NDLI: Lipase maturation factor 1 (lmf1) is induced by endoplasmic reticulum stress through activating transcription factor 6 (Atf6 ) signaling.

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Lipase maturation factor 1 (lmf1) is induced by endoplasmic reticulum stress through activating transcription factor 6 (Atf6 ) signaling.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dezwaan-mccabe, Diane Kaufman, Randal J. Mao, Hui Z. Ehrhardt, Nicole Bedoya, Candy Mungrue, Imran N. Rutkowski, D. Thomas Péterfy, Miklós Gomez, Javier A.
Description	Author Affiliation: Mao HZ ( From the Medical Genetics Research Institute and.); Ehrhardt N ( From the Medical Genetics Research Institute and.); Bedoya C ( Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California 90048.); Gomez JA ( Department of Anatomy and Cell Biology and Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.); DeZwaan-McCabe D ( Department of Anatomy and Cell Biology and Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.); Mungrue IN ( the Department of Pharmacology and Experimental Therapeutics, Louisiana State University School of Medicine, New Orleans, Louisiana 70112.); Kaufman RJ ( Degenerative Disease Research, Sanford-Burnham Medical Research Institute, La Jolla, California 92037, and.); Rutkowski DT ( Department of Anatomy and Cell Biology and Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.); Péterfy M ( From the Medical Genetics Research Institute and Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California 90048, the Department of Medicine, David Geffen School of Medicine at the University of California, Los Angeles, California 90095 mpeterfy@ucla.edu.)
Abstract	Lipase maturation factor 1 (Lmf1) is a critical determinant of plasma lipid metabolism, as demonstrated by severe hypertriglyceridemia associated with its mutations in mice and human subjects. Lmf1 is a chaperone localized to the endoplasmic reticulum (ER) and required for the post-translational maturation and activation of several vascular lipases. Despite its importance in plasma lipid homeostasis, the regulation of Lmf1 remains unexplored. We report here that Lmf1 expression is induced by ER stress in various cell lines and in tunicamycin (TM)-injected mice. Using genetic deficiencies in mouse embryonic fibroblasts and mouse liver, we identified the Atf6 arm of the unfolded protein response as being responsible for the up-regulation of Lmf1 in ER stress. Experiments with luciferase reporter constructs indicated that ER stress activates the Lmf1 promoter through a GC-rich DNA sequence 264 bp upstream of the transcriptional start site. We demonstrated that Atf6 is sufficient to induce the Lmf1 promoter in the absence of ER stress, and this effect is mediated by the TM-responsive cis-regulatory element. Conversely, Atf6 deficiency induced by genetic ablation or a dominant-negative form of Atf6 abolished TM stimulation of the Lmf1 promoter. In conclusion, our results indicate that Lmf1 is an unfolded protein response target gene, and Atf6 signaling is sufficient and necessary for activation of the Lmf1 promoter. Importantly, the induction of Lmf1 by ER stress appears to be a general phenomenon not restricted to lipase-expressing cells, which suggests a lipase-independent cellular role for this protein in ER homeostasis.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	35
Volume Number	289
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2014-08-29
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Activating Transcription Factor 6 Metabolism Endoplasmic Reticulum Membrane Proteins Physiology Oxidative Stress Signal Transduction Animals Genetics Mice Mice, Inbred C57BL Promoter Regions, Genetic Real-Time Polymerase Chain Reaction Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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