Selenium (Se) is an essential trace element required for the biosynthesis of selenoproteins, and selenocysteine insertion sequence (SECIS) binding protein 2 (SECISBP2, or SBP2) represents a key trans-acting factor for the cotranslational insertion of selenocysteine into selenoproteins. Defects in SBP2 are a cause of abnormal thyroid hormone metabolism (ATHYHM) associated with a reduction in type II iodothyronine deiodinase activity. Mutations in this gene have been associated with a reduction in activity of a specific thyroxine deiodinase, a selenocysteine-containing enzyme, and abnormal thyroid hormone metabolism. Cells depleted of SBP2 have increased levels of ROS, which lead to cellular oxidative stress manifested as DNA lesions, stress granules, and lipid peroxidation, induction of caspase- and cytochrome c-dependent apoptosis, indicating that SBP2 is required for protection against ROS-induced cellular damage and cell survival.
Western Blot: HeLa Cells, 1:500-1:5000; IP: Mouse Testis Tissue, 1:200-1:2000
Type: Primary
Antigen: SECISBP2
Clonality: Polyclonal
Clone:
Conjugation: Unconjugated
Epitope:
Host: Rabbit
Isotype: IgG
Reactivity: Human, Mouse, Rat