Abstract
Background and Aims: PLIN2 is the most prominent lipid droplet (LD)-associated protein in foam cells. PLIN2 stabilizes LDs and LDs protect PLIN2 from rapid degradation. LD-bound PLIN2 degradation is dependent on AMPK-phosphorylation via chaperone-mediated autophagy (CMA). PLIN2 is vital to maintain certain LD size and number. We have recently shown that the Ser251Pro SNP in PLIN2 influences macroautophagy, cholesterol efflux, cholesterol accumulation and is associated with subclinical atherosclerosis development in humans. Since a direct crosstalk between macroautophagy and CMA has been proposed, we aim to investigate whether the Ser251Pro SNP affects CMA and the degradation of PLIN2, thereby influencing lipophagy.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
