ACSVL4 Antibody (B-5): sc-101271
- ACSVL4 Antibody (B-5) is a mouse monoclonal IgG1 κ, cited in 3 publications, provided at 100 µg/ml
- raised against recombinant ACSVL4 of human origin
- recommended for detection of ACSVL4 of human origin by WB, IP and ELISA
- At present, we have not yet completed the identification of the preferred secondary detection reagent(s) for ACSVL4 Antibody (B-5). This work is in progress.
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ACSVL4 Antibody (B-5) is a mouse monoclonal IgG1 antibody that detects acyl-coenzyme A synthetase very long-chain 4 (ACSVL4) in human samples through applications such as western blotting (WB), immunoprecipitation (IP), and enzyme-linked immunosorbent assay (ELISA). ACSVL4 is a member of the acyl-coenzyme A synthetase family, specifically classified as a solute carrier family 27A (SLC27A) gene product, and plays a crucial role in fatty acid metabolism by facilitating the transport of very long-chain fatty acids across the plasma membrane. This transport is vital for cellular energy production and lipid biosynthesis, as very long-chain fatty acids are essential components of various biological membranes and signaling molecules. ACSVL4 is predominantly expressed in tissues with high fatty acid metabolism, such as the liver, heart, and adipose tissue, where ACSVL4 contributes to the regulation of lipid homeostasis. The unique expression pattern of ACSVL4, along with ACSVL4′s ability to activate and transport fatty acids, underscores its importance in metabolic processes and potential implications in metabolic disorders. Anti-ACSVL4 antibody (B-5) is an invaluable tool for researchers studying fatty acid metabolism and its associated pathways, providing insights into the physiological and pathological roles of this critical protein.
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ACSVL4 Antibody (B-5) References:
- Overexpressed FATP1, ACSVL4/FATP4 and ACSL1 increase the cellular fatty acid uptake of 3T3-L1 adipocytes but are localized on intracellular membranes. | Zhan, T., et al. 2012. PLoS One. 7: e45087. PMID: 23024797
- Interactions between FATP4 and ichthyin in epidermal lipid processing may provide clues to the pathogenesis of autosomal recessive congenital ichthyosis. | Li, H., et al. 2013. J Dermatol Sci. 69: 195-201. PMID: 23290633
- A Novel SLC27A4 Splice Acceptor Site Mutation in Great Danes with Ichthyosis. | Metzger, J., et al. 2015. PLoS One. 10: e0141514. PMID: 26506231
- Investigation of the fatty acid transporter-encoding genes SLC27A3 and SLC27A4 in autism. | Maekawa, M., et al. 2015. Sci Rep. 5: 16239. PMID: 26548558
- SLC27A4 regulate ATG4B activity and control reactions to chemotherapeutics-induced autophagy in human lung cancer cells. | Wu, S., et al. 2016. Tumour Biol. 37: 6943-52. PMID: 26662804
- Solute Carrier Family 27 Member 4 (SLC27A4) Enhances Cell Growth, Migration, and Invasion in Breast Cancer Cells. | Yen, MC., et al. 2018. Int J Mol Sci. 19: PMID: 30388870
- Skin permeability barrier formation by the ichthyosis-causative gene FATP4 through formation of the barrier lipid ω-O-acylceramide. | Yamamoto, H., et al. 2020. Proc Natl Acad Sci U S A. 117: 2914-2922. PMID: 31974308
- SLC27A4-mediated selective uptake of mono-unsaturated fatty acids promotes ferroptosis defense in hepatocellular carcinoma. | Li, Z., et al. 2023. Free Radic Biol Med. 201: 41-54. PMID: 36924851
- PLIN5 interacts with FATP4 at membrane contact sites to promote lipid droplet-to-mitochondria fatty acid transport. | Miner, GE., et al. 2023. Dev Cell. 58: 1250-1265.e6. PMID: 37290445
- Hepatocyte-specific SLC27A4 deletion ameliorates nonalcoholic fatty liver disease in mice via suppression of phosphatidylcholine-mediated PXR activation. | Shen, C., et al. 2025. Metabolism. 162: 156054. PMID: 39489412
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ACSVL4 Antibody (B-5) | sc-101271 | 100 µg/ml | $333.00 |