abeta

Beta-amyloid 39/Beta-APP39 Protein, Human, Recombinant (aa 672-710, His & GST) is expressed in E. coli expression system with His and GST tag. The predicted molecular weight is 32.2 kDa and the accession number is P05067-1.

APP/Protease nexin-II Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 101 kDa and the accession number is P05067-8.

Beta-amyloid 42/Beta-APP42 Protein, Human, Recombinant (His & GST) is expressed in E. coli expression system with His and GST tag. The predicted molecular weight is 32.4 kDa and the accession number is P05067-1.

Insulin-Degrading Enzyme (IDE) is a secreted enzyme that belongs to the peptidase M16 family. IDE is a large zinc-binding protease and cleaves multiple short polypeptides that vary considerably in sequence. IDE plays a role in the cellular breakdown of insulin, IAPP, glucagon, bradykinin, kallidin, and other peptides, and thereby plays a role in intercellular peptide signaling. IDE degrades amyloid formed by APP and IAPP. IDE may participate in the degradation and clearance of naturally secreted amyloid β-protein by neurons and microglia. IDE, which migrates at 110 kDa during gel electrophoresis under denaturing conditions, has since been shown to have additional substrates, including the signaling peptides glucagon, TGF α and β-endorphin.

Beta-amyloid 40/Beta-APP40 Protein, Human, Recombinant (His & GST) is expressed in E. coli expression system with His and GST tag. The predicted molecular weight is 31.8 kDa and the accession number is P05067-1.

Beta-amyloid 38/Beta-APP38 Protein, Human, Recombinant (aa 672-709, His & GST) is expressed in E. coli expression system with His and GST tag. The predicted molecular weight is 32.1 kDa and the accession number is P05067-1.

G protein-coupled receptor kinase 5, also known as G protein-coupled receptor kinase GRK5 and GRK5, is a member of the protein kinase superfamily, AGC Ser/Thr protein kinase family, and GPRK subfamily. GRKs specifically phosphorylate agonist-occupied G protein-coupled receptors at the inner surface of the plasma membrane (PM), leading to receptor desensitization. GRKs utilize a variety of mechanisms to bind tightly, and sometimes reversibly, to cellular membranes. GRKs play an important role in mediating agonist-specific desensitization of numerous G protein-coupled receptors.GRK5 contains one AGC-kinase C-terminal domain, one protein kinase domain, and one RGS domain. GRK5 specifically phosphorylates the activated forms of G protein-coupled receptors. Phospholipid-stimulated autophosphorylation may represent a novel mechanism for membrane association and regulation of GRK5 activity. GRK5 deficiency significantly exaggerates microgliosis and astrogliosis in the presence of an inflammatory initiator, such as the excess fibrillar Abeta and the subsequent active inflammatory reactions. GRK5 deficiency has been linked to early Alzheimer's disease in humans and mouse models of the disease.

THOP1, also known as Thimet oligopeptidase 1, Thimet oligopeptidase, EC 3.4.24.15, or EP24.15, is a zinc(II) endopeptidase implicated in the processing of numerous physiological peptides. As an intracellular enzyme, highly expressed in the brain, kidneys and neuroendocrine tissue, THOP1 has been proposed to metabolize peptides within cells, thereby affecting antigen presentation and G protein-coupled receptor signal transduction. Its substrates is gonadotrophin-releasing hormone (GnRH), an important hypothalamic hormone that regulates the synthesis and release of oestradiol and facilitates female sexual behaviour. THOP1 against toxic effects of Abeta in the early stages of Alzheimer disease (AD) pathology, and suggest that the observed increase in THOP1 expression might be part of a compensatory defense mechanism of the brain against an increased Abeta load.