Product: ACSL4/FACL4 Antibody
Catalog: DF12141
Description: Rabbit polyclonal antibody to ACSL4/FACL4
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 79 kDa,74 kDa; 79kD(Calculated).
Uniprot: O60488
RRID: AB_2844946

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(83%)
Clonality:
Polyclonal
Specificity:
ACSL4/FACL4 Antibody detects endogenous levels of total ACSL4/FACL4.
RRID:
AB_2844946
Cite Format: Affinity Biosciences Cat# DF12141, RRID:AB_2844946.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

ACS 4; ACS4; ACSL 4; Acsl4; ACSL4_HUMAN; acyl CoA synthetase 4; Acyl CoA synthetase long chain family member 4; FACL 4; FACL4; Fatty acid Coenzyme A ligase; fatty acid Coenzyme A ligase long-chain 4; LACS 4; LACS4; Lignoceroyl CoA synthase; Long chain 4; long chain acyl CoA synthetase 4; long chain fatty acid CoA ligase 4; long chain fatty acid Coenzyme A ligase 4; Long-chain acyl-CoA synthetase 4; Long-chain-fatty-acid--CoA ligase 4; MRX63; MRX68;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Sequence:
MKLKLNVLTIILLPVHLLITIYSALIFIPWYFLTNAKKKNAMAKRIKAKPTSDKPGSPYRSVTHFDSLAVIDIPGADTLDKLFDHAVSKFGKKDSLGTREILSEENEMQPNGKVFKKLILGNYKWMNYLEVNRRVNNFGSGLTALGLKPKNTIAIFCETRAEWMIAAQTCFKYNFPLVTLYATLGKEAVVHGLNESEASYLITSVELLESKLKTALLDISCVKHIIYVDNKAINKAEYPEGFEIHSMQSVEELGSNPENLGIPPSRPTPSDMAIVMYTSGSTGRPKGVMMHHSNLIAGMTGQCERIPGLGPKDTYIGYLPLAHVLELTAEISCFTYGCRIGYSSPLTLSDQSSKIKKGSKGDCTVLKPTLMAAVPEIMDRIYKNVMSKVQEMNYIQKTLFKIGYDYKLEQIKKGYDAPLCNLLLFKKVKALLGGNVRMMLSGGAPLSPQTHRFMNVCFCCPIGQGYGLTESCGAGTVTEVTDYTTGRVGAPLICCEIKLKDWQEGGYTINDKPNPRGEIVIGGQNISMGYFKNEEKTAEDYSVDENGQRWFCTGDIGEFHPDGCLQIIDRKKDLVKLQAGEYVSLGKVEAALKNCPLIDNICAFAKSDQSYVISFVVPNQKRLTLLAQQKGVEGTWVDICNNPAMEAEILKEIREAANAMKLERFEIPIKVRLSPEPWTPETGLVTDAFKLKRKELRNHYLKDIERMYGGK

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Chicken
100
Rabbit
100
Xenopus
83
Zebrafish
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - O60488 As Substrate

Site PTM Type Enzyme
S23 Phosphorylation
Y31 Phosphorylation
T34 Phosphorylation
K47 Ubiquitination
K49 Ubiquitination
K54 Ubiquitination
S57 Phosphorylation
T63 Phosphorylation
K89 Acetylation
K89 Ubiquitination
K92 Acetylation
S95 Phosphorylation
K113 Ubiquitination
K117 Ubiquitination
S140 Phosphorylation
T143 Phosphorylation
K148 Ubiquitination
K150 Ubiquitination
K211 Ubiquitination
C221 S-Nitrosylation
K223 Ubiquitination
Y227 Phosphorylation
K231 Ubiquitination
K312 Ubiquitination
S352 Phosphorylation
S353 Phosphorylation
K354 Ubiquitination
K356 Ubiquitination
K360 Ubiquitination
K367 Ubiquitination
K383 Ubiquitination
K388 Ubiquitination
K397 Acetylation
K397 Ubiquitination
K401 Acetylation
K401 Ubiquitination
Y404 Phosphorylation
K407 Ubiquitination
K413 Ubiquitination
Y415 Phosphorylation
K426 Ubiquitination
S447 Phosphorylation
Y483 Phosphorylation
T485 Phosphorylation
K498 Ubiquitination
K500 Ubiquitination
T508 Phosphorylation
K512 Ubiquitination
K536 Ubiquitination
Y541 Phosphorylation
Y582 Phosphorylation
S584 Phosphorylation
K587 Ubiquitination
K593 Ubiquitination
S607 Phosphorylation
K621 Ubiquitination
K651 Ubiquitination
K661 Ubiquitination
K670 Ubiquitination
S674 Phosphorylation
T679 Phosphorylation
T682 Phosphorylation
T686 Phosphorylation
K690 Acetylation
K690 Ubiquitination
K702 Ubiquitination

Research Backgrounds

Function:

Catalyzes the conversion of long-chain fatty acids to their active form acyl-CoA for both synthesis of cellular lipids, and degradation via beta-oxidation. Preferentially activates arachidonate and eicosapentaenoate as substrates. Preferentially activates 8,9-EET > 14,15-EET > 5,6-EET > 11,12-EET. Modulates glucose-stimulated insulin secretion by regulating the levels of unesterified EETs (By similarity). Modulates prostaglandin E2 secretion.

Subcellular Location:

Mitochondrion outer membrane>Single-pass type III membrane protein. Peroxisome membrane>Single-pass type III membrane protein. Microsome membrane>Single-pass type III membrane protein. Endoplasmic reticulum membrane>Single-pass type III membrane protein. Cell membrane.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Family&Domains:

Belongs to the ATP-dependent AMP-binding enzyme family.

Research Fields

· Cellular Processes > Transport and catabolism > Peroxisome.   (View pathway)

· Cellular Processes > Cell growth and death > Ferroptosis.   (View pathway)

· Metabolism > Lipid metabolism > Fatty acid biosynthesis.

· Metabolism > Lipid metabolism > Fatty acid degradation.

· Metabolism > Global and overview maps > Metabolic pathways.

· Metabolism > Global and overview maps > Fatty acid metabolism.

· Organismal Systems > Endocrine system > PPAR signaling pathway.

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

References

1). Microbial metabolite deoxycholic acid-mediated ferroptosis exacerbates high-fat diet-induced colonic inflammation. Molecular metabolism, 2024 (PubMed: 38642891) [IF=8.1]

Application: WB    Species: Rat    Sample: IEC-6 cells and Caco-2 cells

Figure 3 Deoxycholic acid enhanced lipopolysaccharide-induced ferroptosis in intestinal epithelial cells (A–H) IEC-6 cells and Caco-2 cells were incubated with or without 10 ng/mL LPS for 12 h, followed by 200 μM DCA for 2 h. They were divided into four group (n = 6 in each group): control group, DCA group, LPS group and LPS + DCA group. (A) The relative mRNA expression level of GPX4 in each group of IEC-6 cells and Caco-2 cells (n = 6 in each group). (B) The relative mRNA expression level of ACSL4 in each group of IEC-6 cells and Caco-2 cells (n = 6 in each group). (C) The protein level of GPX4, ACSL4 and β-actin in each group of IEC-6 cells and Caco-2 cells. (D) Representative transmission electron microscopy images (scale bars, 1 μm) of cell and mitochondria, and Fe2+/Hoechst immunofluorescence in each group of IEC-6 cells. Mitochondria was showed by white arrows in the pictures. The red fluorescence is indicative of the presence of ferrous ions. (E) The content of Fe2+ in each group of IEC-6 cells and Caco-2 cells (n = 6 in each group). (F) The content of GSH in each group of IEC-6 cells and Caco-2 cells (n = 6 in each group). (G) The content of ROS in each group of IEC-6 cells and Caco-2 cells (n = 6 in each group). (H) The content of MDA in each group of IEC-6 cells and Caco-2 cells (n = 6 in each group). (I-K) IEC-6 cells were incubated 2 μM ferrostatin-1 (Fer-1) for 16 h, and then incubated with or without 10 ng/mL LPS for 12 h, followed by 200 μM DCA for 2 h. They were divided into six group (n = 5 or 6 in each group): control group, LPS group, LPS + DCA group, Fer-1 group, LPS + Fer-1 group and LPS + DCA + Fer-1 group. (I) The relative mRNA expression level of GPX4, ACSL4 and DMT1 in each group of IEC-6 cells (n = 6 in each group). (J) The content of GSH in each group of IEC-6 cells (n = 5 in each group). (K) The content of MDA in each group of IEC-6 cells (n = 5 in each group). Data are represented as mean ± SEM. ns P > 0.05, ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. ##P < 0.01, ####P < 0.0001. ∗ LPS group vs control group, LPS + DCA group vs LPS group. # LPS + Fer-1 group vs LPS group, LPS + DCA + Fer-1 group vs LPS + DCA group.

Application: IHC    Species: Mouse    Sample: colonic tissues

Figure 3 Deoxycholic acid enhanced lipopolysaccharide-induced ferroptosis in intestinal epithelial cells (A–H) IEC-6 cells and Caco-2 cells were incubated with or without 10 ng/mL LPS for 12 h, followed by 200 μM DCA for 2 h. They were divided into four group (n = 6 in each group): control group, DCA group, LPS group and LPS + DCA group. (A) The relative mRNA expression level of GPX4 in each group of IEC-6 cells and Caco-2 cells (n = 6 in each group). (B) The relative mRNA expression level of ACSL4 in each group of IEC-6 cells and Caco-2 cells (n = 6 in each group). (C) The protein level of GPX4, ACSL4 and β-actin in each group of IEC-6 cells and Caco-2 cells. (D) Representative transmission electron microscopy images (scale bars, 1 μm) of cell and mitochondria, and Fe2+/Hoechst immunofluorescence in each group of IEC-6 cells. Mitochondria was showed by white arrows in the pictures. The red fluorescence is indicative of the presence of ferrous ions. (E) The content of Fe2+ in each group of IEC-6 cells and Caco-2 cells (n = 6 in each group). (F) The content of GSH in each group of IEC-6 cells and Caco-2 cells (n = 6 in each group). (G) The content of ROS in each group of IEC-6 cells and Caco-2 cells (n = 6 in each group). (H) The content of MDA in each group of IEC-6 cells and Caco-2 cells (n = 6 in each group). (I-K) IEC-6 cells were incubated 2 μM ferrostatin-1 (Fer-1) for 16 h, and then incubated with or without 10 ng/mL LPS for 12 h, followed by 200 μM DCA for 2 h. They were divided into six group (n = 5 or 6 in each group): control group, LPS group, LPS + DCA group, Fer-1 group, LPS + Fer-1 group and LPS + DCA + Fer-1 group. (I) The relative mRNA expression level of GPX4, ACSL4 and DMT1 in each group of IEC-6 cells (n = 6 in each group). (J) The content of GSH in each group of IEC-6 cells (n = 5 in each group). (K) The content of MDA in each group of IEC-6 cells (n = 5 in each group). Data are represented as mean ± SEM. ns P > 0.05, ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. ##P < 0.01, ####P < 0.0001. ∗ LPS group vs control group, LPS + DCA group vs LPS group. # LPS + Fer-1 group vs LPS group, LPS + DCA + Fer-1 group vs LPS + DCA group.

2). d-Borneol enhances cisplatin sensitivity via autophagy dependent EMT signaling and NCOA4-mediated ferritinophagy. PHYTOMEDICINE, 2022 (PubMed: 36030746) [IF=7.9]

3). Human umbilical cord mesenchymal stem cells ameliorate erectile dysfunction in rats with diabetes mellitus through the attenuation of ferroptosis. Stem Cell Research & Therapy, 2022 (PubMed: 36064453) [IF=7.5]

4). Med1 inhibits ferroptosis and alleviates liver injury in acute liver failure via Nrf2 activation. Cell & bioscience, 2024 (PubMed: 38678227) [IF=7.5]

5). The ERK-cPLA2-ACSL4 axis mediating M2 macrophages ferroptosis impedes mucosal healing in ulcerative colitis. Free radical biology & medicine, 2024 (PubMed: 38367927) [IF=7.4]

6). Astragaloside IV attenuates myocardial dysfunction in diabetic cardiomyopathy rats through downregulation of CD36-mediated ferroptosis. Phytotherapy Research, 2023 (PubMed: 36882189) [IF=7.2]

7). Erythropoietin inhibits ferroptosis and ameliorates neurological function after spinal cord injury. Neural Regeneration Research, 2023 (PubMed: 36204858) [IF=6.1]

Application: WB    Species: Rat    Sample: spinal cord

Figure 3 EPO regulates the expression of ferroptotic biomarkers after SCI. (A) Western blot of the indicated proteins in injured tissues from the treatment groups. (B–H) Quantitative analysis of Tfr, Fpn, Fth, Acsl4 and 4-Hne protein expression at 14 dpi. Gapdh was used as the reference protein. (I, J) Quantitative reverse transcription polymerase chain reaction results of xCT and Gpx4 mRNA extracted from injured tissue at 7 dpi. β-Actin mRNA was used as the reference gene. (K) Quantitative analysis of reduced GSH from injured tissue at 7 dpi. All data are expressed as the mean ± SD (n = 5 in each group). *P < 0.05, **P < 0.01, ***P < 0.001 (one-way analysis of variance followed by Dunnett’s multiple comparisons test). 4-Hne: 4-Hydroxynonenal; Acsl4: acyl-coenzyme A synthetase long chain family member 4; dpi: day(s) post injury; EPO: erythropoietin; Fpn: ferroportin or solute carrier family 40 member 1; Fth: ferritin heavy chain; Gapdh: glyceraldehyde-3-phosphate dehydrogenase; Gpx4: glutathione peroxidase 4; GSH: glutathione; ns: not significant; SCI: spinal cord injury; Tfr: transferrin receptor; xCT: the solute carrier family 7 member 11.

8). Panax notoginseng Saponins Activate Nuclear Factor Erythroid 2-Related Factor 2 to Inhibit Ferroptosis and Attenuate Inflammatory Injury in Cerebral Ischemia-Reperfusion. The American journal of Chinese medicine, 2024 (PubMed: 38699996) [IF=5.7]

9). Protective Role of Dioscin against Doxorubicin-Induced Chronic Cardiotoxicity: Insights from Nrf2-GPX4 Axis-Mediated Cardiac Ferroptosis. Biomolecules, 2024 (PubMed: 38672439) [IF=5.5]

Application: WB    Species: Rat    Sample:

Figure 2 Dioscin alleviates cardiac ferroptosis in DOX-induced rats. (A) Representative Prussian blue staining images of DOX-induced rats treated with or without dioscin. The arrows indicate iron deposition in cardiac tissue. (B) Bar charts indicate cardiac tissue iron in DOX-induced rats treated with or without dioscin. Data are mean ± SD (n = 6). (C–G) Bar charts indicate serum 4-HNE levels and cardiac tissue MDA, glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) levels of DOX-induced rats treated with or without dioscin. Data are mean ± SD (n = 6). (H) The mitochondrial structure of cardiac tissues of DOX-induced rats treated with or without dioscin. (I) Representative images of immunofluorescence analysis of GPX4 expression were captured by fluorescence microscopy. (J) The bar chart indicates the GPX4 intensity in cardiac tissue. Data are mean ± SD (n = 3). (K) Representative Western blotting images of GPX4 and ACSL4 in DOX-induced rats treated with or without dioscin. (L,M) Bar charts indicate the protein expression levels of ACSL4 and GPX4 in cardiac tissues. Data are mean ± SD (n = 3). (N,O) Bar charts indicate the mRNA expression levels of ACSL4 and GPX4 in cardiac tissues. Data are mean ± SD (n = 6). * p < 0.05, ** p < 0.01, *** p < 0.001 vs. DOX treatment group; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. control group. (K) Original western blotting figures can be found in Figure S3.

10). Herceptin induces ferroptosis and mitochondrial dysfunction in H9c2 cells. International Journal of Molecular Medicine, 2022 (PubMed: 34935058) [IF=5.4]

Application: WB    Species: Rat    Sample: H9c2 cells

Figure 3 Fer-1 protects H9c2 cells against Herceptin-induced cell injury and ferroptosis. Fer-1 and DFO reversed the (A) Herceptin-induced reduction in cell viability, (B) Herceptin-induced decrease in GPX4 and SLC7A11 protein expression and Herceptin-induced increase in ACSL4 protein expression. Fer-1 and DFO reversed the Herceptin-induced (C) reduction in GSH content. (D) Fer-1 and DFO did not affect GSSG content. (E) Fer-1 and DFO reversed the Herceptin-induced reduction in the ratio of GSH/GSSG in H9c2 cells. Fer-1 and DFO reversed the Herceptin-induced increase in (F) intracellular and (G) mitochondrial iron levels in H9c2 cells. However, compared with DFO, the effects of Fer-1 were less potent. **P<0.01 and ***P<0.001 vs. NC. #P<0.05 and ##P<0.01 vs. Herceptin (10 µM). Fer-1, ferrostatin-1; GPX4, glutathione peroxidase 4; SLC7A11, recombinant solute carrier family 7 member 11; ACSL4, acyl-CoA synthetase long chain family member 4; GSH, reduced glutathione; GSSG, oxidized glutathione; DFO, deferoxamine; OD, optical density.

Application: WB    Species: rat    Sample: H9c2 cells

Figure 3. | Fer‑1 protects H9c2 cells against Herceptin‑induced cell injury and ferroptosis. Fer‑1 and DFO reversed the (A) Herceptin‑induced reduction in cell viability, (B) Herceptin‑induced decrease in GPX4 and SLC7A11 protein expression and Herceptin‑induced increase in ACSL4 protein expression.

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