FACL4 Antibody (Rabbit mAb) [C8B1]

Catalog No.: F7018

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Biological Description

Specificity FACL4 Antibody (Rabbit mAb) [C8B1] detects endogenous levels of total FACL4 protein.
Background FACL4, now designated ACSL4, belongs to the long-chain acyl-CoA synthetase family and catalyzes the esterification of polyunsaturated fatty acids, most notably arachidonic acid and adrenic acid, into their corresponding coenzyme A thioesters, generating the fatty acyl-CoA species AA-CoA and AdA-CoA that serve as the direct substrates for downstream membrane phospholipid remodeling. Once activated by ACSL4, these polyunsaturated fatty acyl-CoAs are incorporated into phosphatidylethanolamine by lysophosphatidylcholine acyltransferase 3, generating polyunsaturated phosphatidylethanolamine species that are the primary substrates for lipid peroxidation within cellular membranes, positioning ACSL4 as the initiating enzyme in a defined biosynthetic sequence that determines a cell's membrane lipid peroxidation potential rather than acting as a generic fatty acid-activating enzyme. This ACSL4-generated pool of polyunsaturated phospholipids is subsequently oxidized by lipoxygenases or through iron-catalyzed non-enzymatic Fenton chemistry, producing lipid hydroperoxides that destabilize membrane bilayer structure and drive ferroptosis, an iron-dependent form of regulated cell death, making ACSL4 expression level and enzymatic activity a determinant of a cell's intrinsic susceptibility to this death pathway. ACSL4 activity is itself subject to direct post-translational regulation: protein kinase C beta II phosphorylates ACSL4 at threonine 328 in response to sensing an initial, moderate accumulation of lipid peroxides, and this phosphorylation event activates ACSL4, increasing PUFA-CoA production and amplifying lipid peroxide accumulation to lethal levels, forming a positive feedback loop that converts an early peroxidation signal into a full ferroptotic response; interferon-gamma secreted by CD8-positive T cells further stimulates ACSL4 expression and PUFA-CoA biosynthesis, coupling this lipid peroxidation pathway to anti-tumor immune signaling. ACSL4 also functions as a broader regulator of fatty acid metabolism, remodeling the phospholipid composition of cellular membranes, participating in steroidogenesis, and balancing eicosanoid biosynthesis, giving the enzyme a role in membrane lipid homeostasis distinct from its lipid peroxidation-initiating function. ACSL4 is highly expressed across multiple human tumor types, and because its enzymatic output directly determines the polyunsaturated phospholipid substrate pool available for peroxidation, ACSL4 has emerged as a candidate node for therapeutically inducing tumoral ferroptosis, particularly in combination strategies pairing immune checkpoint inhibition with polyunsaturated fatty acid supplementation or direct pharmacological activation of the PKCβII-ACSL4 axis.

Usage Information

Application WB, IP, IHC, IF, FCM Dilution
WB IP IHC IF FCM
1:1000 1:40 1:500 1:50 1:120
Reactivity Mouse, Human
Source Rabbit Monoclonal Antibody MW 79 kDa
Storage Buffer PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
Storage
(from the date of receipt)		 -20°C (avoid freeze-thaw cycles), 2 years

References

  • https://pubmed.ncbi.nlm.nih.gov/40932861/
  • https://pubmed.ncbi.nlm.nih.gov/35674490/

Application Data