Isolation and mapping to 17p12 – 13 of the human homologous of the murine growth arrest specific Gas-3 gene

Martinotti, Alessia; Cariani, Claudia T.; Melani, Cecilia; Sozzi, Gabriella; Spurr, Nigel K.; Colombo, Mario P.

doi:10.1093/hmg/1.5.331

Cited by 11 publications

(5 citation statements)

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“…These data confirm that Cop‐1 expression behaves in the manner expected for a gas gene in that Cop‐1 levels rise relatively early in the shift from proliferation to quiescence. Less than a dozen gas genes have been described and even fewer gas gene products have been characterized (Schneider et al, 1988; Manfioletti et al, 1990a, b; Brancolini et al, 1992; Coccia et al, 1992; Del Sal et al, 1992; Martinotti et al, 1992; Manfioletti et al, 1993; Vacha et al, 1997; Gonos, 1998; Evdokiou and Cowled, 1998a, b; Whitmore et al, 1998) thus this observation is of potential significance with respect to mechanisms regulating growth arrest in cells.…”

Section: Discussionmentioning

confidence: 99%

COP‐1, a member of the CCN family, is a heparin‐induced growth arrest specific gene in vascular smooth muscle cells

Delmolino

Stearns

Castellot

2001

Journal Cellular Physiology

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Vascular smooth muscle cell (VSMC) hyperplasia is responsible for the failure of 15-30% of vascular surgical procedures such as coronary artery bypass grafts and angioplasties. We and others have shown that heparin suppresses VSMC proliferation in vivo and in cell culture. We hypothesize that heparin inhibits VSMC proliferation by binding to cell surface receptors, resulting in selective modulation of mitogenic signal transduction pathways and altered transcription of a specific subset of growth regulatory genes. To test this idea, we used subtractive hybridization to identify differentially expressed mRNAs in heparin-treated and untreated VSMC. We identified a heparin induced mRNA identical to Cop-1, a member of the CCN family of proteins which are secreted, cysteine-rich modular proteins involved in growth regulation and migration. Cop-1 from smooth muscle cells appears to have a different expression pattern and possibly different functions than Cop-1 from other cells. Cop-1 mRNA is expressed at high levels in quiescent VSMC and at low levels in proliferating VSMC, an expression pattern highly characteristic of growth arrest specific genes. Cop-1 mRNA is expressed at high levels in heparin treated VSMC and COP-1 protein is secreted into culture medium. In tissues, Cop-1 expression is observed in the uninjured rat aorta suggesting a possible role for Cop-1 in vivo. We found PDGF, but not EGF, inhibits the expression of Cop-1 in VSMC. Neither TGF-beta nor interferon-beta, two inhibitors of VSMC proliferation, were able to induce Cop-1 expression. In addition, heparin does not induce Cop-1 mRNA in endothelial cells and VSMC resistant to the antiproliferative effect of heparin. Conditioned medium from cells over-expressing COP-1 protein inhibits VSMC proliferation in culture. Together, our data indicate that COP-1 may play a role in the antiproliferative mechanism of action of heparin.

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Section: Discussionmentioning

confidence: 99%

COP‐1, a member of the CCN family, is a heparin‐induced growth arrest specific gene in vascular smooth muscle cells

Delmolino

Stearns

Castellot

2001

Journal Cellular Physiology

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“…CL-20 is localized on chromosome 12 while PMP22 has been mapped at 17p12-13 (27,(31)(32)(33). Genetic alterations in the expression of PMP22 have been implicated in several neuropathies specific for the peripheral nervous system.…”

Section: Discussionmentioning

confidence: 99%

“…The open reading frame (ORF) of CL-20 exhibits substantial sequence similarity to three cDNA sequences, Gas3 (23), SR13 (24), and PMP22 (25)(26)(27) encoding the mouse, rat, and human peripheral myelin protein, respectively. The peripheral myelin protein is highly expressed in peripheral nerves (25,26) and is induced in growth-arrested Balb/c3T3 cells (23).…”

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confidence: 99%

Identification and Characterization of a Novel Squamous Cell-associated Gene Related to PMP22

Marvin¹,

Fujimoto²,

Jetten³

1995

Journal of Biological Chemistry

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In this study, we identify and characterize a novel gene, CL-20, that encodes a 17.8-kDa protein with sequence and structural similarity to the growth arrestspecific gene gas3/peripheral myelin protein gene PMP22. The CL-20 protein exhibits a 43% identity with PMP22. The positions of the four lipophilic domains and the N-glycosylation site of PMP22 are conserved in CL-20, suggesting that it also is an integral membrane glycoprotein. The CL-20 gene is located on human chromosome 12 rather than 17 and encodes a 2.8-kilobase mRNA instead of 1.7-kilobase mRNA. These observations indicate that the CL-20 gene is related to but distinct from PMP22. In contrast to PMP22, CL-20 mRNA and protein are induced during squamous differentiation of rabbit tracheal epithelial cells in vitro, and Northern blot analysis and in situ hybridization demonstrated that CL-20 mRNA is most abundant in squamous epithelia. These results indicate that the high expression of CL-20 is closely correlated with squamous differentiation. The differences in tissue-specific expression and regulation between CL-20 and PMP22 suggest different roles for these two proteins. Retinoids, which inhibit squamous differentiation, repress the induction of CL-20. The retinoic acid receptor-selective retinoid SRI-6751-84 is the most effective in suppressing CL-20, suggesting that the activation of the retinoic acid receptor signaling pathway is important in this suppression.Squamous differentiation can be observed in many tissues including the trachea, bronchus, and skin. The lining of the trachea and bronchi normally consists of a pseudostratified columnar epithelium (1). During vitamin A deficiency or after toxic assault or mechanical injury (2-4), regions of the mucociliary epithelium are replaced by a stratified squamous epithelium. Tracheobronchial epithelial cells also undergo squamous differentiation when cultured in medium deficient in retinoids (5-7). In many respects, squamous differentiation in the tracheobronchial epithelial cells resembles differentiation in epidermal keratinocytes and other squamous differentiating tissues (8). The histologically distinct layers constituting the squamous epithelium (8) exhibit distinctive patterns of expression of specific genes and are evidence that squamous differentiation is a multistage process (5, 9, 10). Early in this differentiation process, cells irreversibly lose their proliferative potential and down-regulate the expression of the cell cycleassociated genes cdc2 and E2F-1 (11, 12). This is followed by the expression of squamous-specific genes such as transglutaminase type I (7, 13-15), the cross-linked envelope precursors involucrin, loricrin, and cornifin (16 -19), cholesterol sulfotransferase (20), and specific keratins (9, 21). These genes have been cloned and are shown to be regulated by a variety of agents including retinoids, which suppress the expression of squamous-specific genes (7-21).In this study, we describe the isolation and characterization of a cDNA CL-20 that was isolated from a cDNA libra...

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“…The incidence of HNPP is about 1 in 6250 [4]. CMT type 1 (CMT1A) and HNPP are autosomal dominant disorders caused by duplication or deletion of a 1.5 Mb genomic fragment of the PMP22 gene located at 17p11.2-12 [5][6][7]. CMT1A and HNPP are reciprocal products of the same unequal crossing-over recombination.…”

Section: Introductionmentioning

confidence: 99%

Identification of deletion and duplication genotypes of thePMP22gene using PCR‐RFLP, competitive multiplex PCR, and multiplex ligation‐dependent probe amplification: A comparison

et al. 2008

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We evaluated the efficacy of PCR-RFLP, competitive multiplex PCR, and a commercially available system of multiplex ligation-dependent probe amplification (MLPA) for the determination of deletion and duplication genotypes of the PMP22 gene. We compared the methods for efficiency, sensitivity, and specificity. We determined the gene dosage of the PMP22 gene via PCR-RFLP, competitive multiplex PCR, and MLPA. To demonstrate the sensitivity and accuracy of these three methods, a total of 185 samples from 42 patients with hereditary neuropathy with liability to pressure palsies (HNPP), 57 patients with Charcot-Marie-Tooth disease type 1A (CMT1A), and 86 unaffected individuals, were analyzed. Molecular diagnosis by PCR-RFLP was performed on all 185 samples; 24 HNPP deletions and 33 CMT1A duplications were identified. In contrast, 25 HNPP deletions and 38 CMT1A duplications were identified correctly using competitive multiplex PCR and MLPA. Six samples were incorrectly identified by PCR-RFLP (one HNPP deletion and five CMT1A duplications). Competitive multiplex PCR and MLPA demonstrated reliability and relative speed compared to PCR-RFLP; they were superior to PCR-RFLP for gene dosage quantification. Multiplex PCR and MLPA should be the methods of choice for detection of deletion and duplication genotypes in molecular genetic diagnoses.

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Isolation and mapping to 17p12 – 13 of the human homologous of the murine growth arrest specific Gas-3 gene

Cited by 11 publications

References 0 publications

COP‐1, a member of the CCN family, is a heparin‐induced growth arrest specific gene in vascular smooth muscle cells

COP‐1, a member of the CCN family, is a heparin‐induced growth arrest specific gene in vascular smooth muscle cells

Identification and Characterization of a Novel Squamous Cell-associated Gene Related to PMP22

Identification of deletion and duplication genotypes of thePMP22gene using PCR‐RFLP, competitive multiplex PCR, and multiplex ligation‐dependent probe amplification: A comparison

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