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Description
FDX1 Recombinant Rabbit mAb (S-3587-58)Product Specification Host Rabbit Antigen FDX1 Synonyms Adrenodoxin, mitochondrial; Adrenal ferredoxin; Ferredoxin 1; Hepatoredoxin; ADX Immunogen Recombinant Protein Location Mitochondrion Accession P10109 Clone Number S 3587 58 Antibody Type Recombinant mAb Isotype IgG Application WB, IHC P Reactivity Hu, Ms, Rt Positive Sample A549, HepG2, PC 3, Caco 2, mouse kidney, mouse testis, rat kidney, rat testis, COS 7 Predicted Reactivity Bv, Pg, Sh, Ck
Product Specification
| Host | Rabbit |
| Antigen | FDX1 |
| Synonyms | Adrenodoxin, mitochondrial; Adrenal ferredoxin; Ferredoxin-1; Hepatoredoxin; ADX |
| Immunogen | Recombinant Protein |
| Location | Mitochondrion |
| Accession | P10109 |
| Clone Number | S-3587-58 |
| Antibody Type | Recombinant mAb |
| Isotype | IgG |
| Application | WB, IHC-P |
| Reactivity | Hu, Ms, Rt |
| Positive Sample | A549, HepG2, PC-3, Caco-2, mouse kidney, mouse testis, rat kidney, rat testis, COS-7 |
| Predicted Reactivity | Bv, Pg, Sh, Ck |
| Purification | Protein A |
| Concentration | 0.5 mg/ml |
| Conjugation | Unconjugated |
| Physical Appearance | Liquid |
| Storage Buffer | PBS, 40% Glycerol, 0.05% BSA, 0.03% Proclin 300 |
| Stability & Storage | 12 months from date of receipt / reconstitution, -20 °C as supplied |
Dilution
| application | dilution | species |
| WB | 1:1000-1:2000 | Hu, Ms, Rt, Mk |
| IHC-P | 1:200 | Hu, Ms, Rt |
Background
FDX1 (Ferredoxin 1) is a crucial mitochondrial iron-sulfur cluster protein that serves as an essential electron donor for the biosynthesis of iron-sulfur clusters and steroid hormones, functioning primarily by transferring electrons from NADPH via ferredoxin reductase (FDXR) to various target enzymes such as ferredoxin-dependent sulfite reductase and cytochrome P450 family members involved in processes like heme synthesis, vitamin D activation, and cortisol production; notably, recent groundbreaking research has identified FDX1 as the central upstream regulator of cuproptosis, a distinct form of regulated cell death triggered by excessive copper accumulation, wherein FDX1 directly reduces Cu2+ to the more toxic Cu+ state and facilitates the lipoylation of tricarboxylic acid cycle proteins, leading to their aggregation and subsequent proteotoxic stress that ultimately causes cell demise, thereby establishing FDX1 not only as a vital metabolic hub but also as a potential therapeutic target for cancer treatment and copper-related disorders.
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