β-Amyloid (pE3 Peptide) (D5N5H) Rabbit mAb #14975
- WB
- IHC
- IF
Supporting Data
REACTIVITY | H |
SENSITIVITY | Endogenous |
MW (kDa) | 4 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Immunohistochemistry (Paraffin) | 1:100 |
Immunofluorescence (Frozen) | 1:200 |
Storage
For a carrier free (BSA and azide free) version of this product see product #76486.
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
Aβ peptides can be further modified by amino-terminal truncation that exposes a free glutamate residue to the enzyme glutaminyl cyclase, which catalyzes the formation of an amino-terminal pyroglutamate (pE) (7,8). Aβ (pE3) peptides exhibit increased stability relative to non-modified peptides due to an enhanced resistance to peptidase-mediated degradation (9) and a higher propensity to form β-sheets and aggregate (10). Antibodies targeting Aβ (pE3) peptides may be plaque-specific as there is no evidence for circulating Aβ (pE3) peptides (11).
- Selkoe, D.J. (1996) J Biol Chem 271, 18295-8.
- Caporaso, G.L. et al. (1992) Proc Natl Acad Sci USA 89, 3055-9.
- Hung, A.Y. and Selkoe, D.J. (1994) EMBO J 13, 534-42.
- Suzuki, T. et al. (1994) EMBO J 13, 1114-22.
- Ando, K. et al. (1999) J Neurosci 19, 4421-7.
- Iijima, K. et al. (2000) J Neurochem 75, 1085-91.
- Jawhar, S. et al. (2011) J Biol Chem 286, 38825-32.
- Saido, T.C. et al. (1995) Neuron 14, 457-66.
- Saido, T.C. et al. (1996) Neurosci Lett 215, 173-6.
- He, W. and Barrow, C.J. (1999) Biochemistry 38, 10871-7.
- Demattos, R.B. et al. (2012) Neuron 76, 908-20.
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