R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
ACSL4 (F6T3Z) Rabbit mAb #38493
Filter:
- WB
- IP
- IF
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 80 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
| Immunofluorescence (Immunocytochemistry) | 1:200 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
ACSL4 (F6T3Z) Rabbit mAb recognizes endogenous levels of total ACSL4 protein. Species reactivity for immunofluorescence is human only.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human ACSL4 protein.
Background
The long-chain fatty acyl-CoA synthetase (ACSL) family of enzymes convert free long-chain fatty acids into their active form, acyl-coenzyme A (acyl-CoA), and play dominant roles in both anabolic (fatty acid synthesis and lipogenesis) and catabolic (lipolysis and fatty acid β-oxidation) pathways (1). Acyl-CoA synthetase long-chain family member 4 (ACSL4) preferentially catalyzes the formation of arachidonoyl-coenzyme A (AA-CoA) by inserting coenzyme A (CoA) into arachidonic acid (AA) (1). ACSL4-catalyzed acyl-CoAs also participate in the regulation of steroidogenesis (2), eicosanoid biosynthesis (3), and phospholipid remodeling (4). ACSL4 is an essential enzyme for the conversion of two key ferroptosis-inducing signals, oxidized arachidonic and adrenic phosphatidylethanolamines (5,6). Genome-wide CRISPR/Cas9-based genetic screens have demonstrated that ACSL4 is an essential component for ferroptosis execution (6), and genetic or pharmacological inhibition of ACSL4 can initiate a specific anti-ferroptotic rescue pathway (5). ACSL4 expression is upregulated in ferroptosis-sensitive cancer cells compared with ferroptosis-resistant cells (7) and has been shown to predict sensitivity to ferroptosis in a panel of basal-like breast cancer cell lines (6). Moreover, high ACSL4 protein expression in hepatocellular carcinoma (HCC) clinical tissue specimens is associated with improved patient outcomes after sorafenib treatment and could serve as a predictive biomarker (8).
- Quan, J. et al. (2021) Eur J Pharmacol 909, 174397.
- Cornejo Maciel, F. et al. (2005) J Mol Endocrinol 34, 655-66.
- Kuwata, H. et al. (2014) Biochim Biophys Acta 1841, 44-53.
- Killion, E.A. et al. (2018) Mol Metab 9, 43-56.
- Kagan, V.E. et al. (2017) Nat Chem Biol 13, 81-90.
- Doll, S. et al. (2017) Nat Chem Biol 13, 91-98.
- Yuan, H. et al. (2016) Biochem Biophys Res Commun 478, 1338-43.
- Feng, J. et al. (2021) Acta Pharmacol Sin 42, 160-170.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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