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Protease Inhibitors

Protease inhibitors are chemicals that effectively halt the function of proteases. Proteases are enzymes involved in protein metabolism or breaking down proteins into their constituent parts. Proteases function by hydrolysis of the peptide bonds between the amino acids in the protein chain. These free amino acids are then available to be utilized by the body. The protease inhibitors interfere with this process by using chelating agents, inhibiting the action of protein protease, inhibiting the transition state of proteolysis, or becoming a suicide inhibitor. There are many classes of protease inhibitors including aspartic, cysteine, metalloprotease, serine, and trypsin. Protease inhibition is especially useful in the treatment of viral infections. Protease inhibitors can inhibit viral action by stopping the virus in its efforts to utilize host proteins for its own metabolism. For example, the human immunodeficiency virus (HIV) uses proteases in the final stages of its replication process. The protease inhibitor drugs can help treat HIV infections by effectively causing the virus to replicate producing inert or defective progeny viruses that are not able to infect new cells. Therefore, the drugs can help to reduce symptoms and suppress the viruses, but does not kill all of them and thus the protease inhibitors do not provide a cure.

The anti- neuroserpin antibody has roles in serine protease inhibitors. It may be involved in the protein that reorganizes synaptic connections and protects neurons from cell damage. Defects in neuroserpin cause genetic encephalopathy characterized by inherited dementia. Anti-SERPINB6 antibody binds against the target SERPINB6. SERPINB6 is involved in the regulation of serine proteinases in the brain and blood. SERPINB6 is localized in the cytoplasm and specified in keratinocytes, skeletal muscle, placenta, cardiac muscle, lung, kidney, and pancreas. SERPINB6 inhibits cathepsin G, kallikrein-8, and thrombin. Defects in SERPINB6 are the cause of deafness autosomal recessive type 91. Deafness autosomal recessive type 91 is a form on non-syndromic deafness characterized by progressive sensorineural hearing loss that worsens with age. Affected individuals gradually lose their hearing but remain in control of their vestibular responses.

 
Product Number Title Applications Host Clonality
AC16-0012 Anti-TIMP1 Antibody ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (7-6C1)
AC16-0013 Anti-TIMP1 Antibody WB, IHC(F), IHC(P), ICC, IF, IP, FC Mouse Monoclonal (147-6D11)
AC16-0012-01 Anti-TIMP1 Antibody (AMCA) ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (7-6C1)
AC16-0012-02 Anti-TIMP1 Antibody (AP) ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (7-6C1)
AC16-0012-03 Anti-TIMP1 Antibody (APC) ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (7-6C1)
AC16-0012-04 Anti-TIMP1 Antibody (APC-Cy5.5) ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (7-6C1)
AC16-0012-05 Anti-TIMP1 Antibody (APC-Cy7) ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (7-6C1)
AC16-0012-06 Anti-TIMP1 Antibody (Avidin) ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (7-6C1)
AC16-0012-07 Anti-TIMP1 Antibody (Biotin) ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (7-6C1)
AC16-0012-08 Anti-TIMP1 Antibody (BPE) ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (7-6C1)
AC16-0012-09 Anti-TIMP1 Antibody (Cy3) ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (7-6C1)
AC16-0012-10 Anti-TIMP1 Antibody (Cy5) ELISA, WB, IHC(F), IHC(P), IP Mouse Monoclonal (7-6C1)