Is the Golgi apparatus the obligatory final step for lipoprotein secretion by intestinal cells?
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The GTPase ARFRP1 affects lipid droplet protein composition and triglyceride release from intracellular storage of intestinal Caco-2 cells
2018, Biochemical and Biophysical Research CommunicationsCitation Excerpt :CM production begins in the ER lumen of intestinal enterocytes, where one molecule of apolipoprotein B48 (ApoB48) binds TGs. Further TG incorporation is mediated by microsomal triglyceride transfer protein (MTP) [1,2], and more surface proteins such as apolipoprotein A4 (ApoA4) attach and CMs exit the ER in pre-chylomicron transport vesicles (PCTV) towards the Golgi [3,4], where further surface proteins like apolipoprotein A1 (ApoA1) are acquired [5,6], before CMs are released at the basolateral side of enterocytes into the lymph. Although lipid absorption and CM production are highly efficient processes, a fraction of dietary TGs is transiently stored in cytosolic lipid droplets (LDs) [7].
Further studies on the mechanism of inhibition of intestinal chylomicron transport by Pluronic L-81
1989, Biochimica et Biophysica Acta (BBA)/Lipids and Lipid MetabolismThe surface extracellular coat of the midgut in Triatoma infestans I. Mechanism of development
1986, Journal of Ultrastructure Research and Molecular Structure Research
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