Tailor-made Antibodies
and Tools for Life Science
Home|||||Technical Support

Abeta-pE3 antibody - 218 311

Abeta peptides are major components of neuritic plaques in Alzheimer's disease
Mouse monoclonal purified IgG
Cat. No.: 218 311
Amount: 100 µg
Price: $415.00
Cat. No. 218 311 100 µg purified IgG, lyophilized. Albumin and azide were added for stabilization. For reconstitution add 100 µl H2O to get a 1mg/ml solution in PBS. Then aliquot and store at -20°C to -80°C until use.
Antibodies should be stored at +4°C when still lyophilized. Do not freeze!
Applications
 
WB: 1 : 1000 (see remarks) gallery  
IP: yes
ICC: not tested yet
IHC: 1 : 100 (see remarks)
IHC-P: 1 : 1000 up to 1 : 5000 gallery  
Clone 1-57
Subtype IgG2b (κ light chain)
Immunogen Synthetic peptide corresponding to AA 3 to 7 from human Abeta-pE3 (UniProt Id: P05067)
Epitop Epitop: AA 3 to 5 from human Abeta-pE3 (UniProt Id: P05067)
Reactivity Reacts with: human (P05067), rat (P08592), mouse (P12023).
Other species not tested yet.
Specificity Specific for Abeta-pE3.
Remarks

WB: Detects purified Abeta pE3. Complex samples like brain extracts still have to be tested.
Boil membrane after blotting for 3min.
IHC: Antigen retrieval with formic acid is required.

Data sheet 218_311.pdf

References for Abeta-pE3 - 218 311

N-truncated Abeta starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody.
Antonios G, Saiepour N, Bouter Y, Richard BC, Paetau A, Verkkoniemi-Ahola A, Lannfelt L, Ingelsson M, Kovacs GG, Pillot T, Wirths O, et al.
Acta neuropathologica communications (2013) 1: 56. 218 311 IHC, WB; tested species: human
Pyroglutamate amyloid β (Aβ) aggravates behavioral deficits in transgenic amyloid mouse model for Alzheimer disease.
Wittnam JL, Portelius E, Zetterberg H, Gustavsson MK, Schilling S, Koch B, Demuth HU, Blennow K, Wirths O, Bayer TA
The Journal of biological chemistry (2012) 28711: 8154-62. 218 311 IP
N-truncated Abeta starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody.
Antonios G, Saiepour N, Bouter Y, Richard BC, Paetau A, Verkkoniemi-Ahola A, Lannfelt L, Ingelsson M, Kovacs GG, Pillot T, Wirths O, et al.
Acta neuropathologica communications (2013) 1: 56. 218 311 IHC, WB; 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. 218 311 IHC-P; tested species: human
Cat. No.: 218 311
Amount: 100 µg
Price: $415.00
N-truncated Abeta starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody.
Antonios G, Saiepour N, Bouter Y, Richard BC, Paetau A, Verkkoniemi-Ahola A, Lannfelt L, Ingelsson M, Kovacs GG, Pillot T, Wirths O, et al.
Acta neuropathologica communications (2013) 1: 56. 218 311 IHC, WB; tested species: human
Pyroglutamate amyloid β (Aβ) aggravates behavioral deficits in transgenic amyloid mouse model for Alzheimer disease.
Wittnam JL, Portelius E, Zetterberg H, Gustavsson MK, Schilling S, Koch B, Demuth HU, Blennow K, Wirths O, Bayer TA
The Journal of biological chemistry (2012) 28711: 8154-62. 218 311 IP
N-truncated Abeta starting with position four: early intraneuronal accumulation and rescue of toxicity using NT4X-167, a novel monoclonal antibody.
Antonios G, Saiepour N, Bouter Y, Richard BC, Paetau A, Verkkoniemi-Ahola A, Lannfelt L, Ingelsson M, Kovacs GG, Pillot T, Wirths O, et al.
Acta neuropathologica communications (2013) 1: 56. 218 311 IHC, WB; 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. 218 311 IHC-P; tested species: human
Background

Amyloid deposits, also called plaques, of Alzheimer's patients consist of several protein components like the amyloid beta-peptides (Abeta, ) 1-40/42 and additional C- and N-terminally truncated and modified fragments. Very abundant are the isoaspartate (isoAsp)-Abeta and pyroglutamyl (pGlu)-Abeta peptides. The latter are formed by cyclization of the N-terminal glutamate at position 3 or 11 catalyzed by glutaminyl cyclase (QC) resulting in very amyloidogenic and neurotxic variants of Abeta; Abeta-pE3 and Abeta pE11.
In contrast to extracellular plaques that do not perfectly correlate with Alzheimer´s disease intraneuronal Abeta accumulation and vascular Abeta deposits have gained more and more evidence to be among the crucial factors responsible for progressive neuron loss.