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Abeta 1-5 - 218 231

A major component of neuritic plaques in Alzheimer's disease
Monoclonal mouse purified IgG
Cat. No.: 218 231
Amount: 100 µg
Price: 415.00 €
Cat. No. 218 231 100 µg purified IgG, lyophilized. Azide was added before lyophilization. For reconstitution add 100 µl H2O to get a 1mg/ml solution in PBS. Then aliquot and store at -20°C until use.
Applications WB: not tested yet
IP: not tested yet
ICC: not tested yet
IHC: 1 : 100 up to 1 : 500 gallery  
IHC-P/FFPE: 1 : 100 up to 1 : 200 gallery  
Clone 80C2
Subtype IgG2a (κ light chain)
Immunogen Synthetic peptide corresponding to AA 1 to 5 from human Abeta (UniProt Id: P05067)
Epitop Epitop: AA 1 to 5 from human Abeta (UniProt Id: P05067)
Reactivity Reacts with: human (P05067), mouse (P12023).
Other species not tested yet.
Specificity Specific for Abeta 38, 40, 42, 43. No cross-reactivity to N-terminally truncated Abeta species.
Data sheet 218_231.pdf

References for Abeta 1-5 - 218 231

N-terminal heterogeneity of parenchymal and vascular amyloid-β deposits in Alzheimer's disease.
Zampar S, Klafki HW, Sritharen K, Bayer TA, Wiltfang J, Rostagno A, Ghiso J, A Miles L, Wirths O
Neuropathology and applied neurobiology (2020) : . 218 231 WB, IHC-P; tested species: human
N-terminal heterogeneity of parenchymal and vascular amyloid-β deposits in Alzheimer's disease.
Zampar S, Klafki HW, Sritharen K, Bayer TA, Wiltfang J, Rostagno A, Ghiso J, A Miles L, Wirths O
Neuropathology and applied neurobiology (2020) : . 218 231 WB, IHC-P; tested species: human
The presubiculum is preserved from neurodegenerative changes in Alzheimer's disease.
Murray CE, Gami-Patel P, Gkanatsiou E, Brinkmalm G, Portelius E, Wirths O, Heywood W, Blennow K, Ghiso J, Holton JL, Mills K, et al.
Acta neuropathologica communications (2018) 61: 62. 218 231 IHC-P; tested species: human
The metalloprotease ADAMTS4 generates N-truncated Aβ4-x species and marks oligodendrocytes as a source of amyloidogenic peptides in Alzheimer's disease.
Walter S, Jumpertz T, Hüttenrauch M, Ogorek I, Gerber H, Storck SE, Zampar S, Dimitrov M, Lehmann S, Lepka K, Berndt C, et al.
Acta neuropathologica (2018) : . 218 231 IHC-P; tested species: mouse
Cat. No.: 218 231
Quantity: 100 µg
Price: 415.00 €
N-terminal heterogeneity of parenchymal and vascular amyloid-β deposits in Alzheimer's disease.
Zampar S, Klafki HW, Sritharen K, Bayer TA, Wiltfang J, Rostagno A, Ghiso J, A Miles L, Wirths O
Neuropathology and applied neurobiology (2020) : . 218 231 WB, IHC-P; tested species: human
N-terminal heterogeneity of parenchymal and vascular amyloid-β deposits in Alzheimer's disease.
Zampar S, Klafki HW, Sritharen K, Bayer TA, Wiltfang J, Rostagno A, Ghiso J, A Miles L, Wirths O
Neuropathology and applied neurobiology (2020) : . 218 231 WB, IHC-P; tested species: human
The presubiculum is preserved from neurodegenerative changes in Alzheimer's disease.
Murray CE, Gami-Patel P, Gkanatsiou E, Brinkmalm G, Portelius E, Wirths O, Heywood W, Blennow K, Ghiso J, Holton JL, Mills K, et al.
Acta neuropathologica communications (2018) 61: 62. 218 231 IHC-P; tested species: human
The metalloprotease ADAMTS4 generates N-truncated Aβ4-x species and marks oligodendrocytes as a source of amyloidogenic peptides in Alzheimer's disease.
Walter S, Jumpertz T, Hüttenrauch M, Ogorek I, Gerber H, Storck SE, Zampar S, Dimitrov M, Lehmann S, Lepka K, Berndt C, et al.
Acta neuropathologica (2018) : . 218 231 IHC-P; tested species: mouse
Background

Amyloid deposits, also called plaques, of Alzheimer's patients consist of several protein components like the amyloid beta-peptides (Abeta, Aβ) 1-40/42/43 and additional C- and N-terminally modified fragments of Abeta as for instance Abeta pE3 and Abeta pE11.
An additional Abeta variant, Abeta 38, is more soluble compared to other Abeta species and is not found in plaques of sporadic Alzheimer´s cases. However, it is detected in the blood-vessel walls of a subset of patients with severe cerebral amyloid angiopathy. It especially accumulates in brains of patients carrying mutations in the Abeta coding region.
Cleavage of amyloid precursor protein APP by β- and γ- secretases results in the generation of the Aβ (βA4)peptide, whereas α-secretase cleaves within the Aβ sequence and prevents the formation of Abeta from APP.