Anti-Human PEN2 (CT)

Leinco Technologies
Product Code: LEI-P205
Product Group: Primary Antibodies
CodeSizePrice
LEI-P205-20ug20 ug£199.00
Quantity:
LEI-P205-0.1mg0.1 mg£591.00
Quantity:
Prices exclude any Taxes / VAT

Overview

Host Type: Rabbit
Antibody Clonality: Polyclonal
Regulatory Status: RUO
Target Species: Human
Application: Western Blot (WB)
Shipping:
Ambient
Storage:
This polyclonal antibody is stable for at least one week when stored at 2-8°C. For long term storage aliquot in working volumes without diluting and store at -20°C in a manual defrost freezer. Avoid Repeated Freeze Thaw Cycles.

Further Information

Concentration:
0.5 mg/ml
Conjugate/Tag/Label:
Purified No Carrier Protein
Format:
This polyclonal antibody is formulated in phosphate buffered saline (PBS) pH 7.4 containing 0.02% sodium azide as a preservative.
Formulation:
This polyclonal antibody is formulated in phosphate buffered saline (PBS) pH 7.4 containing 0.02% sodium azide as a preservative.
Immunogen:
PN:P215
Long Description:
PEN2, in addition to presenilin, nicastrin, and APH-1 forms the γ-secretase protein complex, a membrane-bound aspartyl protease that can cleave certain proteins at peptide bonds buried within the hydrophobic environment of the lipid bilayer. This cleavage is responsible for a key step in signaling from several cell-surface receptors and is thought to be required for the generation of the neurotoxic amyloid peptides that are central to the pathogenesis of Alzheimer?s disease(1,2 for review). Like the tumor necrosis factor-α-converting enzyme (TACE) and the β-site cleavage enzyme (BACE) protease families, γ-secretase will cleave the amyloid precursor protein (APP), but within the intramembrane region of APP, resulting in either the non-toxic p3 (from the α and γ cleavage site) or the toxic A/β amyloid peptide (from the β and γ cleavage site)(3). It is thought that accumulation of the Aβ peptide is the precursor to Alzheimer?s disease(4).
NCBI Gene:
55851
Target:
PEN2

References

1. Weihofen, A. et al. (2003) Trends Cell Biol. 13:71 2. Periz, G. et al. (2004) J. Neurosci. Res. 77:309 3. Selkoe, D. J. (1998) Trends Cell Biol. 8:447 4. Selkoe, S. J. (1999) Nature 399:A23

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