Cloning, Sequencing, Gene Organization, and Localization of the Human Ribosomal Protein RPL23A Gene

Fan, Wufang; Christensen, Mari; Eichler, Evan E.; Zhang, Xiaoxiao; Lennon, Greg

doi:10.1006/geno.1997.5038

Cited by 15 publications

(9 citation statements)

References 28 publications

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“…We show that the gene structure is quite similar to the other human ubiquitin fusion protein, Uba52, although the ubiquitin-coding portion of the gene has been split into an additional exon in this gene. Although 2 ribosomal genes contain TATA and/or CAAT elements in their promoters have been described (10,11), the large majority of ribosomal gene promoters are similar to that reported here. Specifically, the regulatory elements of these genes consist of a TATA-less promoter within a CpG-rich island, with the transcriptional start site located within a polypyrimidine tract.…”

Section: Vol 270 No 3 2000supporting

confidence: 84%

Structure of the Human Ubiquitin Fusion Gene Uba80 (RPS27a) and One of Its Pseudogenes

Kirschner

Stratakis

2000

Biochemical and Biophysical Research Communications

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Ubiquitin is a highly conserved 76 amino acid protein that is generated in the cell by proteolysis of larger proteins containing either polyubiquitin chains or ubiquitin fused to carboxyl extension proteins (CEPs). In humans, the two human ubiquitin-CEP genes are Uba80 and Uba52, which code for ubiquitin fused to ribosomal protein S27a and L40, respectively. Working from a recently generated physical map of human chromosome 2p16, we determined the genetic and physical location and the genomic structure of the Uba80 gene in its entirety. A comparison of Uba80 to Uba52 revealed that the two genes share a conserved 5-end structure, but that the structure of the ubiquitin coding regions was not conserved. Analysis of 400 bp of the promoter of Uba80 revealed strong similarity not only to the Uba52 promoter, but also to the other known human ribosomal gene promoters that have been identified to date. Homology searches also detected the presence of a pseudogene for Uba80, and the structure of this sequence feature is also reported.

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Section: Vol 270 No 3 2000supporting

confidence: 84%

Structure of the Human Ubiquitin Fusion Gene Uba80 (RPS27a) and One of Its Pseudogenes

Kirschner

Stratakis

2000

Biochemical and Biophysical Research Communications

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“…A good example represents the human genomic sequence proximal to WEE1 which contains a processed pseudogene flanked by a 13 bp direct sequence repeat on each side. It displays significant homology to the gene RPL23A (Fan et al, 1997), which maps to 17q11 and codes for a ribosomal protein. In the murine genomic sequence no such pseudogene can be found (Fig.…”

Section: Resultsmentioning

confidence: 99%

Comparative architectural aspects of regions of conserved synteny on human chromosome 11p15.3 and mouse chromosome 7 (including genes WEE1 and LMO1)

Cichutek

Brueckmann²,

Seipel³

et al. 2001

Cytogenet Genome Res

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Human chromosome 11p15.3 is associated with chromosome aberrations in the Beckwith Wiedemann Syndrome and implicated in the pathogenesis of different tumor types including lung cancer and leukemias. To date, only single tumor-relevant genes with linkage to this region (e.g. LMO1) have been found suggesting that this region may harbor additional potential disease associated genes. Although this genomic area has been studied for years, the exact order of genes/chromosome markers between D11S572 and the WEE1 gene locus remained unclear. Using the FISH technique and PAC clones of the flanking markers we determined the order of the genomic markers. Based on these clones we established a PAC contig of the respective region. To analyse the chromosome area in detail the synteny of the orthologous region on distal mouse chromosome 7 was determined and a corresponding mouse clone contig established, proving the conserved order of the genes and markers in both species: “cen–WEE1–D11S2043–ZNF143–RANBP7–CEGF1– ST5–D11S932–LMO1–D11S572–TUB–tel”, with inverted order of the murine genes with respect to the telomere/centromere orientation. The region covered by these contigs comprises roughly 1.6 MB in human as well as in mouse. The genomic sequence of the two subregions (around WEE1 and LMO1) in both species was determined using a shotgun sequencing strategy. Comparative sequence analysis techniques demonstrate that the content of repetitive elements seems to decline from centromere to telomere (52.6% to 34.5%) in human and in the corresponding murine region from telomere to centromere (41.87% to 27.82%). Genomic organisation of the regions around WEE1 and LMO1 was conserved, although the length of gene regions varied between the species in an unpredictable ratio. CpG islands were found conserved in putative promoter regions of the known genes but also in regions which so far have not been described as harboring expressed sequences.

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“…2A). Mass spectrometric analysis identified this protein as RPL23A, a component of the 60S subunit of ribosome (17, 18) (fig. S11).…”

mentioning

confidence: 99%

“…2B). The amino acid sequence of RPL23A is 100% conserved between mice and humans (18). The sera from the B cell-reconstituted R7–39 mice indeed recognized recombinant RPL23A, but not histone H1.2 protein, another candidate protein indicated by the mass spectrometric analysis (Fig.…”

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confidence: 99%

Detection of T cell responses to a ubiquitous cellular protein in autoimmune disease

Ito

Hashimoto

Hirota

et al. 2014

Science

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T cells mediating autoimmune diseases, such as rheumatoid arthritis (RA), are difficult to characterize because they are likely to be deleted or inactivated in the thymus if the self-antigens they recognize are ubiquitously expressed. One way to obtain and analyze these autoimmune T cells is to alter T cell receptor (TCR) signaling in developing T cells to change their sensitivity to thymic negative selection, thereby allowing their thymic production. From mice thus engineered to generate T cells mediating autoimmune arthritis, we have isolated arthritogenic TCRs and characterized the self-antigens they recognized. One of them was the ubiquitously expressed 60S ribosomal protein L23a (RPL23A), with which T cells and autoantibodies from RA patients reacted. This strategy may improve our understanding of the underlying drivers of autoimmunity.

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Cloning, Sequencing, Gene Organization, and Localization of the Human Ribosomal Protein RPL23A Gene

Cited by 15 publications

References 28 publications

Structure of the Human Ubiquitin Fusion Gene Uba80 (RPS27a) and One of Its Pseudogenes

Structure of the Human Ubiquitin Fusion Gene Uba80 (RPS27a) and One of Its Pseudogenes

Comparative architectural aspects of regions of conserved synteny on human chromosome 11p15.3 and mouse chromosome 7 (including genes WEE1 and LMO1)

Detection of T cell responses to a ubiquitous cellular protein in autoimmune disease

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