Publication | Open Access
Endoplasmic reticulum polymers impair luminal protein mobility and sensitize to cellular stress in alpha1-antitrypsin deficiency
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Citations
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References
2012
Year
Changes in protein diffusion provide an explanation for the cellular consequences of ER protein overload in mutants that cause inclusion body formation and α1AT deficiency.
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A lag in intracellular degradation of mutant alpha 1-antitrypsin correlates with the liver disease phenotype in homozygous PiZZ alpha 1-antitrypsin deficiency. Yu‐Ling Wu, I. P. Whitman, Ernesto P. Molmenti, Proceedings of the National Academy of Sciences Common Er DegradationImmunologyPathologyAsialoglycoprotein Receptor SubunitsProtein Expression | 1994 | 291 |
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