GPX4 Antibody - #DF6701

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Product: GPX4 Antibody
Catalog: DF6701
Description: Rabbit polyclonal antibody to GPX4
Application: WB IHC IF/ICC
Cited expt.: WB, IHC, IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Chicken
Mol.Wt.: 22kDa; 22kD(Calculated).
Uniprot: P36969
RRID: AB_2838663

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Related Downloads
MS Report
HPLC Report
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

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. For optimal experimental results, antibody reuse is not recommended.
*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(90%), Bovine(100%), Chicken(80%)
Clonality:
Polyclonal
Specificity:
GPX4 Antibody detects endogenous levels of total GPX4.
RRID:
AB_2838663
Cite Format: Affinity Biosciences Cat# DF6701, RRID:AB_2838663.
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

Glutathione peroxidase 4; GPX 4; GPX-4; GPX4; GPX4_HUMAN; GSHPx-4; MCSP; mitochondrial; PHGPx; Phospholipid hydroperoxidase; Phospholipid hydroperoxide glutathione peroxidase; Phospholipid hydroperoxide glutathione peroxidase mitochondrial; snGPx; snPHGPx; Sperm nucleus glutathione peroxidase;

Immunogens

Immunogen:

A synthesized peptide derived from human GPX4, corresponding to a region within C-terminal amino acids.

Uniprot:

P36969(GPX4_HUMAN) >>Visit HPA database.

Gene(ID):
GPX4(2879)
Expression:
P36969 GPX4_HUMAN:

Present primarily in testis.

Description:
Glutathione peroxidase catalyzes the reduction of hydrogen peroxide, organic hydroperoxide, and lipid peroxides by reduced glutathione and functions in the protection of cells against oxidative damage. Human plasma glutathione peroxidase has been shown to be a selenium-containing enzyme and the UGA codon is translated into a selenocysteine. Through alternative splicing and transcription initiation, rat produces proteins that localize to the nucleus, mitochondrion, and cytoplasm. In humans, experimental evidence for alternative splicing exists; alternative transcription initiation and the cleavage sites of the mitochondrial and nuclear transit peptides need to be experimentally verified. [provided by RefSeq, Jul 2008]
Sequence:
MSLGRLCRLLKPALLCGALAAPGLAGTMCASRDDWRCARSMHEFSAKDIDGHMVNLDKYRGFVCIVTNVASQUGKTEVNYTQLVDLHARYAECGLRILAFPCNQFGKQEPGSNEEIKEFAAGYNVKFDMFSKICVNGDDAHPLWKWMKIQPKGKGILGNAIKWNFTKFLIDKNGCVVKRYGPMEEPLVIEKDLPHYF

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
Bovine
100
Pig
90
Chicken
80
Horse
0
Sheep
0
Dog
0
Xenopus
0
Zebrafish
0
Rabbit
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

Research Backgrounds

Function:

Essential antioxidant peroxidase that directly reduces phospholipid hydroperoxide even if they are incorporated in membranes and lipoproteins (By similarity). Can also reduce fatty acid hydroperoxide, cholesterol hydroperoxide and thymine hydroperoxide (By similarity). Plays a key role in protecting cells from oxidative damage by preventing membrane lipid peroxidation (By similarity). Required to prevent cells from ferroptosis, a non-apoptotic cell death resulting from an iron-dependent accumulation of lipid reactive oxygen species. The presence of selenocysteine (Sec) versus Cys at the active site is essential for life: it provides resistance to overoxidation and prevents cells against ferroptosis (By similarity). The presence of Sec at the active site is also essential for the survival of a specific type of parvalbumin-positive interneurons, thereby preventing against fatal epileptic seizures (By similarity). May be required to protect cells from the toxicity of ingested lipid hydroperoxides (By similarity). Required for normal sperm development and male fertility (By similarity). Essential for maturation and survival of photoreceptor cells (By similarity). Plays a role in a primary T-cell response to viral and parasitic infection by protecting T-cells from ferroptosis and by supporting T-cell expansion (By similarity).

Subcellular Location:

Mitochondrion.

Cytoplasm.

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

Present primarily in testis.

Family&Domains:

Belongs to the glutathione peroxidase family.

Research Fields

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

· Metabolism > Metabolism of other amino acids > Glutathione metabolism.

References

1). Polyamine-mediated ferroptosis amplification acts as a targetable vulnerability in cancer. Nature communications, 2024 (PubMed: 38504107) [IF=16.6]
2). Mesenchymal Stem Cells Prevent SLC39A14-Dependent Hepatocyte Ferroptosis through Exosomal miR-16-5p in Liver Graft. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025 (PubMed: 39680749) [IF=15.1]
3). Piezo1 Upregulation in Monocyte-Derived Macrophages Impairs Post-Myocardial Infarction Cardiac Repair via Defective Efferocytosis and Enhanced Ferroptosis. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025 (PubMed: 41214880) [IF=15.1]
4). Disruption of Gut Microbiota-Mediated De Novo NAD+ Synthesis Contributes to the Development of Polycystic Ovary Syndrome. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025 (PubMed: 41082373) [IF=15.1]

Application: WB    Species: Mouse    Sample:

Figure 6 NAD+ inhibits DHEA-induced ferroptosis in PCOS mice. A,B) Ovarian GSH and MDA levels in NMN- and 3-HAA-treated mice (n = 5). C,D) Representative 4-HNE-stained images of ovarian tissues from the indicated groups of mice (scale bar, 20 µm). E,F) Representative TUNEL-stained images of ovarian tissues from the indicated groups of mice (scale bar, 50 µm). G) Ovarian PTGS2 mRNA expression in the indicated groups of mice (n = 5). H,I) Ovarian PTGS2 and GPX4 protein levels analyzed by western blotting in DHEA-treated mice subjected to NMN and 3-HAA treatments (n = 3). J) Ovarian Fe2+ levels in DHEA-induced PCOS mice treated with NMN and 3-HAA (n = 5). For K,L), KGN cells were pretreated with Fer-1 (2 µM) and NMN (1 mM) for 2 h, followed by treatment with DHEA (20 µM) for 24 h. (K) Cell viability assay (n = 5). (L) PTGS2 and GPX4 protein levels in NMN- and Fer-1-treated KGN cells were analyzed by western blotting (n = 3). M. Prepubertal female mice (21-day-old) were intraperitoneally injected with 3-HAA (200 mg kg−1) and Fer-1 (10 mg kg−1), and subcutaneously injected with DHEA (60 mg kg−1) daily for 21 days. Representative H&E-stained images of ovarian tissues from the indicated groups of mice (scale bar, 200 µm) and analysis of the number of cystic follicles and corpora lutea based on H&E-stained sections (n = 5). Data are expressed as mean ± SD. Statistical significance was determined using one-way ANOVA followed by Tukey's test (A, B, and G-M). *p < 0.05, **p < 0.01, and ***p < 0.001 indicate significance.
5). Identification and analysis of microplastic aggregation in CAR-T cells. Journal of hazardous materials, 2024 (PubMed: 39488976) [IF=13.6]
6). Retinol Saturase Mediates Retinoid Metabolism to Impair a Ferroptosis Defense System in Cancer Cells. Cancer research, 2023 (PubMed: 37184371) [IF=12.5]
7). PRODH2-Mediated Metabolism in the Bone Microenvironment Promotes Breast Cancer Metastasis. Cancer research, 2025 (PubMed: 40749014) [IF=12.5]

Application: WB    Species: Mouse    Sample:

Figure 4. PRODH2 suppresses ferroptosis and regulates osteoclast differentiation. A, Untargeted metabolomics analysis in PRODH2-overexpressing cells vs. vector cells with treatment of Hyp. B, Changes in intracellular GSH levels upon PRODH2 overexpression (OE) or knockout in SCP2 cells with treatment of Hyp. C, Western blot analysis of ferroptosis-related proteins in indicated cells following Hyp treatment. Band intensities were normalized to β-actin and expressed as fold change relative to control. D, mRNA expression levels of SLC7A11 in different PRODH2 expression conditions with treatment of Hyp. E, Relative expression levels of intracellular GSH in breast cancer indicated cells with treatment of Hyp. F, Representative images and quantitative analysis of C11-BODIPY oxidation (green)/reduction (red) ratio in cells. Scale bar, 100 μm. G, Representative staining images and quantification of osteoclast differentiation in the presence of CM from indicated cells with treatment of Hyp. Black arrows, multinuclear TRAP+ osteoclasts. Scale bar, 100 μm. H, Left, μCT, hematoxylin and eosin (H&E), and TRAP staining images of bone metastasis in mice after intracardiac injection. Right, quantification of the positive area of Sirius red staining, BLI signals, μCT osteolytic lesion sites, and TRAP+ osteoclasts along the bone–tumor interface of metastases. n = 6 mice per group. Each experiment was performed in triplicate and independently repeated three times. Data are presented as the mean ± SD of n = 3 biologically independent samples. Scale bar, 100 μm. *, P < 0.05; **, P < 0.01. B, bone, T, tumor; M, marrow; NC, negative control.
8). Berberine suppresses colorectal cancer progression by inducing ferroptosis-mediated energy metabolism disorders. Journal of advanced research, 2025 (PubMed: 41139018) [IF=11.4]

Application: WB    Species: human    Sample: HCT116 cells

Fig. 6. BBR regulates the Gli1/STAT3-FNR signaling axis involved in the ferroptosis of HCT116 cells and CT26 cells. (A) Scheme of BBR regulating Gli1/STAT3-FNR signaling axis in vitro. (B) Principal component analysis in RNA-sequence of HCT116 cells. (C) Correlation plot in RNA-sequence of HCT116 cells. (D) Volcano plot illustrating differentially regulated gene number of HCT116 cells. (E) Kyoto encyclopedia of genes and genomes enrichment analysis in RNA-sequence of HCT116 cells. (F) gene set enrichment analysis of selected pathways including FNR signatures and Hedgehog signaling axis of HCT116 cells. (G) Represented western blot bands of Gli1, STAT3, GPX4, SLC7A11, and FTH1 of HCT116 cells. N = 3. (H) Represented western blot bands of Gli1, STAT3, GPX4, SLC7A11, and FTH1 of CT26 cells. N = 3. Values represented mean ± SD. *p < 0.05 and **p < 0.01.
9). Thymosin α1 alleviates pulpitis by inhibiting ferroptosis of dental pulp cells. International journal of oral science, 2025 (PubMed: 41087337) [IF=10.8]

Application: WB    Species: Rat    Sample:

Fig. 3 The effect of thymosin α1 on the ferroptosis of dental pulp cells (DPCs). a CCK8 assay: The effect of different concentrations of Tα1 on the growth of DPCs. b The expression of PTGS2, FTL, and GPX4 proteins was evaluated using western blot in four groups of DPCs including Control group, LPS-stimulated DPCs (LPS group), LPS-stimulated DPCs with Tα1 addition (LPS + Tα1 group), and LPS-stimulated DPCs with Ptma gene silenced (LPS + shPTMA group). The statistical analysis of PTGS2 (c), FTL (d), and GPX4 (e) proteins expression in four groups of DPCs. (f) Intracellular Fe2+ levels in DPCs were measured by the FerroOrange fluorescent probe (orange). Cell nuclei were stained with DAPI (blue). A ferroptosis inhibitor, ferrostatin-1, was added into LPS-stimulated DPCs (LPS + Fer-1). Scale bars: 50 μm. g Quantitative analysis of the FerroOrange fluorescent intensity of the four groups of DPCs. Bars represent means ± SD. h Flow cytometry of JC-10 of the four groups. Accumulation of JC-10 aggregates in the mitochondrial matrix can be detected by red fluorescence (Ex/Em: 540/590 nm). At mitochondrial depolarization, JC-10 diffuses out of the mitochondria and returns to its monomeric form which exhibits green fluorescence (Ex/Em: 490/525 nm). i Statistical analysis of JC-10 red/green fluorescence ratio among the four groups. The expression of the inflammatory factor TNF-α (j), IL-1β (k), and IL-6 (l) among the four groups of DPCs. *P 

Application: WB    Species: Rat    Sample:

Fig. 2 Evaluation of ferroptosis in pulpitis. a Pattern of ferroptosis in pulpitis. b KEGG enrichment analysis of ferroptosis in single-cell RNA sequencing between pulpitis and healthy pulp tissue. c The levels of ROS in pulpitis and control pulp tissue were measured by the DCFH-DA fluorescent probe (green). d Intracellular Fe2+ levels in pulpitis and control pulp tissue were detected with the FerroOrange fluorescent probe (orange). Scale bars: 20 μm. Immunohistochemistry of GPX4 (e) and PTGS2 (f) in human pulpitis and control pulp tissue. D: dentin; P: tooth pulp. g Quantitative analysis of ROS fluorescence intensity in pulpitis and control pulp tissue. h Quantitative analysis of Fe2+ fluorescence intensity in pulpitis and control pulp tissue. Cell nuclei were stained with DAPI (blue). Integrated optical density (IOD) of GPX4 (i) and PTGS2 (j) in human pulpitis and control pulp tissue by Image J Pro software. Values are represented as mean ± SD. *P
10). Silibinin attenuates ferroptosis in acute kidney injury by targeting FTH1. Redox biology, 2024 (PubMed: 39326069) [IF=10.7]
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