ArticleThe Biochemical journal2006
Interaction of human GTP cyclohydrolase I with its splice variants.
Article in The Biochemical journal, 2006. 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, 15 citations in OpenAlex.
- Genetic co-regulation of neopterin and Parkinson's disease.NPJ Parkinson's disease · 2026Article
- A novel FADS2 isoform identified in human milk fat globule suppresses FADS2 mediated Δ6-desaturation of omega-3 fatty acids.Prostaglandins, leukotrienes, and essential fatty acids · 2018Article
- Preparation and characterization of monoclonal antibodies against VSTM1.Monoclonal antibodies in immunodiagnosis and immunotherapy · 2013Article
- The Epithelial Sodium Channel alpha subunit (alpha ENaC) alternatively spliced form "b" in Dahl rats: What's next?International archives of medicine · 2010Article
- Regulation of the epithelial sodium channel [ENaC] in kidneys of salt-sensitive Dahl rats: insights on alternative splicing.International archives of medicine · 2009Article
- Characterization of the epithelial sodium channel alpha subunit coding and non-coding transcripts and their corresponding mRNA expression levels in Dahl R versus S rat kidney cortex on normal and high salt diet.International archives of medicine · 2009Article
- Deficient BH4 production via de novo and salvage pathways regulates NO responses to cytokines in adult cardiac myocytes.American journal of physiology. Heart and circulatory physiology · 2008Article
- Cytokines and lipopolysaccharides induce inducible nitric oxide synthase but not enzyme activity in adult rat cardiomyocytes.Free radical biology & medicine · 2008Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tetrahydrobiopterin is an essential cofactor for aromatic amino acid hydroxylases, ether lipid oxidase and nitric oxide synthases. Its biosynthesis in mammals is regulated by the activity of the homodecameric enzyme GCH (GTP cyclohydrolase I; EC 3.5.4.16). In previous work, catalytically inactive human GCH splice variants differing from the wild-type enzyme within the last 20 C-terminal amino acids were identified. In the present study, we searched for a possible role of these splice variants. Gel filtration profiles of purified recombinant proteins showed that variant GCHs form high-molecular-mass oligomers similar to the wild-type enzyme. Co-expression of splice variants together with wild-type GCH in mammalian cells revealed that GCH levels were reduced in the presence of splice variants. Commensurate with these findings, the GCH activity obtained for wild-type enzyme was reduced 2.5-fold through co-expression with GCH splice variants. Western blots of native gels suggest that splice variants form decamers despite C-terminal truncation. Therefore one possible explanation for the effect of GCH splice variants could be that inactive variants are incorporated into GCH heterodecamers, decreasing the enzyme stability and activity.
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