Insulin-Degrading Enzyme: Difference between revisions
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IDE could help creating IDE-based therapies to control cerebral Aβ and blood sugar concentrations thanks to the understanding of its molecular mechanisms. | IDE could help creating IDE-based therapies to control cerebral Aβ and blood sugar concentrations thanks to the understanding of its molecular mechanisms. | ||
IDE is an unusual enzyme because of its high affinity for substrates that are widely diverse in sequence and structure. IDE prefers to degrade <6 kDa bioactive peptides such as insulin, Aβ, glucagon, atrial natriuretic peptides or transforming growth factor α. Paradoxally, even though IDE targets a broad range of substrates, it shows a remarkable capacity to selectively cleave some peptides without degrading related family members. | IDE is an unusual enzyme because of its high affinity for substrates that are widely diverse in sequence and structure. IDE prefers to degrade <6 kDa bioactive peptides such as insulin, Aβ, glucagon, atrial natriuretic peptides or transforming growth factor α. Paradoxally, even though IDE targets a broad range of substrates, it shows a remarkable capacity to selectively cleave some peptides without degrading related family members. | ||
See [[Human Insulin Degrading Enzyme (Hebrew)]]. | |||
== How are the structure and the functions of IDE related? == | == How are the structure and the functions of IDE related? == | ||