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Abeta-pE3 antibody - 218 003

Abeta peptides are major components of neuritic plaques in Alzheimer's disease
Rabbit polyclonal purified antibody
Cat. No.: 218 003
Amount: 50 µg
Price: $370.00
Cat. No. 218 003 50 µg specific antibody, lyophilized. Affinity purified with the immunogen. Albumin was added for stabilization. For reconstitution add 50 µl H2O to get a 1mg/ml solution in PBS. Then aliquot and store at -20°C to -80°C until use.
Applications WB: 1 : 1000 (see remarks) gallery  
IP: not tested yet
ICC: not tested yet
IHC: 1 : 500 (see remarks) gallery  
IHC-P/FFPE: 1 : 200 (see remarks) gallery  
Immunogen Synthetic peptide corresponding to AA 3 to 7 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.
IHC-P: Antigen retrieval with formic acid is required.

Data sheet 218_003.pdf

References for Abeta-pE3 - 218 003

Prion-like behaviour and tau-dependent cytotoxicity of pyroglutamylated amyloid-β.
Nussbaum JM, Schilling S, Cynis H, Silva A, Swanson E, Wangsanut T, Tayler K, Wiltgen B, Hatami A, Rönicke R, Reymann K, et al.
Nature (2012) 4857400: 651-5. 218 003 WB, IHC
Posttranslational modification impact on the mechanism by which amyloid-β induces synaptic dysfunction.
Grochowska KM, Yuanxiang P, Bär J, Raman R, Brugal G, Sahu G, Schweizer M, Bikbaev A, Schilling S, Demuth HU, Kreutz MR, et al.
EMBO reports (2017) 186: 962-981. 218 003 ICC; tested species: rat
Brain pyroglutamate amyloid-β is produced by cathepsin B and is reduced by the cysteine protease inhibitor E64d, representing a potential Alzheimer's disease therapeutic.
Hook G, Yu J, Toneff T, Kindy M, Hook V
Journal of Alzheimer's disease : JAD (2014) 411: 129-49. 218 003 IHC; tested species: mouse
Glutaminyl cyclase in human cortex: correlation with (pGlu)-amyloid-β load and cognitive decline in Alzheimer's disease.
Morawski M, Schilling S, Kreuzberger M, Waniek A, Jäger C, Koch B, Cynis H, Kehlen A, Arendt T, Hartlage-Rübsamen M, Demuth HU, et al.
Journal of Alzheimer's disease : JAD (2014) 392: 385-400. 218 003 IHC; tested species: human
Glutaminyl cyclase-mediated toxicity of pyroglutamate-beta amyloid induces striatal neurodegeneration.
Becker A, Kohlmann S, Alexandru A, Jagla W, Canneva F, Bäuscher C, Cynis H, Sedlmeier R, Graubner S, Schilling S, Demuth HU, et al.
BMC neuroscience (2013) 14: 108. 218 003 IHC; tested species: human
Prion-like behaviour and tau-dependent cytotoxicity of pyroglutamylated amyloid-β.
Nussbaum JM, Schilling S, Cynis H, Silva A, Swanson E, Wangsanut T, Tayler K, Wiltgen B, Hatami A, Rönicke R, Reymann K, et al.
Nature (2012) 4857400: 651-5. 218 003 WB, IHC
Involvement of perineuronal and perisynaptic extracellular matrix in Alzheimer's disease neuropathology.
Morawski M, Brückner G, Jäger C, Seeger G, Matthews RT, Arendt T
Brain pathology (Zurich, Switzerland) (2012) 224: 547-61. 218 003 IHC; tested species: human
Selective hippocampal neurodegeneration in transgenic mice expressing small amounts of truncated Aβ is induced by pyroglutamate-Aβ formation.
Alexandru A, Jagla W, Graubner S, Becker A, Bäuscher C, Kohlmann S, Sedlmeier R, Raber KA, Cynis H, Rönicke R, Reymann KG, et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience (2011) 3136: 12790-801. 218 003 IHC
Glutaminyl cyclase contributes to the formation of focal and diffuse pyroglutamate (pGlu)-Aβ deposits in hippocampus via distinct cellular mechanisms.
Hartlage-Rübsamen M, Morawski M, Waniek A, Jäger C, Zeitschel U, Koch B, Cynis H, Schilling S, Schliebs R, Demuth HU, Rossner S, et al.
Acta neuropathologica (2011) 1216: 705-19. 218 003 IHC
Cat. No.: 218 003
Quantity: 50 µg
Price: $370.00
Prion-like behaviour and tau-dependent cytotoxicity of pyroglutamylated amyloid-β.
Nussbaum JM, Schilling S, Cynis H, Silva A, Swanson E, Wangsanut T, Tayler K, Wiltgen B, Hatami A, Rönicke R, Reymann K, et al.
Nature (2012) 4857400: 651-5. 218 003 WB, IHC
Posttranslational modification impact on the mechanism by which amyloid-β induces synaptic dysfunction.
Grochowska KM, Yuanxiang P, Bär J, Raman R, Brugal G, Sahu G, Schweizer M, Bikbaev A, Schilling S, Demuth HU, Kreutz MR, et al.
EMBO reports (2017) 186: 962-981. 218 003 ICC; tested species: rat
Brain pyroglutamate amyloid-β is produced by cathepsin B and is reduced by the cysteine protease inhibitor E64d, representing a potential Alzheimer's disease therapeutic.
Hook G, Yu J, Toneff T, Kindy M, Hook V
Journal of Alzheimer's disease : JAD (2014) 411: 129-49. 218 003 IHC; tested species: mouse
Glutaminyl cyclase in human cortex: correlation with (pGlu)-amyloid-β load and cognitive decline in Alzheimer's disease.
Morawski M, Schilling S, Kreuzberger M, Waniek A, Jäger C, Koch B, Cynis H, Kehlen A, Arendt T, Hartlage-Rübsamen M, Demuth HU, et al.
Journal of Alzheimer's disease : JAD (2014) 392: 385-400. 218 003 IHC; tested species: human
Glutaminyl cyclase-mediated toxicity of pyroglutamate-beta amyloid induces striatal neurodegeneration.
Becker A, Kohlmann S, Alexandru A, Jagla W, Canneva F, Bäuscher C, Cynis H, Sedlmeier R, Graubner S, Schilling S, Demuth HU, et al.
BMC neuroscience (2013) 14: 108. 218 003 IHC; tested species: human
Prion-like behaviour and tau-dependent cytotoxicity of pyroglutamylated amyloid-β.
Nussbaum JM, Schilling S, Cynis H, Silva A, Swanson E, Wangsanut T, Tayler K, Wiltgen B, Hatami A, Rönicke R, Reymann K, et al.
Nature (2012) 4857400: 651-5. 218 003 WB, IHC
Involvement of perineuronal and perisynaptic extracellular matrix in Alzheimer's disease neuropathology.
Morawski M, Brückner G, Jäger C, Seeger G, Matthews RT, Arendt T
Brain pathology (Zurich, Switzerland) (2012) 224: 547-61. 218 003 IHC; tested species: human
Selective hippocampal neurodegeneration in transgenic mice expressing small amounts of truncated Aβ is induced by pyroglutamate-Aβ formation.
Alexandru A, Jagla W, Graubner S, Becker A, Bäuscher C, Kohlmann S, Sedlmeier R, Raber KA, Cynis H, Rönicke R, Reymann KG, et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience (2011) 3136: 12790-801. 218 003 IHC
Glutaminyl cyclase contributes to the formation of focal and diffuse pyroglutamate (pGlu)-Aβ deposits in hippocampus via distinct cellular mechanisms.
Hartlage-Rübsamen M, Morawski M, Waniek A, Jäger C, Zeitschel U, Koch B, Cynis H, Schilling S, Schliebs R, Demuth HU, Rossner S, et al.
Acta neuropathologica (2011) 1216: 705-19. 218 003 IHC
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.