ArticleThe Journal of biological chemistry2010
A role for Sp1 in transcriptional regulation of phosphatidylethanolamine N-methyltransferase in liver and 3T3-L1 adipocytes.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Emerging complexities of phospholipid metabolism in adipose tissue.Molecules and cells · 2026Review
- Disruption of Hepatic Insulin Signaling Causes Phospholipid Dysregulation in Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Pathogenesis and intervention strategies for metabolic dysfunction-associated fatty liver disease from the perspective of the gut-microbiota-liver axis.Frontiers in immunology · 2026Review
- Genetic variation shapes the chromatin accessibility landscape and transcriptional responses in mouse adipose tissue.PLoS genetics · 2026Article
- The Role of Phosphatidylethanolamine N-Methyltransferase (International journal of molecular sciences · 2023Article
- Phosphatidylethanolamine N-methyltransferase: from Functions to Diseases.Aging and disease · 2023Review
- An organelle-specific photoactivation and dual-isotope labeling strategy reveals phosphatidylethanolamine metabolic flux.Chemical science · 2023Article
- Distinct infrastructure of lipid networks in visceral and subcutaneous adipose tissues in overweight humans.The American journal of clinical nutrition · 2020Article
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- Sequential synthesis and methylation of phosphatidylethanolamine promote lipid droplet biosynthesis and stability in tissue culture and in vivo.The Journal of biological chemistry · 2011Article
- N-Myc and SP regulate phosphatidylserine synthase-1 expression in brain and glial cells.The Journal of biological chemistry · 2011Article
- Homocysteine as a risk factor for atherosclerosis: is its conversion to s-adenosyl-L-homocysteine the key to deregulated lipid metabolism?Journal of lipids · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Phosphatidylcholine is made in all nucleated mammalian cells via the CDP-choline pathway. Another major pathway for phosphatidylcholine biosynthesis in liver is catalyzed by phosphatidylethanolamine N-methyltransferase (PEMT). We have now identified 3T3-L1 adipocytes as a cell culture model that expresses PEMT endogenously. We have found that PEMT mRNA and protein levels increased dramatically in 3T3-L1 cells upon differentiation to adipocytes. 5'-Deletion analysis of the PEMT promoter-luciferase constructs stably expressed in 3T3-L1 adipocytes identified a regulatory region between -471 and -371 bp (relative to the transcriptional start site). Competitive and supershift assays demonstrated binding sites for transcription factors Sp1, Sp3 (-408 to -413), and YY1 (-417 to -420). During differentiation of 3T3-L1 cells to adipocytes, the amount of Sp1 protein decreased by approximately 50% just prior to activation of PEMT. Transduction of 3T3-L1 adipocytes with retrovirus containing Sp1 cDNA demonstrated that Sp1 inhibited PEMT transcriptional activity. Similarly, short hairpin RNA directed against Sp1 in 3T3-L1 adipocytes enhanced PEMT transcriptional activation. Chromatin immunoprecipitation assays confirmed that Sp1 binds to the PEMT promoter, and this interaction decreases upon differentiation to adipocytes. These experiments directly link increased PEMT expression in adipocytes to decreased transcriptional expression of Sp1. In addition, our data established that Sp1 binding was required for tamoxifen-mediated inhibition of Pemt promoter activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.