Butyrylcholinesterase (BCHE)

Specification

• Cat#: THP-0279
• Product Name: Butyrylcholinesterase (BCHE)
• Description: Recombinant Human Butyrylcholinesterase protein (29-602 aa) is produced by HEK 293 cells expression system. This protein carries a His tag at C-Terminus.
• Sequences: EDDIIIATKNGKVRGMNLTVFGGTVTAFLGIPYAQPPLGRLRFKKPQSLT KWSDIWNATKYANSCCQNIDQSFPGFHGSEMWNPNTDLSEDCLYLNVWIP APKPKNATVLIWIYGGGFQTGTSSLHVYDGKFLARVERVIVVSMNYRVGA LGFLALPGNPEAPGNMGLFDQQLALQWVQKNIAAFGGNPKSVTLFGESAG AASVSLHLLSPGSHSLFTRAILQSGSFNAPWAVTSLYEARNRTLNLAKLT GCSRENETEIIKCLRNKDPQEILLNEAFVVPYGTPLSVNFGPTVDGDFLT DMPDILLELGQFKKTQILVGVNKDEGTAFLVYGAPGFSKDNNSIITRKEF QEGLKIFFPGVSEFGKESILFHYTDWVDDQRPENYREALGDVVGDYNFIC PALEFTKKFSEWGNNAFFYYFEHRSSKLPWPEWMGVMHGYEIEFVFGLPL ERRDNYTKAEEILSRSIVKRWANFAKYGNPNETQNNSTSWPVFKSTEQKY LTLNTESTRIMTKLRAQQCRFWTSFFPKVLEMTGNIDEAEWEWKAGFHRW NNYMMDWKNQFNDYTSKKESCVGLVDHHHHHH
• Species: Human
• Molecular Weight: 66 kDa including tags
• Source: HEK293 cells
• Introduction: Butyrylcholinesterase (BCHE) is a major acetylcholine hydrolyzing enzyme in the circulation. Although it is present in significant amounts in human plasma, no endogenous physiological substrate has been described for this enzyme. It can degrade a large number of ester-containing compounds besides acylcholines, including neurotoxic organophosphate esters. Thus, it plays significant pharmacological and toxicological roles. It is thought to be involved in the pathological progression of Alzheimer’s disease (AD) by depleting acetylcholine. In contrast to ACHE, it attenuates amyloid fibril formation in vitro. BCHE inhibitors have been used to delay symptoms of AD patients by virtue of their ability to enhance ACH availability. Its involvement in the cholinergic anti-inflammatory pathway connects BCHE and ACHE as possible markers of low-grade systemic inflammation observed in Type-2 diabetes, obesity, hypertension, coronary heart disease, and AD. BCHE can exist as monomers, dimers, or tetramers.
• Purity: >95% by SDS-PAGE.
• Application: It is thought to be involved in the pathological progression of Alzheimer’s disease (AD) by depleting acetylcholine. Its involvement in the cholinergic anti-inflammatory pathway connects BCHE and ACHE as possible markers of low-grade systemic inflammation observed in Type-2 diabetes, obesity, hypertension, coronary heart disease, and AD.