ArticleJournal of lipid research2011
Tyrosine phosphatase SHP2 regulates the expression of acyl-CoA synthetase ACSL4.
Article in Journal of lipid research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 50 citations in OpenAlex.
- The SREBF2-ACOT7 axis promotes tumor progression and predicts prognosis in diffuse large b-cell lymphoma.Scientific reports · 2025Article
- Targeting Acyl-CoA synthetase long-chain family member 4: a potential approach for the treatment of cerebral ischemia/reperfusion injury.Metabolic brain disease · 2025Review
- ACSL4-Mediated Ferroptosis and Its Potential Role in Central Nervous System Diseases and Injuries.International journal of molecular sciences · 2023Review
- Review
- Mitochondrial Dynamics as Potential Modulators of Hormonal Therapy Effectiveness in Males.Biology · 2023Review
- New insights into signal transduction pathways in adrenal steroidogenesis: role of mitochondrial fusion, lipid mediators, and MAPK phosphatases.Frontiers in endocrinology · 2023Review
- Lipidomic and Membrane Mechanical Signatures in Triple-Negative Breast Cancer: Scope for Membrane-Based Theranostics.Molecular and cellular biochemistry · 2022Review
- New inhibitor targeting Acyl-CoA synthetase 4 reduces breast and prostate tumor growth, therapeutic resistance and steroidogenesis.Cellular and molecular life sciences : CMLS · 2021Article
- Evaluation of long-chain acyl-coenzyme A synthetase 4 (ACSL4) expression in human breast cancer.Research in pharmaceutical sciences · 2020Article
- Small Molecule Amyloid-β Protein Precursor Processing Modulators Lower Amyloid-β Peptide Levels via cKit Signaling.Journal of Alzheimer's disease : JAD · 2019Article
- Baicalin inhibits PDGF-BB-induced hepatic stellate cell proliferation, apoptosis, invasion, migration and activation via the miR-3595/ACSL4 axis.International journal of molecular medicine · 2018Article
- Human MicroRNA-548p Decreases Hepatic Apolipoprotein B Secretion and Lipid Synthesis.Arteriosclerosis, thrombosis, and vascular biology · 2017Article
- Fatty acid metabolism in breast cancer subtypes.Oncotarget · 2017Review
- Role of Protein Phosphorylation and Tyrosine Phosphatases in the Adrenal Regulation of Steroid Synthesis and Mitochondrial Function.Frontiers in endocrinology · 2016Review
- Article
- Long-chain acyl-CoA synthetase in fatty acid metabolism involved in liver and other diseases: an update.World journal of gastroenterology · 2015Review
- Polymorphisms of PTPN11 gene could influence serum lipid levels in a sex-specific pattern.Lipids in health and disease · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acyl-CoA synthetase 4 (ACSL4) is implicated in fatty acid metabolism with marked preference for arachidonic acid (AA). ACSL4 plays crucial roles in physiological functions such as steroid synthesis and in pathological processes such as tumorigenesis. However, factors regulating ACSL4 mRNA and/or protein levels are not fully described. Because ACSL4 protein expression requires tyrosine phosphatase activity, in this study we aimed to identify the tyrosine phosphatase involved in ACSL4 expression. NSC87877, a specific inhibitor of the tyrosine phosphatase SHP2, reduced ACSL4 protein levels in ACSL4-rich breast cancer cells and steroidogenic cells. Indeed, overexpression of an active form of SHP2 increased ACSL4 protein levels in MA-10 Leydig steroidogenic cells. SHP2 has to be activated through a cAMP-dependent pathway to exert its effect on ACSL4. The effects could be specifically attributed to SHP2 because knockdown of the phosphatase reduced ACSL4 mRNA and protein levels. Through the action on ACSL4 protein levels, SHP2 affected AA-CoA production and metabolism and, finally, the steroidogenic capacity of MA-10 cells: overexpression (or knockdown) of SHP2 led to increased (or decreased) steroid production. We describe for the first time the involvement of SHP2 activity in the regulation of the expression of the fatty acid-metabolizing enzyme ACSL4.
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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.