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una/protease

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Alpha-ketoamides, alpha-ketoesters and alpha-diketones as HCV NS3 protease inhibitors.

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Peptide-based alpha-ketoamides, alpha-ketoesters and alpha-diketones were designed, synthesized and evaluated against HCV NS3 protease. Alpha-ketoamides have the highest affinity among the three classes, with 8 being the most potent inhibitor with an IC50 of 340 nM.

Peptide alpha-keto ester, alpha-keto amide, and alpha-keto acid inhibitors of calpains and other cysteine proteases.

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A series of dipeptidyl and tripeptidyl alpha-keto esters, alpha-keto amides, and alpha-keto acids having leucine in the P2 position were synthesized and evaluated as inhibitors for the cysteine proteases calpain I, calpain II, cathepsin B, and papain. In general, peptidyl alpha-keto acids were more
An ELISA test system has been developed for the quantification of the two distinct forms of the proteinase inhibitor alpha 2-macroglobulin (alpha 2M): (i) free alpha 2M (functionally active), which is the electrophoretically slow form (alpha 2 MS), and (ii) the alpha 2 M-proteinase complex
N alpha-(N,N-dimethylcarbamoyl)-alpha-azaornitine and N alpha-(N,N-dimethylcarbamoyl)-alpha-azalysine phenyl and p-nitrophenyl esters (7-10) were synthesized and tested as inhibitors of trypsin, chymotrypsin and thrombin. The N,N-dimethylcarbamoyl group was chosen to decrease the tendency of

[Substitution therapy in alpha 1-protease inhibitor deficiency (alpha 1-antitrypsin deficiency)].

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Deficiency of alpha 1-protease inhibitor is a dominant autosomally inherited error of metabolism leading to destruction of alveolar septa by proteolytic enzymes mainly released by neutrophils often before the fifth decade. Diagnosis and determination of phenotype are achieved by serologic tests.

Protease susceptibilities of HMW, 1 alpha, 2 alpha, but not 3 alpha cartilage collagens are similar to type V collagen.

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Binding of alpha 1 antitrypsin (alpha 1 protease inhibitor) to human lymphocytes.

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[Protease inhibitors, alpha-1-antitrypsin and alpha-2-macroglobulin, in liver processes].

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Immunoelectrophoretic pattern of alpha 2-macroglobulin and alpha 2-macroglobulin-protease complexes.

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Biosynthesis of a alpha-amylase and protease by Streptomyces olivaceus 142. III. Some aspects of alpha-amylase induction.

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The induction of alpha-amylase in Streptomyces olivaceus 142 depends on the phase of growth of culture and the nature of the carbon sources upon which the cells were grown prior to exposure to inducer. The most susceptible to induction are cells from the initial hours of growth and glycerol -- grown
Tumor necrosis factor alpha (TNF-alpha) is a potent cytokine in neurodegenerative disorders, but its precise role in particular brain disorders is ambiguous. In motor neuron (MN) disease of the mouse, exemplified by the model wobbler (WR), TNF-alpha causes upregulation of the

Effect of alpha,alpha-dialkyl amino acids on the protease resistance of peptides.

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A tryptic [EC 3.4.21.4] digestion assay of 2-aminoisobutyric acid (Aib)-containing peptides was carried out to investigate the effect of alpha,alpha-dialkyl amino acid residues on the protease resistance. The introduction of Aib residues to the P1' positions exhibited a 19-fold higher protease

Aralast: an alpha 1-protease inhibitor for the treatment of alpha-antitrypsin deficiency.

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Alpha-antitrypsin (AAT) is a serine protease inhibitor, which inhibits the proteolytic enzyme elastase. Individuals with a deficiency of AAT may develop clinical manifestations that include a decline in lung function. Deficiency of AAT can lead to many clinical manifestations, most commonly chronic

Alzheimer's alpha-secretase may be a calcium-dependent protease.

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Proteolytic processing of beta-amyloid precursor protein (APP) is believed to be fundamental to the understanding of Alzheimer's disease. The identities and the regulatory elements of the proteases involved in the process, known as alpha/beta/gamma secretases, are unclear. In this study, by

Treatment of panniculitis associated with alpha-1-antitrypsin deficiency with alpha-1-protease inhibitor.

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