ArticleJournal of lipid research2015
Sin3A-associated protein, 18 kDa, a novel binding partner of TRIB1, regulates MTTP expression.
Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Article
- Review
- Targeting cis-regulatory elements of FOXO family is a novel therapeutic strategy for induction of leukemia cell differentiation.Cell death & disease · 2023Article
- [Quantitative analysis of lipid metabolism-related differential proteins in patients with alcoholic liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023Article
- The genetic interactions between non-alcoholic fatty liver disease and cardiovascular diseases.Frontiers in genetics · 2022Review
- TRIB1 regulates LDL metabolism through CEBPα-mediated effects on the LDL receptor in hepatocytes.The Journal of clinical investigation · 2021Article
- Review
- Current Progress in Delineating the Roles of Pseudokinase TRIB1 in Controlling Human Diseases.Journal of Cancer · 2021Review
- A C21-steroidal derivative suppresses T-cell lymphoma in mice by inhibiting SIRT3 via SAP18-SIN3.Communications biology · 2020Article
- Suppression of the SAP18/HDAC1 complex by targeting TRIM56 and Nanog is essential for oncogenic viral FLICE-inhibitory protein-induced acetylation of p65/RelA, NF-κB activation, and promotion of cell invasion and angiogenesis.Cell death and differentiation · 2019Article
- TRIB1 rs17321515 gene polymorphism increases the risk of coronary heart disease in general population and non-alcoholic fatty liver disease patients in Chinese Han population.Lipids in health and disease · 2019Article
- CXCR2 expression on granulocyte and macrophage progenitors under tumor conditions contributes to mo-MDSC generation via SAP18/ERK/STAT3.Cell death & disease · 2019Article
- Trouble With Tribbles-1.Arteriosclerosis, thrombosis, and vascular biology · 2019Review
- TRIB1 is a positive regulator of hepatocyte nuclear factor 4-alpha.Scientific reports · 2017Article
- Differential variation patterns between hubs and bottlenecks in human protein-protein interaction networks.BMC evolutionary biology · 2016Article
- From Loci to Biology: Functional Genomics of Genome-Wide Association for Coronary Disease.Circulation research · 2016Review
- Experimental Biology for the Identification of Causal Pathways in Atherosclerosis.Cardiovascular drugs and therapy · 2016Review
- Insights from Genome-Wide Association Analyses of Nonalcoholic Fatty Liver Disease.Seminars in liver disease · 2015Review
- Tribbles-1: a novel regulator of hepatic lipid metabolism in humans.Biochemical Society transactions · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian tribbles homolog 1 (TRIB1) is a human locus that has been shown to significantly impact plasma lipid levels across several ethnic groups. In addition, the gene has been associated with the occurrence of nonalcoholic fatty liver disease. In the present study, a yeast-two-hybrid system was used to screen for novel molecular targets of TRIB1 binding. Loci corresponding to clones that were positive for TRIB1 binding subsequently were assessed for roles in lipid metabolism in mice using adenoviral constructs to induce knockdown or overexpression. Sin3A-associated protein, 18 kDa (SAP18) was identified as a novel binding partner of TRIB1. Knockdown of the Sap18 in mouse liver decreased plasma lipid levels and increased hepatic lipid levels; SAP18 overexpression showed the opposite effects. Transcriptome analysis of the mouse liver revealed that Sap18 knockdown decreased and SAP18 overexpression increased microsomal TG transfer protein (MTTP) expression levels. Chromatin immunoprecipitation analysis showed that halo-tagged SAP18, halo-tagged TRIB1, and anti-mSin3A antibody enriched precipitates for regulatory sequences of the MTTP gene. Enforced expression of SAP18 enhanced and SAP18 knockdown conversely attenuated the enrichment of MTTP regulatory sequences seen with anti-mSin3A antibody. These studies indicated that SAP18 expression enhanced the recruitment of mSin3A in coordination with TRIB1 to MTTP regulatory elements and increased MTTP expression.
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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.