signal recognition particle 14kDa (homologous Alu RNA binding protein) | OKDB#: 4995 |
Symbols: | SRP14 | Species: | human | ||
Synonyms: | ALURBP, | Locus: | 15q22 in Homo sapiens |
For retrieval of Nucleotide and Amino Acid sequences please go to:
OMIM
Entrez Gene
Mammalian Reproductive Genetics Endometrium Database Resource Orthologous Genes UCSC Genome Browser GEO Profiles new! Amazonia (transcriptome data) new! R-L INTERACTIONS MGI |
General Comment |
The SRP9/14 subunit of the signal recognition particle (SRP) is present in more than 20-fold excess over SRP in primate cells and exists primarily free but also in complex with small cytoplasmic Alu RNAs. Bovia F 1995 et al.
The heterodimeric protein SRP9/14 bound to the Alu sequences of SRP RNA is essential for the translational control function of the signal recognition particle (SRP). The Alu RNAs of primate cells are believed to be derived from SRP RNA and have been shown to bind to an SRP14-related protein in vitro. We have used antibodies to characterize SRP9/14 and examine its association with small RNAs in vivo. Although SRP9 proteins are the same size in both rodent and primate cells, SRP14 subunits are generally larger in primate cells. An additional alanine-rich domain at the C-terminus accounts for the larger size of one human isoform. Although the other four SRP proteins are largely assembled into SRP in both rodent and primate cells, we found that the heterodimer SRP9/14 is present in 20-fold excess over SRP in primate cells. An increased synthesis rate of both proteins may contribute to their accumulation. The majority of the excess SRP9/14 is cytoplasmic and does not appear to be bound to any small RNAs; however, a significant fraction of a small cytoplasmic Alu RNA is complexed with SRP9/14 in a 8.5 S particle. Our findings that there is a large excess of SRP9/14 in primate cells and that Alu RNAs are bound to SRP9/14 in vivo suggest that this heterodimeric protein may play additional roles in the translational control of gene expression and/or Alu transcript metabolism.
/////////////////////////
|
||||
General function | RNA binding | ||||
Comment | |||||
Cellular localization | Cytoplasmic, Nuclear | ||||
Comment | |||||
Ovarian function | |||||
Comment | |||||
Expression regulated by | |||||
Comment | |||||
Ovarian localization | Oocyte | ||||
Comment | Gene expression profiling of human GV oocytes: an analysis of a profile obtained by Serial Analysis of Gene Expression (SAGE). Stanton JL 2001 et al. A gene expression profile of the human GV oocyte has recently been established by Serial Analysis of Gene Expression (SAGE). A significant number of the genes identified in this profile had not previously been associated with mammalian oocytes. We sought to confirm gene matches by RT-PCR amplification of candidate transcripts using mouse eggs. Attention focused on receptors, proteins involved in apoptosis, and cytoskeletal proteins. Two receptors found in the human catalogue, CCR6 and PAR3, were not found in mouse eggs, whereas myosin light chain, LLGL, beta-actin, 5HT receptor, bad, bak, DFF45, and Caspase homologue (cash) were. Individual SAGEtags can match more than one gene and, in some cases, more than ten. Examination of transcript sequences that generate multiple gene assignments identified a common denominator of short interspersed elements or Alu sequences. For reasons which are, as yet, unclear, the human GV oocyte SAGE catalogue contains relatively high abundances of SAGEtags in Alu sequences. This may reflect normal expression of Alu-containing genes in eggs or upregulated expression of Alu elements following stress. The degeneracy of gene matches in SAGE generated by Alu sequences makes independent confirmation of candidate genes essential. ///////////////////////// | ||||
Follicle stages | |||||
Comment | |||||
Phenotypes | |||||
Mutations | 0 mutations | ||||
Genomic Region | show genomic region | ||||
Phenotypes and GWAS | show phenotypes and GWAS | ||||
Links |
|
created: | March 27, 2014, 2:09 p.m. | by: |
hsueh email:
home page: |
last update: | March 27, 2014, 2:15 p.m. | by: | hsueh email: |
Click here to return to gene search form