|Ring-box 1||OKDB#: 2013|
|Synonyms:||REGULATOR OF CULLINS 1, ROC1|||Locus:||3q21 in Homo sapiens|
For retrieval of Nucleotide and Amino Acid sequences please go to:
Mammalian Reproductive Genetics Endometrium Database Resource Orthologous Genes UCSC Genome Browser
R-L INTERACTIONS MGI
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Control of the oocyte-to-embryo transition by the ubiquitin-proteolytic system in mouse and C. elegans. Verlhac MH et al. In metazoans the oocyte-to-embryo transition occurs in the absence of mRNA transcription and relies entirely on maternally provided mRNA and proteins. We review here recent findings illustrating the importance of degradation of key proteins allowing essential cell cycle transitions as well as important remodelling of the oocyte to produce a totipotent zygote. By following the chronological order of events, we update recent discoveries on the instrumental role of the cullin-RING and APC/C ubiquitin-ligases in promoting meiosis resumption and the oocyte-to-embryo transition.
NCBI Summary: This gene encodes an evolutionarily conserved protein that interacts with cullins. The protein plays a unique role in the ubiquitination reaction by heterodimerizing with cullin-1 to catalyze ubiquitin polymerization. It also may be involved in the regulation of protein turn-over.
|General function||Cell cycle regulation|
|Expression regulated by|
|Comment||Polycystic ovary syndrome (PCOS) affects 5% of reproductive aged women and is the leading cause of anovulatory infertility. A hallmark of PCOS is excessive theca cell androgen secretion, which is directly linked to the symptoms of PCOS. Our previous studies demonstrated that theca cells from PCOS ovaries maintained in long term culture persistently secrete significantly greater amounts of androgens than normal theca cells, suggesting an intrinsic abnormality. Furthermore, previous studies suggested that ovarian hyperandrogenemia is inherited as an autosomal dominant trait. However, the genes responsible for ovarian hyperandrogenemia of PCOS have not been identified. In this present study, Wood JR, et al carried out microarray analysis to define the gene networks involved in excess androgen synthesis by the PCOS theca cells in order to identify candidate PCOS genes. Analysis revealed that PCOS theca cells have a gene expression profile that is distinct from normal theca cells. Included in the cohort of genes with increased mRNA abundance in PCOS theca cells were aldehyde dehydrogenase 6 and retinol dehydrogenase 2, which play a role in all-trans-retinoic acid biosynthesis and the transcription factor GATA6. We demonstrated that retinoic acid and GATA6 increased the expression of 17alpha-hydroxylase, providing a functional link between altered gene expression and intrinsic abnormalities in PCOS theca cells. Thus, the analyses have 1) defined a stable molecular phenotype of PCOS theca cells, 2) suggested new mechanisms for excess androgen synthesis by PCOS theca cells, and 3) identified new candidate genes that may be involved in the genetic etiology of PCOS. This is one of the genes with Altered mRNA Abundance in PCOS Theca Cells as compared with normal theca cells Maintained Under Basal Conditions.|
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|last update:||2010-10-21 20:00:59||by:||Aaron J Hsueh, hsuehlab email: email@example.com|