GPX4 Antibodies

Phospholipid hydroperoxide glutathione peroxidase (GPX4)

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 crucial role in protecting cells from oxidative damage by preventing tissue 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 (PubMed:24439385).

Gene Information

Human
Gene Name:	GPX4
Uniprot:	P36969
Entrez:	2879

Family

Belongs to:
glutathione peroxidase family

Alternative Names

EC 1.11.1; EC 1.11.1.12; glutathione peroxidase 4 (phospholipid hydroperoxidase); Glutathione Peroxidase 4; GPX4; GPx-4; GSHPx-4; MCSP; PHGPx; PHGPxsnGPx; phospholipid hydroperoxidase; phospholipid hydroperoxide glutathione peroxidase, mitochondrial; snGPx; snPHGPx; sperm nucleus glutathione peroxidase

Molecular Weight

Mass (kDA):
22.175 kDA

Genomic Context

Human
Location:	19p13.3
Sequence:	19; NC_000019.10 (1103994..1106779)

Tissue Specificity

Present primarily in testis.

Subcellular Localizations

[Isoform Mitochondrial]: Mitochondrion.; [Isoform Cytoplasmic]: Cytoplasm.

Diseases

• Malignant Neoplasms
• Neoplasms
• Mammary Neoplasms
• Malignant Neoplasm Of Breast
• Infertility
• Colorectal Cancer
• Infection By Cryptococcus Neoformans
• Hypokinesia
• Malignant Neoplasm Of Prostate
• Cholangiocarcinoma
• Acquired Immunodeficiency Syndrome
• Pituitary Diseases

• Adenocarcinoma
• Congenital Abnormality
• Liver Carcinoma
• Prostatic Neoplasms
• Male Infertility
• Nerve Degeneration
• Retinitis Pigmentosa

Pathways

• Cell Death
• Aging
• Fertilization
• Translation
• Protein Oxidation
• Localization
• Cell Growth
• Pathogenesis
• Embryo Development
• Necrotic Cell Death
• Hatching
• Transport
• Programmed Cell Death

• Dna Hypermethylation
• Osteoblast Differentiation
• Electron Transport
• Electron Transport Chain
• Dna Demethylation
• Immune Response
• Pigmentation

PTMs

• Reduction
• Oxidation
• Demethylation

• Phosphorylation
• Glycosylation
• Cleavage

• Methylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/GPX4

Best Uses Of The GPX4 Marker

The GPX4 marker is used to study the iron transport in ferroptosis. Its target is common to both TransOmics and Elucidator analysis tools. Scientists can submit their results for specimens, species, or applications. These results are eligible for product credits. This is applicable for scientists across the globe. Below are some examples of the best use of the GPX4 marking.

GPX4 is a crucial regulator of ferroptosis

GPX4 is an important regulator of ferroptosis, and is involved in the death of cardiac cells induced by DOX. It has been shown that heterodeletion of GPX4 in cardiomyocytes exacerbates these cardiac abnormalities. This study has shown that heterodeletion GPX4 in cardiomyocytes decreases the number of TUNEL+ cells and also increases ferroptosis.

GPX4 is vital for ferroptosis that is known as the death of cancer cells. It also mediates ferritin degradation and contributes to iron homeostasis in COPD lung tissue. While the exact relationship between NCOA4 and GPX4 is unclear, it could be an undiscovered therapeutic target in different types of cancer. GPX4 inhibition can inhibit the growth of some cancers such as clear cell carcinomas which are sensitive to HIF-2a and the HIFDA axis.

Inhibitors of ferroptosis may include NRF2 or other inhibitors of the protein SRF2. These compounds reduce the production of ROS as well as iron and can cause ferroptosis to be prevented. Further research is required to identify the targets of the effectors of GPX4 inhibitors. This information could contribute to new treatments and therapies for ferroptosis. Although there is not any specific evidence as to how iron or GPX4 inhibit ferroptosis, it is important to comprehend how this process operates.

Lipoxygenases are closely related to ferroptosis. Alongside the GPX4, lipoxygenases play an important role in the regulation of ferroptosis. Additionally, NAC counteracts the toxic lipids generated by nuclear ALOX5.

It is common to both TransOmics and Elucidator analysis tools

The TransOmics and Elucidator protomics analysis tools use the same approach to analyze the data. The results obtained with the TransOmics algorithm were consistent with the results obtained using the Elucidator analysis tool. Both cases demonstrated that GPX4 is a significant enhanced protein. Furthermore, other candidate proteins did not affect the (1S, 3R)-RSL3 sensitivity or cell killing.

It is a typical target for siRNAs

SiRNAs are small RNAs that inhibit specific gene expression. They are the most frequent targets of GPX4. Cardiomyocytes die via ferroptosis, when GPX4 is destroyed by siRNAs and the chemical inhibitor RSL3. Surprisingly, NRVMs were less susceptible to siRNAs than H9c2 cells. Cells from differentiated C2C12 tissues were less sensitive to GPX4 inhibition than NRVMs. Additionally, C2C12 cells were able deplete the GPX4 receptor within two days.

These siRNAs can be used to reduce GPX4 levels within many host cells including cancer cells as well as human cells. These siRNAs are engineered to be non-toxic and have no off-target effects. These products should not be utilized to treat or diagnose diseases. They are designed for research purposes only. They have been proven to be effective in knockdown studies of a variety of other cancer-related genes.

GPX4 is an essential regulator of the death of ferroptotic cells. There are eight GPX enzyme isoforms in human. Each has its own substrate specificity and expression in the tissue. Six of these enzymes are expressed in BJeLR cells and knockdown of any of them can cause negative effects on the viability of cells. Knockdown of GPX4 causes ferroptosis in RCC cells.

A pool siRNAs that target the GPX4 gene have been found to be more effective than single-clone siRNAs. This is why it is a better choice than one siRNA. Additionally, it was found that siRNAs targeting GPX4 were rescued through a combination of an iron chelator, DFOM Vitamin E and an MEK inhibitor known as U0126.

It is a protein that can be used in both TransOmics analysis tools and Elucidator analysis tools.

GPX4 is a selenoprotein which inhibits the synthesis of the phospholipid hydroperoxides, which play a role in a myriad of pathophysiologic conditions such as atherogenesis and inflammation. GPX4 is also sensitive towards selenium, which is incorporated into selenoproteins like the selenocysteine.

It is an essential regulator of ferroptosis

GPX4 is an essential regulator of the process of ferroptosis. It is essential for ferritin deposition that is iron-dependent and cell-to-cell exchangethat are vital for ferroptosis. This death sentence involves GPx4 and reduced glutathione and a-tocopherol. It also includes iron, oxygen and LOX activities. The mechanism of ferroptosis is not completely understood, but the concept of synergy is established.

This study found that GPX4 regulates ferroptosis in cells that are sensitive to erastin. It is a powerful inhibitor of the system xc as well as GPX4. Researchers employed (1S,3R)-RSL3 to stimulate ferroptosis, without diminishing GSH. These results proved the efficacy of Erastin in the BJeLR model of cancer xenografts.

For a long time, the molecular mechanisms that regulate ferroptosis have been studied. GPX4 activation inhibits the process by reducing the concentration of cysteine within the cell. Inactivation of CREB decreases cysteine and glutathione levels. Inhibition of glutathione peroxidase inhibits the production of PLOOH, a critical ferroptosis metabolite.

The transcription element CREB connected to GPX4 activates cAMP reaction element binding protein (CREB). CREB is also able to inhibit ferroptosis, and also stimulate the growth of NSCLC cells. Thus, CREB is a vital regulator of ferroptosis. These factors play many roles in ferroptosis control and ought to be considered as an important target for development of drugs.

Genetic studies have shown that ferrostatin-1 is an effective inhibitor of ferroptosis. As a free radical scavenger, the mechanism of ferroptosis inhibitor has been proposed. It is unclear what the effect of these inhibitors is in vivo. The inhibitors have been able to inhibit ferroptosis, but only in mice. To fully comprehend how these compounds hinder ferroptosis, more research is needed.