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- W1987228909 abstract "The object of this work was to test the hypothesis that failure to secrete the Z variant of human α 1 ‐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." @default.
- W1987228909 created "2016-06-24" @default.
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- W1987228909 date "1987-05-25" @default.
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- W1987228909 title "Disruption of the Lys-290-Glu-342 salt bridge in human α<sub>1</sub>-antitrypsin does not prevent its synthesis and secretion" @default.
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- W1987228909 doi "https://doi.org/10.1016/0014-5793(87)80760-3" @default.
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