ArticleMolecular and cellular biochemistry2011
Acyl-CoA binding proteins interact with the acyl-CoA binding domain of mitochondrial carnitine palmitoyl transferase I.
Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
- In vivo CRISPR activation screen identifies acyl-CoA-binding protein as a driver of bone metastasis.Science translational medicine · 2025Article
- CYP2C9, CYP3A and CYP2C19 metabolize Δ9-tetrahydrocannabinol to multiple metabolites but metabolism is affected by human liver fatty acid binding protein (FABP1).Biochemical pharmacology · 2024Article
- Drugs Form Ternary Complexes with Human Liver Fatty Acid Binding Protein 1 (FABP1) and FABP1 Binding Alters Drug Metabolism.Molecular pharmacology · 2024Article
- Article
- Drugs Form Ternary Complexes with Human Liver Fatty Acid Binding Protein (FABP1) and FABP1 Binding Alters Drug Metabolism.bioRxiv : the preprint server for biology · 2024Article
- Impact of Intracellular Lipid Binding Proteins on Endogenous and Xenobiotic Ligand Metabolism and Disposition.Drug metabolism and disposition: the biological fate of chemicals · 2023Review
- Targeting fatty acid oxidation via Acyl-CoA binding protein hinders glioblastoma invasion.Cell death & disease · 2023Article
- Article
- From benzodiazepines to fatty acids and beyond: revisiting the role of ACBP/DBI.Trends in endocrinology and metabolism: TEM · 2021Review
- Proteomic analysis of mitochondrial biogenesis in cardiomyocytes differentiated from human induced pluripotent stem cells.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Review
- The diversity of ACBD proteins - From lipid binding to protein modulators and organelle tethers.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Ablating both Fabp1 and Scp2/Scpx (TKO) induces hepatic phospholipid and cholesterol accumulation in high fat-fed mice.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Article
- Loss of fatty acid binding protein-1 alters the hepatic endocannabinoid system response to a high-fat diet.Journal of lipid research · 2017Article
- 4-1BB signaling activates glucose and fatty acid metabolism to enhance CD8Cellular & molecular immunology · 2017Article
- Impact ofJournal of lipid research · 2017Article
- Impact of dietary phytol on lipid metabolism in SCP2/SCPX/L-FABP null mice.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017Article
- Review
- Loss of L-FABP, SCP-2/SCP-x, or both induces hepatic lipid accumulation in female mice.Archives of biochemistry and biophysics · 2015Article
- The PDZ3 domain of the cellular scaffolding protein MAGI-1 interacts with the Coxsackievirus and adenovirus receptor (CAR).The international journal of biochemistry & cell biology · 2015Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Although the rate limiting step in mitochondrial fatty acid oxidation, catalyzed by carnitine palmitoyl transferase I (CPTI), utilizes long-chain fatty acyl-CoAs (LCFA-CoA) as a substrate, how LCFA-CoA is transferred to CPTI remains elusive. Based on secondary structural predictions and conserved tryptophan residues, the cytoplasmic C-terminal domain was hypothesized to be the LCFA-CoA binding site and important for interaction with cytoplasmic LCFA-CoA binding/transport proteins to provide a potential route for LCFA-CoA transfer. To begin to address this question, the cytoplasmic C-terminal region of liver CPTI (L-CPTI) was recombinantly expressed and purified. Data herein showed for the first time that the L-CPTI C-terminal 89 residues were sufficient for high affinity binding of LCFA-CoA (K (d) = 2-10 nM) and direct interaction with several cytoplasmic LCFA-CoA binding proteins (K (d) < 10 nM), leading to enhanced CPTI activity. Furthermore, alanine substitutions for tryptophan in L-CPTI (W391A and W452A) altered secondary structure, decreased binding affinity for LCFA-CoA, and almost completely abolished L-CPTI activity, suggesting that these amino acids may be important for ligand stabilization necessary for L-CPTI activity. Moreover, while decreased activity of the W452A mutant could be explained by decreased binding of lipid binding proteins, W391 itself seems to be important for activity. These data suggest that both interactions with lipid binding proteins and the peptide itself are important for optimal enzyme activity.
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