ArticleBiochemical and biophysical research communications2010
Human selenophosphate synthetase 1 has five splice variants with unique interactions, subcellular localizations and expression patterns.
Article in Biochemical and biophysical research communications, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- SEPHS1: Its evolution, function and roles in development and diseases.Archives of biochemistry and biophysics · 2022Article
- Constitutive Oxidative Stress by SEPHS1 Deficiency Induces Endothelial Cell Dysfunction.International journal of molecular sciences · 2021Article
- Cell Proliferation and Motility Are Inhibited by G1 Phase Arrest in 15-kDa Selenoprotein-Deficient Chang Liver Cells.Molecules and cells · 2015Article
- Deficiency of the 15-kDa selenoprotein led to cytoskeleton remodeling and non-apoptotic membrane blebbing through a RhoA/ROCK pathway.Biochemical and biophysical research communications · 2015Article
- Function of alternative splicing.Gene · 2013Review
- Selenium, selenoprotein genes and Crohn's disease in a case-control population from Auckland, New Zealand.Nutrients · 2012Article
- l(2)01810 is a novel type of glutamate transporter that is responsible for megamitochondrial formation.The Biochemical journal · 2011Article
- Drosophila selenophosphate synthetase 1 regulates vitamin B6 metabolism: prediction and confirmation.BMC genomics · 2011Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Selenophosphate synthetase 1 (SPS1) is an essential cellular gene in higher eukaryotes. Five alternative splice variants of human SPS1 (major type, DeltaE2, DeltaE8, +E9, +E9a) were identified wherein +E9 and +E9a make the same protein. The major type was localized in both the nuclear and plasma membranes, and the others in the cytoplasm. All variants form homodimers, and in addition, the major type forms a heterodimer with DeltaE2, and DeltaE8 with +E9. The level of expression of each splice variant was different in various cell lines. The expression of each alternative splice variant was regulated during the cell cycle. The levels of the major type and DeltaE8 were gradually increased until G2/M phase and then gradually decreased. DeltaE2 expression peaked at mid-S phase and then gradually decreased. However, +E9/+E9a expression decreased gradually after cell cycle arrest. The possible involvement of SPS1 splice variants in cell cycle regulation is discussed.
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