracer [68Ga]Ga-TC3-OGDOTA
Hindawi; https://doi.org/10.1155/2019/6403274.
Valeriy G. Ostapchenko, Jonatan Snir, Mojmir Suchy, Jue Fan, M. Rebecca Cobb, Blaine A. Chronik, Michael Kovacs, Vania F. Prado, Robert H. E. Hudson, Stephen H. Pasternak, Marco A. M. Prado, Robert Bartha

Selective inhibition of phosphodiesterases 4, 5 and 9 induces HSP20 phosphorylation and attenuates amyloid beta 1–42-mediated cytotoxicity.
FEBS Open Bio; doi: 10.1002/2211-5463.12156.
Cameron, RT.; Whiteley, E.; Day, JP.; Parachikova, AI.; Baillie, GS.

The Luminescent Oligothiophene p-FTAA Converts Toxic Aβ1–42 Species into Nontoxic Amyloid Fibers with Altered Properties.
Journal of Biological Chemistry; doi: 10.1074/jbc.M115.696229..
Livia Civitelli, Linnea Sandin, Erin Nelson, Sikander Iqbal Khattak, Ann-Christin Brorsson, Katarina Kågedal

Amyloid-b peptides act as allosteric modulators of cholinergic signalling through formation of soluble BA b ACs.
Brain; doi: 10.1093/brain/awv318..
Rajnish Kumar, A. Nordberg, Taher Darreh-Shori

Transgenic Mice Overexpressing Amyloid Precursor Protein Exhibit Early Metabolic Deficits and a Pathologically Low Leptin State Associated with Hypothalamic Dys
The Journal of Neuroscience; 10.1523/JNEUROSCI.0872-14.2014.
Makoto Ishii, Gang Wang, Gianfranco Racchumi, Jonathan P. Dyke, and Costantino Iadecola

Beta-Amyloid (1-42), TFA

Product Details

References

Publications