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Loss-of-function PCSK9 mutants evade the unfolded protein response sensor GRP78 and fail to induce endoplasmic reticulum stress when retained
The proprotein convertase subtilisin/kexin type-9 (PCSK9) plays a central role in cardiovascular disease (CVD) by degrading hepatic low-density lipoprotein receptor (LDLR). As such, loss-of-function (LOF) PCSK9 variants that fail to exit the endoplasmic reticulum (ER) increase hepatic LDLR levels an...
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| I publikationen: | J Biol Chem |
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| Huvudupphovsmän: | , , , , , , , , , , , |
| Materialtyp: | Artigo |
| Språk: | Inglês |
| Publicerad: |
American Society for Biochemistry and Molecular Biology
2018
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| Ämnen: | |
| Länkar: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5950004/ https://ncbi.nlm.nih.gov/pubmed/29593095 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1074/jbc.RA117.001049 |
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