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  • RASSF1A, BLU, NORE1A, PTEN and MGMT expression and promoter methylation in gliomas and glioma cell lines and evidence of deregulated expression of de novo DNMTs. 18616639

    Methylation of CpG islands in gene promoters can lead to gene silencing. Together with deletion or mutation, it may cause a loss of function of tumor suppressor genes. RASSF1A (3p21.3), NORE1A (1q32.1) and BLU (3p21.3) have been shown to be downregulated by methylation in cancer, and PTEN (10q23.3) and MGMT (10q26.1) are located in areas commonly deleted in astrocytomas. MGMT methylation predicts a better response and a longer overall survival in patients with glioblastomas treated with temozolomide. We analyzed 53 astrocytoma samples and 10 high-grade glioma cell lines. Gene expression was assessed by RT-PCR. Bisulfite sequencing, MSP and a melting curve analysis-based real-time PCR were performed to detect promoter methylation. Treatments with 5'-aza-2'-deoxicitidine were applied to restore gene expression in cell lines. Ninety-two percent of tumor samples were methylated for RASSF1A, 30%-57% for BLU and 47% for MGMT, suggesting promoter methylation of these genes to be a common event in glioma tumorigenesis. Only 4% of the tumors revealed a methylated promoter for NORE1A. No association between methylation and loss of expression could be established for PTEN. We identified de novo DNMTs overexpression in a subset of tumors which may explain the methylation phenotype of individual gliomas.
    Document Type:
    Reference
    Product Catalog Number:
    05-890

  • RASSF3 and NORE1: identification and cloning of two human homologues of the putative tumor suppressor gene RASSF1. 11965544

    RASSF1A, one of the two major isoforms of the putative tumor suppressor gene RASSF1, located at 3p21.3, is inactivated in a variety of human cancers including lung, breast, bladder and renal cell carcinomas. We have isolated and cloned two human homologues of this gene, RASSF3 and NORE1, located at 12q14.1 and 1q32.1, respectively. Both RASSF3 and NORE1 share almost 60% homology, at the amino acid level, with RASSF1. The RASSF3 gene contains five exons and encodes a 247 amino acid protein (MW of 28.6 kDa) with a highly conserved Ras association (RalGDS/AF-6) (RA) domain at the C-terminus. RASSF3 is ubiquitously expressed in all normal tissues and cancer cell lines analysed. NORE1, which is homologous to the previously described mouse Nore1 gene, exists in at least two spliced isoforms, A and B. Transcript A encodes a protein of 418 amino acids (MW or 47 kDa) while transcript B contains an ORF of 265 aa (MW of 30.5 kDa). Both share a RA domain, encoded by exons 3 through 6. NORE1A and NORE1B are expressed in most of the normal tissues analysed but they appear to be down-regulated in several cancer cell lines. However, contrary to RASSF1A, gene silencing by methylation of the CpG islands at which the two NORE1 transcripts initiate is not a common event in human primary tumors. RASSF3 and NORE1B are very similar, at the N-terminus, to the splice variant C of RASSF1 (RASSF1C), which does not seem to be involved in tumorigenesis. NORE1A is most closely related to RASSF1A, for sequence homology and genomic organization. However, aberrations in tumors have so far not been found. The presence of a Ras association domain common to NORE1, RASSF1, and RASSF3 suggests their possible involvement in Ras-like signaling pathways.
    Document Type:
    Reference
    Product Catalog Number:
    05-890

  • The dark side of Ras: regulation of apoptosis. 14663478

    Mutational activation of Ras promotes oncogenesis by disrupting a multitude of normal cellular processes. Perhaps, best characterized and understood are the mechanisms by which oncogenic Ras promotes deregulated cell cycle progression and uncontrolled cellular proliferation. However, it is now clear that oncogenic Ras can also deregulate processes that control apoptosis. In light of the diversity of downstream effector targets known to facilitate Ras function, it is perhaps not surprising that Ras regulation of cell survival is complex, involving the balance and interplay of multiple signaling networks. While our understanding of these events is still far from complete, and is complicated by cell type and signaling context differences, several important mechanisms have begun to emerge. We review the role and mechanism of specific effectors in regulating the antiapoptotic (Raf, phosphatidylinositol 3-kinase and Tiam1) and apoptotic (Nore1 and RASSF1) actions of oncogenic Ras, and discuss the possibility that the effector actions of p120RasGAP make a significant contribution to Ras regulation of apoptotic events.
    Document Type:
    Reference
    Product Catalog Number:
    05-890

  • Cell signaling: life or death decisions of ras proteins. 11937045

    The discovery of a new downstream target for the Ras GTPases - a Nore1-Mst1 protein complex - reveals a mechanism by which Ras can promote apoptosis, and suggests that the influence of Ras on cell survival or death depends upon the relative level of activation of its various target proteins.
    Document Type:
    Reference
    Product Catalog Number:
    05-890

  • Mesitylene (Iceland)

    Document Type:
    SDS
    Product Catalog Number:
    805890
    Product Catalog Name:
    Mesitylene (Mesitylene)

  • Mesitylene (India)

    Document Type:
    SDS
    Product Catalog Number:
    805890
    Product Catalog Name:
    Mesitylene (Mesitylene)

  • Mesitylene (Éire)

    Document Type:
    SDS
    Product Catalog Number:
    805890
    Product Catalog Name:
    Mesitylene (Mesitylene)