Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
February 1, 1989Journal of Biological ChemistryOpen Access

Disruption of the 290–342 salt bridge is not responsible for the secretory defect of the PiZ α1-antitrypsin variant

View Full Paper
Ask AI
Bookmark
Share

Authors

RSR N SifersBaylor College of MedicineCHChristopher HardickSWSavio L.C. WooKorea Institute of Ocean Science and Technology

Discussion

Loading...

Member takes

Implication

Key Points

Key points are not available for this paper at this time.

Cite This Study

Sifers et al. (1989) studied this question.

synapsesocial.com/papers/6a71b05fb27f15817827d3d8https://doi.org/10.1016/s0021-9258(19)81712-x
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Alpha-1-Antitrypsin Deficiency1971 · 193 citations
  2. 2Recombinant genomes which express chloramphenicol acetyltransferase in mammalian cells.1982 · 7,748 citations
  3. 3Identification of a second mutation in the protein-coding sequence of the Z type alpha 1-antitrypsin gene.1986 · 127 citations