Disruption of the Lys‐290‐Glu‐342 salt bridge in human α1‐antitrypsin does not prevent its synthesis and secretion
- 25 May 1987
- journal article
- Published by Wiley in FEBS Letters
- Vol. 216 (1) , 79-82
- https://doi.org/10.1016/0014-5793(87)80760-3
Abstract
The object of this work was to test the hypothesis that failure to secrete the Z variant of human α1-antitrypsin is related to the loss of a particular structural feature, the Lys-290 to Glu-342 salt bridge. Oligonucleotide-directed mutagenesis was used to disrupt the salt bridge by substituting a glutamic acid for lysine at residue 290. RNA transcripts prepared from this mutant DNA and from the normal cDNA were both able to direct the synthesis of protein in a cell-free system and after injection into Xenopus oocytes. Furthermore, the constructed mutant α-antitrypsin was secreted as readily as the normal inhibitor.Keywords
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