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ACSL3 distribution closely overlapped with proteins involved in trafficking from the trans-Golgi network and endosomes. In contrast, the ACSL4 localisation pattern more closely followed that of calnexin which is an endoplasmic reticulum resident chaperone.
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Subcellular fractionation showed that at least 68% of ACSL3 remain at the ER even during extensive fatty acid supplementation. High resolution single molecule microscopy confirmed the abundance of cytoplasmic ACSL3 outside of LDs.
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ACSL3 is essential for mutant KRAS lung cancer tumorigenesis in vivo and is highly expressed in human lung cancer
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Study shows that ACSL3 contributes to intratumoral steroidogenesis by modulating the steroidogenic genes and plays an important role in the growth of castration-resistant prostate cancer.
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ACLS4 and ACLS3 have roles in insulin secretion
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The prominent expression of ACSL3 in VSMC.
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activation of fatty acid import is linked to the up-regulation of cellular long chain acyl-CoA synthetase activity and identify the long chain acyl-CoA syntheatse3 (Acsl3) as a novel host factor required for polio replication.
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role of N-terminal region of acyl-CoA synthetase 3 in its function and localization on lipid droplets
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expression of ACSL3 was induced by endoplasmic reticulum stress
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Results suggest that initiation of Golgi export of Lyn involves association of ACSL3 with the Lyn C-lobe, which is exposed to the molecular surface in an open conformation.
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Results suggest that liver X receptors play a regulatory role in fatty acid metabolism by direct regulation of ACSL3 in human placental trophoblast cells.
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ACSL3 is a novel molecular target of PPARdelta in HepG2 cells; there is a regulatory mechanism for ACSL3 transcription in liver tissue
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Sequence analysis of genomic clones demonstrates that the human ACS3 gene spans at least 80.6 kb and contains 17 exons.
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Repression of FAS mRNA expression is the consequence of feedback inhibition of FAS expression by long chain fatty acyl-CoAs, which are formed by FACL3 during its upregulation by vitamin D3in prostate cancer cells.
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Oncostatin M directly lowers the plasma triglycerides in hyperlipidemia by stimulating the transcription of ACSL3/5 in the liver.
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Data suggest that endogenous FATP4 does not function to translocate fatty acids across the plasma membrane, but functions more as a very long-chain acyl-CoA synthetase.
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Small interfering RNA targeting ACSL3 inhibits secretion of hepatitis c virus from human hepatoma-derived cells
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Data suggest that methylated ACSL3 5'CpG islands in umbilical cord white blood cell DNA may be a surrogate endpoint for transplacental polycyclic aromatic hydrocarbon exposure and/or a potential biomarker for environmentally-related asthma.
