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Erratum: DGAT2 partially compensates for lipid-induced ER stress in human DGAT1-deficient intestinal stem cells

Open AccessPublished:October 06, 2021DOI:https://doi.org/10.1016/j.jlr.2021.100126
      VOL 60 (2019) PAGES 1787–1800
      The authors regret that Supplemental Table S1 was missing from their published article and several citations to Supplemental Material were incorrect. Supplemental Table S1 is provided with this corrigendum. Below we provide the corrected Supplemental Material citations.
      On page 1789, the citation in “… pLenti-CMV-GFP-Hygro plasmid (21) (supplemental Fig. S5)” should be to supplemental Fig. S3.
      On page 1794, in the Fig. 4 legend, the citation in “Complete dataset in supplemental Fig. S2” should be to supplemental Fig. S1.
      On page 1795, the citation in “… or presence (Fig. 5B, supplemental Fig. S3B)” should be to supplemental Fig. S2B.
      On page 1796, in the Fig. 5 legend, the citation in “Complete data set is in supplemental Fig. S3” should be to supplemental Fig. S2.
      On page 1798, in the Fig. 7 legend, the citation in “PI to measure cell death (supplemental Fig. S3)” should be to supplemental Fig. S4.
      On page 1789, the citation in “Primers are listed in supplemental Table S3” should be to supplemental Table S1.
      The authors would like to apologize for any inconvenience caused.

      Supplemental data

      This article contains supplemental data.

      Supplemental data

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      • DGAT2 partially compensates for lipid-induced ER stress in human DGAT1-deficient intestinal stem cells
        Journal of Lipid ResearchVol. 60Issue 10
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          Dietary lipids are taken up as FAs by the intestinal epithelium and converted by diacylglycerol acyltransferase (DGAT) enzymes into triglycerides, which are packaged in chylomicrons or stored in cytoplasmic lipid droplets (LDs). DGAT1-deficient patients suffer from vomiting, diarrhea, and protein losing enteropathy, illustrating the importance of this process to intestinal homeostasis. Previously, we have shown that DGAT1 deficiency causes decreased LD formation and resistance to unsaturated FA lipotoxicity in patient-derived intestinal organoids.
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