ALKBH7 antibody
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Description
May function as protein hydroxylase; can catalyze auto-hydroxylation at Leu-110(in vitro), but this activity may be due to the absence of the true substrate(PubMed:25122757). Required to induce programmed necrosis in response to DNA damage caused by cytotoxic alkylating agents. Acts by triggering the collapse of mitochondrial membrane potential and loss of mitochondrial function that leads to energy depletion and cell death(PubMed:23666923). ALKBH7-mediated necrosis is probably required to prevent the accumulation of cells with DNA damage(PubMed:23666923). Does not display DNA demethylase activity(PubMed:23666923). Involved in fatty acid metabolism(By similarity).
Documents del producto
Product specifications
| Category | Primary Antibodies |
| Immunogen Target | alkB, alkylation repair homolog 7(E. coli) (ALKBH7) |
| Host | Rabbit |
| Reactivity | Human, Mouse, Rat |
| Recommended Dilution | WB: 1:200-1:2000; IHC: 1:20-1:200 |
| Clonality | polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Observed MW | 25 kDa |
| Purity | ≥95% as determined by SDS-PAGE |
| Purification | Immunogen affinity purified |
| Size 1 | 100µg |
| Form | liquid |
| Tested Applications | ELISA, WB, IHC |
| Storage | PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.) |
| UniProt ID | Q9BT30 |
| Gene ID | 84266 |
| Alias | ALKBH7,ABH7,SPATA11 |
| Background | Antibody anti-ALKBH7 |
| Status | RUO |
| Note | Mol. Weight 25 kDa |
Descripción
ALKBH7 is a mitochondrial dioxygenase that lacks canonical nucleic acid demethylase activity but instead regulates programmed necrosis and mitochondrial integrity. Unlike other ALKB family members, ALKBH7 is primarily involved in cellular energy metabolism and stress responses. It regulates mitochondrial homeostasis by influencing the permeability of the mitochondrial membrane and the release of reactive oxygen species (ROS). ALKBH7 is required for alkylation-induced necrosis, a form of programmed cell death triggered by genotoxic stress, where its loss impairs mitochondrial membrane potential and ROS generation. It has been shown to play a role in lipid metabolism and cellular response to alkylating agents. Dysregulation of ALKBH7 has been associated with resistance to alkylating chemotherapeutic agents, highlighting its importance in cancer cell death pathways. Emerging research suggests ALKBH7 as a potential target for enhancing cancer cell sensitivity to DNA damage-inducing therapies.
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