Anti-Amyloid Beta 3NTyr10 Antibody, clone 4A5E8

Isotype testing: Identity Confirmation by Isotyping Test.

Isotyping Analysis: The identity of this monoclonal antibody is confirmed by isotyping test to be mouse IgG2b .

Anti-Amyloid Beta 3NTyr10 Antibody, clone 4A5E8, Cat. No. MABN779, is a highly specific mouse monoclonal antibody that targets 3NTyr10 and has been tested in ELISA and Immunohistochemistry.

ELISA Analysis: A representative lot detected Amyloid Beta 3NTyr10 in ELISA applications (Heneka, M.T., et. al. (2013). Nature. 493(7434):674-8).

Immunohistochemistry Analysis: A 1:50 dilution from a representative lot detected Amyloid Beta 3NTyr10 in unfixed cortical brain sections from a control verses clinically confirmed AD (Braak stage V) cases. (Courtesy of Dr. Markus Kummer and Prof. Dr. Michael Heneka, MD, University of Bonn, Department of Neurology, Clinical Neurosciences, Germany).

Research Category
Neuroscience

Clone 4A5E8 detects amyloid beta 1-42 nitrated at position 10 in human.

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Deposition of Amyloid beta (Ab) is an early event in the pathogenesis of Alzheimer s disease (AD). Ab peptides originate from the proteolytic cleavage of the amyloid precursor protein (APP). The beta-secretase cleaves APP between residues Met671 and Asp672 and yields sAPP beta and C99. Following the beta-secretase cleavage, a second cleavage occurs at the C-terminus of Ab peptide that releases Ab from C99. This cleavage occurs in the vicinity of residue 712 of the C-terminus. The gamma-secretase can cleave the C-terminal region at either Val711 or Ile713 to produce the shorter Ab peptide (Ab1-40) or the longer Ab peptide (Ab1-42). Ab1-42 occurs more frequently and forms fibrillar aggregates far more readily than the Ab1-40 peptide. In AD, upregulation of inducible nitric oxide synthase (NOS2), results in tyrosine nitration of several proteins, including Ab, which accelerates its aggregation. APP/PS1/Nlrp3 mice display less nitrated Ab and a reduced average plaque size as well as fewer nitrated plaque cores. NOS2 deficiency and treatment with NOS2 inhibitors is shown to reduce 3NTyr (10)-Ab and overall Ab deposition and cognitive dysfunction in APP/PS1 mice. Also, injection of 3NTyr(10)-A into the brain of young APP/PS1 mice leads to induction of beta-amyloidosis. (Ref.: Heneka, MT et al (2013). Nature 493, 674-678; Kummer, MP et al (2011). Neuron. 71(5):833-844).

~4.51 kDa calculated. Beta amyloid peptides aggregate in Alzheimer′s disease brain.

Synthetically nitrated linear peptide corresponding to 12 amino acids in the beta amyloid beta 1-42 peptide.

Concentration: Please refer to lot specific datasheet.

Format: Purified

Protein G purified

Purified mouse monoclonal antibody IgG2b in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Stable for 1 year at 2-8°C from date of receipt.