Protein Catagory: Neutrophil Proteins
CAS Number: 9004-06-2
Molecular Weight: 29,500 Da
Immunogen: No
Compound Purity: ≥95% by SDS-PAGE
Applications: Host Defense, Antimicrobial, Inflammation, Cancer, NETosis, Emphysema, COPD, SARS-CoV-2, Rheumatoid Arthritis, In Vitro Diagnostic
References: - Hiroyasu, S., et al., (2021), 'Granzyme B inhibition reduces disease severity in autoimmune blistering diseases', NATURE COMMUNICATIONS, 12: pp 302. Available at: https://doi.org/10.1038/s41467-020-20604-3 - Nielsen, N. S., et al., (2022), 'Cryo-EM structures of human A2ML1 elucidate the protease-inhibitory mechanism of the A2M family', NATURE COMMUNICATIONS., 13: pp 3033. Available at: https://doi.org/10.1038/s41467-022-30758-x - Li, Y., et al., (2024), 'Cystine-knot peptide inhibitors of HTRA1 bind to a cryptic pocket within the active site region', Nature Communications 15: pp 4359. Available at: https://doi.org/10.1038/s41467-024-48655-w - Lee, C. W., et al., (2017) 'The lysosomal protein cathepsin L is a progranulin protease', Molecular Neurodegeneration, 12: pp 55. Available at: DOI 10.1186/s13024-017-0196-6 - Alatrash, G., et al., (2018), ' Targeting the Leukemia Antigen PR1 with Immunotherapy for the Treatment of Multiple Myeloma', Clin Cancer Res., 24(14): pp 3386-3396. Available at: doi: 10.1158/1078-0432.CCR-17-2626.
Product Description: Neutrophil elastase (NE), a serine protease stored in azurophilic granules of neutrophils, plays critical roles in host defense and tissue remodeling. As a member of the chymotrypsin superfamily, NE hydrolyzes elastin, collagen, and proteoglycans through its catalytic triad (His-Asp-Ser), enabling pathogen clearance via microbial membrane disruption. Beyond direct bactericidal activity, NE modulates immune responses by activating matrix metalloproteinases (MMPs), inducing pro-inflammatory cytokines (TNF-α, IL-1β, IL-8), and promoting neutrophil extracellular trap (NET) formation. However, unchecked NE activity drives extracellular matrix degradation, contributing to chronic inflammatory and degenerative diseases. NE dysregulation is central to pulmonary emphysema, particularly in α1-antitrypsin deficiency, where insufficient protease inhibition leads to alveolar destruction. In chronic obstructive pulmonary disease (COPD), NE excess exacerbates airway inflammation and mucus hypersecretion, perpetuating lung parenchymal damage. NE also directly injures cartilage in rheumatoid arthritis by degrading collagen and activating fibroblast-like synoviocytes, amplifying joint inflammation. Additionally, elevated NE levels correlate with cystic fibrosis progression, acute respiratory distress syndrome (ARDS), and severe COVID-19, where it enhances viral entry and cytokine storms. Balancing NE’s protective and pathogenic roles remains a clinical challenge, necessitating therapies that preserve antimicrobial function while preventing tissue destruction.
English
Deutsch
