| ras related dexamethasone induced 1 | OKDB#: 5430 |
| Symbols: | RASD1 | Species: | human | ||
| Synonyms: | AGS1, DEXRAS1, MGC:26290 | Locus: | 17p11.2 in Homo sapiens |
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| General Comment | NCBI Summary: This gene encodes a member of the Ras superfamily of small GTPases and is induced by dexamethasone. The encoded protein is an activator of G-protein signaling and acts as a direct nucleotide exchange factor for Gi-Go proteins. This protein interacts with the neuronal nitric oxide adaptor protein CAPON, and a nuclear adaptor protein FE65, which interacts with the Alzheimer's disease amyloid precursor protein. This gene may play a role in dexamethasone-induced alterations in cell morphology, growth and cell-extracellular matrix interactions. Epigenetic inactivation of this gene is closely correlated with resistance to dexamethasone in multiple myeloma cells. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Sep 2011] | ||||
| General function | Intracellular signaling cascade | ||||
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| Cellular localization | Cytoplasmic | ||||
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| Ovarian function | Oocyte maturation | ||||
| Comment | RASD1 Knockdown Results in Failure of Oocyte Maturation. Lee Y et al. (2016) Ras dexamethasone-induced protein (RASD1) is a member of Ras superfamily of small GTPases. RASD1 regulates various signaling pathways involved in iron homeostasis, growth hormone secretion, and circadian rhythm. However, RASD1 function in oocyte remains unknown. Using immunohistochemistry, immunofluorescence, and quantitative real-time RT-PCR, RASD1 expression in mouse ovary and RASD1 role in oocyte maturation-related gene expression, spindle formation, and chromosome alignment were analyzed. RNAi microinjection and time-lapse video microscopy were used to examine the effect of Rasd1 knockdown on oocyte maturation. RASD1 was highly detected in oocytes transitioning from primordial to secondary follicles. Rasd1 was highly expressed in germinal vesicle (GV), during GV breakdown, and in metaphase I (MI) stage as oocytes mature, and its expression was significantly downregulated in MII stage. With knockdown of Rasd1, maturation in GV oocytes was arrested at MI stage, showing disrupted meiotic spindling and chromosomal misalignment. In addition, Obox4 and Arp2/3, engaged in MI-MII transition and cytokinesis, respectively, were misregulated in GV oocytes by Rasd1 knockdown. These findings suggest that RASD1 is a novel factor in MI-MII oocyte transition and may be involved in regulating the progression of cytokinesis and spindle formation, controlling related signaling pathways during oocyte maturation.////////////////// | ||||
| Expression regulated by | |||||
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| Ovarian localization | Oocyte | ||||
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| Follicle stages | Antral | ||||
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| Phenotypes | |||||
| Mutations | 0 mutations | ||||
| Genomic Region | show genomic region | ||||
| Phenotypes and GWAS | show phenotypes and GWAS | ||||
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| created: | Dec. 21, 2016, 12:52 p.m. | by: |
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| last update: | Dec. 21, 2016, 12:55 p.m. | by: | hsueh email: |
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