Rabbit Ferroptosis Sampler Kit Monoclonal Antibody

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Cat. No.: DAB-0012019

Size: 20 µL Size: 100 µL Size: Customer Size

Product Information
Clonality	Monoclonal
Host Species	Rabbit
Product Description	Monoclonal antibodies are produced by immunizing animals with synthetic peptides corresponding to residues surrounding Gly213 of human NCOA4, Ala275 of human NRF2, Val509 of human 4F2hc/CD98, Ala224 of human xCT/SLC7A11, residues near the carboxy terminus of human KEAP1 and human FTH1, and residues near the amino terminus of human DMT1. GPX4 Antibody is a polyclonal antibody produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human GPX4 protein. Antibodies are purified by peptide affinity chromatography.
Format	Liquid
Purity	Affinity purity

Target Information
Gene Description	Ferroptosis is an iron-dependent form of regulated cell death associated with an increase in lipid peroxides. Free divalent iron can lead to spontaneous lipid peroxidation through a Fenton reaction. Ferroptosis is regulated by signaling pathways that control iron storage and oxidative stress. Iron homeostasis is controlled, in part, by ferritin, an iron storage protein consisting of a complex of heavy and light chains. Levels of ferritin may be regulated by a selective autophagy process targeting ferritin, termed ferritinophagy. This pathway is mediated by nuclear receptor coactivator 4, a selective cargo receptor for ferritin. The divalent metal transporter SLC11A2/DMT1/NRAMP2 regulates iron homeostasis through non-heme absorption in the intestine. The glutathione peroxidase pathway has been identified as a key antioxidant defense pathway triggering ferroptosis. The compound RSL3, which directly inhibits GPX4, was identified as an activator of ferroptosis. GPX4 converts GSH into oxidized glutathione and reduces cytotoxic lipid peroxides. The glutathione peroxidase pathway is further regulated by System Xc-, an amino acid antiporter consisting of a disulfide-linked heterodimer of SLC7A11/xCT and SLC3A2/4F2hc/CD98, and is inhibited by the ferroptosis inducer erastin. Regulation of genes involved in oxidative stress, including GPX4, are largely controlled by the transcription factor NRF2 and serves as a defense against ferroptosis., der normal conditions, expression of NRF2 is inhibited through interaction with KEAP1, part of a ubiquitin E3 ligase complex that leads to NRF2 proteasomal degradation. Oxidative stress leads to conformational changes in KEAP1 that disrupts this interaction, resulting in stabilization of NRF2. This process is further regulated through the autophagy pathway in which the autophagy cargo receptor p62/SQSTM1 can competitively inhibit the KEAP1-NRF2 complex, leading to upregulation of NRF2.

Target Information

Gene Description

Ferroptosis is an iron-dependent form of regulated cell death associated with an increase in lipid peroxides. Free divalent iron can lead to spontaneous lipid peroxidation through a Fenton reaction. Ferroptosis is regulated by signaling pathways that control iron storage and oxidative stress. Iron homeostasis is controlled, in part, by ferritin, an iron storage protein consisting of a complex of heavy and light chains. Levels of ferritin may be regulated by a selective autophagy process targeting ferritin, termed ferritinophagy. This pathway is mediated by nuclear receptor coactivator 4, a selective cargo receptor for ferritin. The divalent metal transporter SLC11A2/DMT1/NRAMP2 regulates iron homeostasis through non-heme absorption in the intestine. The glutathione peroxidase pathway has been identified as a key antioxidant defense pathway triggering ferroptosis. The compound RSL3, which directly inhibits GPX4, was identified as an activator of ferroptosis. GPX4 converts GSH into oxidized glutathione and reduces cytotoxic lipid peroxides. The glutathione peroxidase pathway is further regulated by System Xc-, an amino acid antiporter consisting of a disulfide-linked heterodimer of SLC7A11/xCT and SLC3A2/4F2hc/CD98, and is inhibited by the ferroptosis inducer erastin. Regulation of genes involved in oxidative stress, including GPX4, are largely controlled by the transcription factor NRF2 and serves as a defense against ferroptosis., der normal conditions, expression of NRF2 is inhibited through interaction with KEAP1, part of a ubiquitin E3 ligase complex that leads to NRF2 proteasomal degradation. Oxidative stress leads to conformational changes in KEAP1 that disrupts this interaction, resulting in stabilization of NRF2. This process is further regulated through the autophagy pathway in which the autophagy cargo receptor p62/SQSTM1 can competitively inhibit the KEAP1-NRF2 complex, leading to upregulation of NRF2.

Shipping & Storage
Shipping	Shipped at 4 °C.
Storage Instructions	Store at +4 °C short term (1-2 weeks). Store at -20 °C long term.
Storage Buffer	Constituent: 100% PBS

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