Human AIF (Apoptosis Inducing Factor) ELISA Kit
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Product specifications
| Category | ELISA Kits |
| Reactivity | Human |
| Detection Method | Colorimetric |
| Assay Data | 4 hours |
| Assay Type | Sandwich ELISA, Double Antibody |
| Test Range | 0.156-10ng/ml |
| Sensitivity | 0.094ng/ml |
| Size 1 | 96T |
| Tested Applications | ELISA |
| Sample Type | Serum, Plasma, Cell Culture Supernatant, cell or tissue lysate, Other liquid samples |
| Availability | Shipped within 10-14 working days. |
| Storage | 2-8 °C for 12 months |
| UniProt ID | O95831 |
| Alias | AIFM1,AIF,PDCD8 |
| Background | Elisa kits for AIF |
| Status | RUO |
Apoptosis Inducing Factor (AIF) is a mitochondrial flavoprotein that plays a dual role in cellular processes, including apoptosis and redox homeostasis. Under normal conditions, AIF resides in the mitochondria, where it participates in oxidative phosphorylation and protects against reactive oxygen species (ROS). During apoptotic signaling, AIF translocates from the mitochondria to the nucleus, where it triggers chromatin condensation and large-scale DNA fragmentation in a caspase-independent manner. This makes AIF a key mediator of programmed cell death in response to mitochondrial dysfunction or oxidative stress. Dysregulation of AIF is implicated in neurodegenerative diseases, such as Parkinson's and Alzheimer's, where mitochondrial dysfunction and cell death contribute to disease progression. Additionally, AIF mutations have been linked to mitochondrial encephalomyopathy and other metabolic disorders. Targeting AIF-related pathways is being explored as a therapeutic strategy for conditions involving excessive cell death or mitochondrial dysfunction.
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This gene encodes a flavoprotein essential for nuclear disassembly in apoptotic cells, and it is found in the mitochondrial intermembrane space in healthy cells. Induction of apoptosis results in the translocation of this protein to the nucleus where it affects chromosome condensation and fragmentation. In addition, this gene product induces mitochondria to release the apoptogenic proteins cytochrome c and caspase-9. Mutations in this gene cause combined oxidative phosphorylation deficiency 6, which results in a severe mitochondrial encephalomyopathy. Alternative splicing results in multiple transcript variants. A related pseudogene has been identified on chromosome 10.
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