Proteolytic cleavage of the Amyloid protein precursor (APP) gives rise to the β-Amyloid and Amyloid A4 proteins, which are present in human platelets. Amyloid deposition is associated with type II diabetes, Down syndrome and a variety of neurological disorders, including Alzheimer’s disease. Proteolytic cleavage of APP leads to the formation of the Amyloid β/A4 Amyloid protein. This protein is involved in the formation of neurofibrillary tangles and plaques that characterize the senile plaques of Alzheimer’s patients. BBP (Beta-amyloid-binding protein), also known as TM2D1 (TM2 domain-containing protein 1), is a 207 amino acid multi-pass membrane protein containing a G protein-coupling module that allows for interaction with the β-amyloid peptide of APP. In cell culture, expression of BBP induces caspase-dependent vulnerability to β-amyloid peptide toxicity, suggesting that it is a target of β-amyloid and may be involved in the molecular pathophysiology of Alzheimer’s disease.
应用类型
WB
免疫原
A synthetic peptide corresponding to residues in Human BBP.
