Selenophosphate synthetase 1 (SEPHS1)

Selenophosphate synthetase 1 (SEPHS1) is an ATP-dependent enzyme that synthesizes selenophosphate from selenide and ATP, a crucial step in selenium metabolism[2][5][7]. Selenophosphate generated by SEPHS1 serves as the selenium donor for synthesis of selenocysteine, which is incorporated into selenoproteins—key regulators of redox balance and oxidative stress resilience[1][2][5]. SEPHS1 belongs to the transferase enzyme family, specifically dikinases (EC 2.7.9.3), and is implicated in biosynthetic and stress-response cellular pathways[2]. Deficiency or downregulation of SEPHS1 impairs selenoprotein biosynthesis, disrupts redox homeostasis, elevates reactive oxygen species, and accelerates cellular senescence, contributing to conditions like osteoarthritis[1][4]. Experimental evidence also links SEPHS1 to cancer progression, notably hepatocellular carcinoma cell invasion[4]. Systemic loss results in embryonic lethality in mice, underlining its fundamental physiological importance[1]. Therapeutic modulation is complicated by its vital metabolic role, and no direct drugs are clinically approved. SEPHS1, alongside its dependent selenoproteins, may serve as a biomarker for selenium status, redox stress, and disease susceptibility[1][4][5].

Other names

Selenide, water dikinase 1SEPHS1SELDSPSSPS1Selenium donor protein 1Selenophosphate synthase 1

Acts as a ROS scavenger, mitigating the effects of SEPHS1 deficiency on oxidative stress and cellular senescence.