This entry represents the N-terminal domain of prolyl 3,4-dihydroxylase Ofd1 from Schizosaccharomyces pombe and homologues in S. cerevisiae (TPA1) and mammals (OGFOD1) [].Ofd1 is a prolyl 4-hydroxylase-like 2-oxoglutarate-Fe(II) dioxygenase that accelerates the degradation of Sre1N (the N-terminal transcription factor domain of Sre1) in the presence of oxygen []. Yeast Sre1 is the orthologue of mammalian sterol regulatory element binding protein (SREBP), and it responds to changes in oxygen-dependent sterol synthesis as an indirect measure of oxygen availability. However, unlike the prolyl 4-hydroxylases that regulate mammalian hypoxia-inducible factor, Ofd1 uses multiple domains to regulate Sre1N degradation by oxygen; the Ofd1 N-terminal dioxygenase domain is required for oxygen sensing and this Ofd1 C-terminal domain accelerates Sre1N degradation in yeasts [, ].
This superfamily entry represents the C-terminal domain of Ofd1 (oxoglutarate and iron-dependent oxygenase, from Schizosaccharomyces pombe), a prolyl 4-hydroxylase-like 2-oxoglutarate-Fe(II) dioxygenase that accelerates the degradation of Sre1N (the N-terminal transcription factor domain of Sre1) in the presence of oxygen []. The domain is conserved from yeasts to humans and was also characterised in S. cerevisiae Tpa1 [, ]. Yeast Sre1 is the orthologue of mammalian sterol regulatory element binding protein (SREBP), and it responds to changes in oxygen-dependent sterol synthesis as an indirect measure of oxygen availability. However, unlike the prolyl 4-hydroxylases that regulate mammalian hypoxia-inducible factor, Ofd1 uses multiple domains to regulate Sre1N degradation by oxygen; the Ofd1 N-terminal dioxygenase domain is required for oxygen sensing and this Ofd1 C-terminal domain accelerates Sre1N degradation in yeasts [].
In fission yeast, Nro1 is a positive regulator of the stability of Sre1N, the sterol regulatory element-binding protein, which is an ER membrane-bound transcription factor that controls adaptation to low oxygen-growth []. In addition, the fission yeast Nro1 is a direct inhibitor of a protein that inhibits SreN1 degradation, Ofd1 (an oxoglutamate deoxygenase). The outcome of this reactivity is that Ofd1 acts as an oxygen sensor that regulates the binding of Nro1 to Ofd1 to control the stability of Sre1N [].This entry also represents ETT1, an Nro1 ortholog []. ETT1 is required for correct translation termination and probably involved in regulation of hypoxic gene expression in association TPA1 []. It inhibits replication of Brome mosaic virus [].
This entry represents the C-terminal degradation domain of oxoglutarate and iron-dependent oxygenase (Ofd1), the domain being conserved from yeasts to humans.Ofd1 is a prolyl 4-hydroxylase-like 2-oxoglutarate-Fe(II) dioxygenase that accelerates the degradation of Sre1N (the N-terminal transcription factor domain of Sre1) in the presence of oxygen []. Yeast Sre1 is the orthologue of mammalian sterol regulatory element binding protein (SREBP), and it responds to changes in oxygen-dependent sterol synthesis as an indirect measure of oxygen availability. However, unlike the prolyl 4-hydroxylases that regulate mammalian hypoxia-inducible factor, Ofd1 uses multiple domains to regulate Sre1N degradation by oxygen; the Ofd1 N-terminal dioxygenase domain is required for oxygen sensing and this Ofd1 C-terminal domain accelerates Sre1N degradation in yeasts [, ].
Serologically defined colon cancer antigen 8 (SDCCAG8), also known as CCCAP (centrosomal colon cancer autoantigen protein), is a family of proteins found in eukaryotes. Mutations of SDCCAG8 are associated with nephronophthisis []and Bardet-Biedl syndrome [], as well as schizophrenia. SDCCAG8 is associated with the centrosome []and interacts with pericentriolar material 1 (PCM1), a centriolar satellite protein crucial for targeting proteins to the centrosome. It regulates centrosomal accumulation of pericentriolar material and neuronal polarisation and migration in the developing mouse cortex [].SDCCAG8 is localized at both centrioles and interacts directly with OFD1 (oral-facial-digital syndrome 1), which is linked to an autosomal recessive cystic kidney disease, NPHP-RC (nephronophthisis-related ciliopathies). Depletion of SDCCAG8 causes kidney cysts and a body axis defect in zebrafish [].
