Abstract
A unique central nervous system (CNS)-specific metalloprotease, DINE / ECEL1 (damage induced neuronal endopeptidase / endothelin converting enzyme-like 1), has recently been added to the M13 / neprilysin (NEP) family. This enzyme was identified by two groups independently using different approaches. In this review, we introduce the characteristics of DINE / ECEL1 and focus on the mechanism underlying the transcriptional regulation of DINE in response to neuronal injury.
Keywords: dine, ecel1, neprilysin, neuron, nerve injury, survival, neuropeptides, leukemia inhibitory, factor (lif)
Protein & Peptide Letters
Title: Dine (Damage-Induced Neuronal Endopeptidase)
Volume: 11 Issue: 5
Author(s): Sumiko Kiryu-Seo and Hiroshi Kiyama
Affiliation:
Keywords: dine, ecel1, neprilysin, neuron, nerve injury, survival, neuropeptides, leukemia inhibitory, factor (lif)
Abstract: A unique central nervous system (CNS)-specific metalloprotease, DINE / ECEL1 (damage induced neuronal endopeptidase / endothelin converting enzyme-like 1), has recently been added to the M13 / neprilysin (NEP) family. This enzyme was identified by two groups independently using different approaches. In this review, we introduce the characteristics of DINE / ECEL1 and focus on the mechanism underlying the transcriptional regulation of DINE in response to neuronal injury.
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Cite this article as:
Kiryu-Seo Sumiko and Kiyama Hiroshi, Dine (Damage-Induced Neuronal Endopeptidase), Protein & Peptide Letters 2004; 11 (5) . https://dx.doi.org/10.2174/0929866043406526
DOI https://dx.doi.org/10.2174/0929866043406526 |
Print ISSN 0929-8665 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5305 |
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Plants are still the major repository of biologically active substances. In the last two decades, however, natural peptides and proteins of plant origin have gained increasing attention due to their pharmacological activities over a variety of human illnesses, including those mediated by infections and parasitosis and those involving different cellular ...read more
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