Structure of the Human Receptor Tyrosine Phosphatase Gamma Gene (PTPRG) and Relation to the Familial RCC t(3;8) Chromosome Translocation

Kastury, Kumar; Ohta, Masataka; Lasota, Jerzy; Moir, Donald T.; Dorman, Thomas E.; LaForgia, Sal; Druck, Teresa; Huebner, Kay

doi:10.1006/geno.1996.0109

Cited by 32 publications

(10 citation statements)

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“…The data generated in this paper is in complete agreement with previously published reports characterizing FRA3B (Kastury et al, 1996;Paradee et al, 1996). The key distinction is that we have now more comprehensively analysed clones from this region to define the ends of decondensation/breakage in the FRA3B region.…”

Section: Discussionsupporting

confidence: 88%

Evidence that instability within the FRA3B region extends four megabases

et al. 2002

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FRA3B is the most frequently expressed common fragile site localized within human chromosomal band 3p14.2, which is frequently deleted in many different cancers, including cervical cancer. Previous reports indicate aphidicolin-induced FRA3B instability occurs over *500 kb which is spanned by the 1.5 Mb fragile histidine triad (FHIT) gene. Recently an HPV16 cervical tumor integration, 2 Mb centromeric to the published FRA3B region, has been identified. FISH-based analysis with a BAC spanning the integration has demonstrated this integration occurs within the FRA3B region of instability. These data suggest that the unstable FRA3B region is much larger than previously reported. FISHbased analysis of aphidicolin-induced metaphase chromosomes allowed for a complete characterization of instability associated with FRA3B. This analysis indicates that fragility extends for 4 Mb. Within this region are a total of five genes, including FHIT. FRA3B gene expression analysis on a panel of cervical tumor-derived cell lines revealed that three of the five genes within FRA3B were aberrantly regulated. A similar analysis of genes outside of FRA3B indicated that the surrounding genes were not aberrantly expressed. These data provide additional support that regions of instability associated with CFSs and the genes contained within them, may play an important role in cancer development.

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Section: Discussionsupporting

confidence: 88%

Evidence that instability within the FRA3B region extends four megabases

et al. 2002

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“…There were several reports of LOH on chromosome 8, which were distributed around 8p11‐p23, among non‐papillary RCC cases [22,36–38]. Detailed analysis of breakpoints of translocation between chromosomes 3 and 8 indicated potential involvement of the FHIT [39], FRA3B [40], or PTP loci located on chromosome 3 [41,42], and the TRC8 locus on chromosome 8 [43]. TRC8 is a 664‐amino acid membrane protein that might function as a receptor in signal transduction.…”

Section: Discussionmentioning

confidence: 99%

A comprehensive analysis of loss of heterozygosity caused by hemizygous deletions in renal cell carcinoma using a subtraction library

Hatano

Nishikawa

McElgunn

et al. 2001

Molecular Carcinogenesis

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Several new loci were identified by a comprehensive analysis of loss of heterozygosity (LOH) using a subtraction library between matched normal and renal cell carcinoma (RCC) tissues. A total of 187 clones from the library, with a complexity of 1x10(4), were mapped, and 44 clusters of the mapped loci were subjected to LOH analysis using microsatellite markers. A total of 27 loci, which exhibited frequencies of LOH of at least 10% among 44 tumors, mostly clear-cell RCC, included several loci that were reported previously, such as, the von Hippel-Lindau gene, adenomatous polyposis coli, and interferon regulatory factor-1, as well as new loci, at 5q32-q34, 6q21-q22, 8p12, and others. These loci exhibited LOH among 11.8-93.8% of tumors, and most, if not all, were derived from the sites of hemizygous deletions. The minimum regions of LOH of chromosomes 5, 6, and 8 were 9.0, 10.3, and 0.775 Mb, respectively. The average distance between the cloned fragments on the chromosomes was 2.2 Mb in 187 clones, indicating that the minimum LOH size expected from this subtraction analysis was roughly 50 kb. Therefore, the strategy described here provides comprehensive analysis of LOH sites, which were mostly caused by hemizygous deletions.

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“…In contrast, exons 20-28 and 29-32 form two tight clusters, which together span approximately 60 kbp. In general, this pattern of exon organization appears to be characteristic of most RPTPs, as it is also observed in RPTPγ [8], LAR [9], CD45 [10] and RPTPα [11]. Each of these phosphatases has at least one very large intron in the 5'-region of the gene.…”

Section: Resultsmentioning

confidence: 76%

“…In RPTPρ, the first and second phosphatase domains are encoded by exons 19-26 and 27-32, respectively (Figure 3A). The exon structure of the RPTPρ phosphatase domains, and that of homologous domains in PCP-2 (NM_005704), RPTPκ (NM 002844), RPTPμ (NM 002845), LAR [9], CD45 [10] RPTPα [11], RPTPγ [8] and rat Esp/mOST-PTP [32, 33], are compared in Figure 4. We have deduced the genomic structure of RPTPκ, RPTPμ and PCP-2 by comparing known cDNA sequences with human genomic clones (NCBI).…”

Section: Resultsmentioning

confidence: 99%

Genomic organization and alternative splicing of the human and mouse RPTPρ genes

et al. 2001

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BackgroundReceptor protein tyrosine phosphatase rho (RPTPρ, gene symbol PTPRT) is a member of the type IIB RPTP family. These transmembrane molecules have been linked to signal transduction, cell adhesion and neurite extension. The extracellular segment contains MAM, Ig-like and fibronectin type III domains, and the intracellular segment contains two phosphatase domains. The human RPTPρ gene is located on chromosome 20q12-13.1, and the mouse gene is located on a syntenic region of chromosome 2. RPTPρ expression is restricted to the central nervous system.ResultsThe cloning of the mouse cDNA, identification of alternatively spliced exons, detection of an 8 kb 3'-UTR, and the genomic organization of human and mouse RPTPρ genes are described. The two genes are comprised of at least 33 exons. Both RPTPρ genes span over 1 Mbp and are the largest RPTP genes characterized. Exons encoding the extracellular segment through the intracellular juxtamembrane 'wedge' region are widely spaced, with introns ranging from 9.7 to 303.7 kb. In contrast, exons encoding the two phosphatase domains are more tightly clustered, with 15 exons spanning ∼ 60 kb, and introns ranging in size from 0.6 kb to 13.1 kb. Phase 0 introns predominate in the intracellular, and phase 1 in the extracellular segment.ConclusionsWe report the first genomic characterization of a RPTP type IIB gene. Alternatively spliced variants may result in different RPTPρ isoforms. Our findings suggest that RPTPρ extracellular and intracellular segments originated as separate modular proteins that fused into a single transmembrane molecule during a later evolutionary period.

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Structure of the Human Receptor Tyrosine Phosphatase Gamma Gene (PTPRG) and Relation to the Familial RCC t(3;8) Chromosome Translocation

Cited by 32 publications

References 0 publications

Evidence that instability within the FRA3B region extends four megabases

Evidence that instability within the FRA3B region extends four megabases

A comprehensive analysis of loss of heterozygosity caused by hemizygous deletions in renal cell carcinoma using a subtraction library

Genomic organization and alternative splicing of the human and mouse RPTPρ genes

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