- ￥5797
- 赛默飞（Thermo Fisher）
- MA514661
- 2025年07月11日
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文献和实验Ier1 p: A Kinase and Site-Specific Endoribonuclease
fibrosis, alpha1-antitrypsin deficiency, and osteogenesis imperfecta (2 ). One way in which cells cope with the accumulation of unfolded proteins in the ER is by activating the unfolded protein response (UPR), an ER-to-nucleus signal transduction pathway
Manipulating the Folding Pathway of ΔF508 CFTR Using Chemical Chaperones
Defects in protein folding constitute the basis of many genetic diseases: cystic fibrosis, alpha-1 antitrypsin deficiency, familial hypercholesterolemia, and congenital nephrogenic diabetes insipidus, to name but a few (see Table 1 for a complete
rAAV Vector Product Characterization and Stability Studies
and safety. In some trials, sustained or transient transgene expression has been demonstrated in humans treated for alpha-1 antitrypsin deficiency, LPL deficiency, hemophilia B and cystic fibrosis, and sustained correction of inherited blindness
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