GPX4 Antibody (YA9649)(PBS only)
(Synonyms: Phospholipid hydroperoxide glutathione peroxidase; mitochondrial; PHGPx; EC 1.11.1.12; Glutathione peroxidase 4; GPx-4; GSHPx-4)Based on 1 Customer Validation
GPX4 Antibody(YA9649)(PBS only) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to GPX4.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-F, IHC-P, ICC/IF
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in PBS, pH 7.4.
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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IHC-F
IHC-F: Immunohistochemistry-Frozen
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
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| Dilution Ratio | 1:1000-1:2000 | 1:100-1:200 | 1:100-1:20 | 1:50-1:200 |
Product Details
GPX4 Antibody(YA9649)(PBS only) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to GPX4.
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Host Rabbit
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Clonality Monoclonal,Recombinant
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 17 kDaNote: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 22 kDa
Entrez Gene: 2879 Human ; 625249 Mouse ; 29328 Rat
SwissProt: P36969 Human ; O70325 Mouse ; P36970 Rat
OMIM: 250220 Human
Synthetic peptide corresponding to Human GPX4 aa18-65.
Endogenous
affinity purified
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS, pH 7.4.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
GPX4 (glutathione peroxidase 4) is a selenium-dependent phospholipid hydroperoxidase that maintains cellular redox homeostasis by reducing complex lipid hydroperoxides to their corresponding lipid alcohols using glutathione as a cofactor, thereby preventing membrane lipid peroxidation and oxidative damage[1][2][3]. Mechanistically, GPX4 functions as the central regulator and major endogenous suppressor of ferroptosis, an iron-dependent form of regulated cell death driven by the accumulation of phospholipid hydroperoxides, and loss of GPX4 activity promotes lipid peroxide accumulation and ferroptotic cell death[2][4][5][6]. Through this lipid peroxide detoxification pathway, GPX4 contributes to the maintenance of cellular viability, immune homeostasis, and tissue integrity, while impaired GPX4 function has been associated with cancer, neurodegenerative disorders, inflammation, ischemia-reperfusion injury, and other ferroptosis-related pathologies[1][7][8]. Compared with other glutathione peroxidase family members, GPX4 possesses a unique ability to directly reduce phospholipid hydroperoxides and oxidized complex lipids, distinguishing it as a specialized phospholipid repair enzyme and a master regulator of ferroptosis[2][9][10]. Distinct cytosolic, mitochondrial, and nuclear GPX4 isoforms have been described, with cytosolic GPX4 identified as essential for embryonic development and cell survival[7][8]. For experimental applications, pharmacological GPX4 inhibitors such as RSL3 and ML162 are widely used to induce ferroptosis, enabling mechanistic studies of lipid peroxidation, redox regulation, cancer vulnerability, and ferroptosis-targeted therapeutic strategies[11][12].
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Subcellular Localization
Cytoplasm; Mitochondrion
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Expression
Tissue_specificity:Present primarily in testis. Expressed in platelets (at protein level). -
Isoforms & Post-Translational Modification
P36969 has 2 isomers: P36969-1: 22175 Da (predicted); P36969-2: 19525 Da (predicted).
Degraded via chaperone-mediated autophagy, promoting ferroptosis. Hydroxylation by EGLN3/PHD3 promotes its stabilization by preventing degradation via chaperone-mediated autophagy. -
Subunit
Monomer. Has a tendency to form higher mass oligomers (PubMed:17630701). Interacts with FUNDC1; this interaction promotes GPX4 recruitment into mitochondria through TOM/TIM complex where it is degraded by mitophagy (PubMed:36828120). Interacts (via KFERQ motif) with HSPA8; promoting its association with LAMP2 and degradation via chaperone-mediated autophagy (By similarity).
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SwissProt ID
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Synonyms
Phospholipid hydroperoxide glutathione peroxidase; mitochondrial; PHGPx; EC 1.11.1.12; Glutathione peroxidase 4; GPx-4; GSHPx-4
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Research Field
Signal Transduction
Documentation
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Data Sheet (263 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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User Guide for Antibodies (1077 KB)
References
[1]. Weaver K, et al. The Selenoprotein Glutathione Peroxidase 4: From Molecular Mechanisms to Novel Therapeutic Opportunities. Biomedicines. 2022 Apr 13;10(4):891. [Content Brief]
[2]. Ma T, et al. GPX4-independent ferroptosis-a new strategy in disease's therapy. Cell Death Discov. 2022 Oct 30;8(1):434. [Content Brief]
[3]. Xia Y, et al. SIRT1 activation ameliorates rhesus monkey liver fibrosis by inhibiting the TGF-β/smad signaling pathway. Chem Biol Interact. 2024 May 1;394:110979. [Content Brief]
[4]. Li J, et al. Ferroptosis: past, present and future. Cell Death Dis. 2020 Feb 3;11(2):88. [Content Brief]
[5]. Ursini F, et al. Lipid peroxidation and ferroptosis: The role of GSH and GPx4. Free Radic Biol Med. 2020 May 20;152:175-185. [Content Brief]
[6]. Ursini F, et al. A white paper on Phospholipid Hydroperoxide Glutathione Peroxidase (GPx4) forty years later. Free Radic Biol Med. 2022 Aug 1;188:117-133. [Content Brief]
[7]. Xie Y, et al. GPX4 in cell death, autophagy, and disease. Autophagy. 2023 Oct;19(10):2621-2638. [Content Brief]
[8]. GPX4 gene information from NCBI.
[9]. Liu Y, et al. GPX4: The hub of lipid oxidation, ferroptosis, disease and treatment. Biochim Biophys Acta Rev Cancer. 2023 May;1878(3):188890. [Content Brief]
[10]. Sciencedirect.topics.
[11]. Cui C, et al. Post-Translational Modification of GPX4 is a Promising Target for Treating Ferroptosis-Related Diseases. Front Mol Biosci. 2022 May 12;9:901565. [Content Brief]
[12]. Sekhar KR, et al. Glutathione peroxidase 4 inhibition induces ferroptosis and mTOR pathway suppression in thyroid cancer. Sci Rep. 2022 Nov 12;12(1):19396. [Content Brief]