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HYB 191-01-02 has specificity for human a-1 AT, native and denatured.
HYB 191-01-02 has been successfully used in Western blotting and ELISA procedures. HYB 191-01-02 reacts strongly with a-1 AT. Strong reaction is seen in ELISA with native and denatured a-1 AT directly coated onto the microtiter well. When tested in sandwich ELISA in combination with a polyclonal antibody against a-1 AT (e.g. DAKO A0012), it only recognizes native a-1 AT. In Western blotting after SDS-PAGE, HYB 191-01-02 reacts with native and denatured a-1 AT in reduced as well as non-reduced forms.
The HYB 191-01-02 immunogen is a-1 AT isolated from human plasma.
The HYB 191-01-02 epitope differs from that of HYB 185-02-02.
NOTE: Concentration is lot-dependent and can vary from 0.85-1.15 mg/mL
Alpha-1-AT is synthesized in the liver and it acts as an inhibitor of proteases such as trypsin, elastase, chymotrypsin, collagenase, leucocytic proteases, plasmin, and thrombin, which may be released during inflammatory reactions in the lung. In the absence of alpha-1-AT, these enzymes are not inhibited and they may digest pulmonary parenchyma. Alpha-1-AT deficiency is associated with chronic obstructive lung disease (emphysema) and less frequently with hepatic cirrhosis in infants and respiratory distress of the newborn. Increase in alpha-1-AT occurs as an acute phase response to tissue necrosis and inflammation. Serum level of alpha-1-AT is elevated in rheumatoid arthritis, bacterial infections, vasculitis, and carcinomatosis.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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