Cloning and Characterization of a Gene (RFN22) Encoding a Novel Brain Expressed Ring Finger Protein (BERP) That Maps to Human Chromosome 11p15.5

El-Husseini, Alaa; Fretier, Pascale; Vincent, Steven R.

doi:10.1006/geno.2000.6452

Cited by 23 publications

(14 citation statements)

References 15 publications

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“…Potential human orthologs of Drosophila brat , based on sequence homology, include TRIM2 [36], TRIM3 [19, 22], TRIM32 [37] and TRIM71 [38], located on chromosomes 4q31.3, 11p15.5, 9q33.1 and 3p22.3, respectively. We focused our investigations on TRIM3 as the human ortholog because: 1) TRIM3 has the highest homology to Drosophila brat [10] (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…TRIM gene clusters are located on chromosomes 1, 4, 5, 6, 7, 11 and 17, and genes for more than 70 TRIM proteins that have been identified thus far[21]. TRIM3 was first identified and characterized as a brain-enriched RING finger protein (BERP) with its gene localized to chromosome 11p15.5 [22]. In this study, we provide functional evidence that TRIM3 is a tumor suppressor in human GBM cell lines, patient-derived neurospheres and in in vivo xenografts.…”

Section: Introductionmentioning

confidence: 99%

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Human Brat Ortholog TRIM3 Is a Tumor Suppressor That Regulates Asymmetric Cell Division in Glioblastoma

et al. 2014

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Cancer stem cells, capable of self-renewal and multipotent differentiation, influence tumor behavior through a complex balance of symmetric and asymmetric cell divisions. Mechanisms regulating the dynamics of stem cells and their progeny in human cancer are poorly understood. In Drosophila, mutation of brain tumor (brat) leads to loss of normal asymmetric cell division by developing neural cells and results in a massively enlarged brain composed of neuroblasts with neoplastic properties. Brat promotes asymmetric cell division and directs neural differentiation at least partially through its suppression on Myc. We identified TRIM3 (11p15.5) as a human ortholog of Drosophila brat and demonstrate its regulation of asymmetric cell division and stem cell properties of glioblastoma (GBM), a highly malignant human brain tumor. TRIM3 gene expression is markedly reduced in human GBM samples, neurosphere cultures and cell lines and its reconstitution impairs growth properties in vitro and in vivo. TRIM3 expression attenuates stem-like qualities of primary GBM cultures, including neurosphere formation and the expression of stem cell markers CD133, Nestin and Nanog. In GBM stem cells, TRIM3 expression leads to a greater percentage dividing asymmetrically rather than symmetrically. As with Brat in Drosophila, TRIM3 suppresses c-Myc expression and activity in human glioma cell lines. We also demonstrate a strong regulation of Musashi-Notch signaling by TRIM3 in GBM neurospheres and neural stem cells that may better explain its effect on stem cell dynamics. We conclude that TRIM3 acts as a tumor suppressor in GBM by restoring asymmetric cell division.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Human Brat Ortholog TRIM3 Is a Tumor Suppressor That Regulates Asymmetric Cell Division in Glioblastoma

et al. 2014

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“…Considering the level of gene and pathway conservation, the similarity of cellular processes, and the emerging evidence of functional conservation of Drosophila genes that are homologous to mammalian oncogenes or tumor suppressor genes [16,17], we wondered whether our data might reveal any parallels to the genetic alterations associated with mammalian cancer formation. This is of particular interest since one of the two human homologs of brat , TRIM3, has been mapped to chromosome 11p15 [75,76], a region that has been termed the "multiple tumor-associated chromosomal region 1" due to the presence of numerous cancer-related genes in this region [77,78]. …”

Section: Resultsmentioning

confidence: 99%

Transcriptional signature of an adult brain tumor in Drosophila

et al. 2004

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Background: Mutations and gene expression alterations in brain tumors have been extensively investigated, however the causes of brain tumorigenesis are largely unknown. Animal models are necessary to correlate altered transcriptional activity and tumor phenotype and to better understand how these alterations cause malignant growth. In order to gain insights into the in vivo transcriptional activity associated with a brain tumor, we carried out genome-wide microarray expression analyses of an adult brain tumor in Drosophila caused by homozygous mutation in the tumor suppressor gene brain tumor (brat).

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“…The gene for BERP is mapped to chromosome 11p15, which is frequently deleted in several human cancers and is speculated to be a tumor suppressor gene (46). However, the exact molecular functions of these cytoplasmic RBCC proteins remain to be elucidated.…”

Section: Tissue Distribution and M-csf-induced Expression Ofmentioning

confidence: 99%

Cloning and Characterization of a Novel RING-B-box-Coiled-coil Protein with Apoptotic Function

Kimura

Suzu

Nakamura

et al. 2003

Journal of Biological Chemistry

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We have identified a novel RING-B-box-coiled-coil (RBCC) protein (MAIR for macrophage-derived apoptosis-inducing RBCC protein) that consists of an Nterminal RING finger, followed by a B-box zinc finger, a coiled-coil domain, and a B30.2 domain. MAIR mRNA was expressed widely in mouse tissues and was induced by macrophage colony-stimulating factor in murine peritoneal and bone marrow macrophages. MAIR protein initially showed a granular distribution predominantly in the cytoplasm. The addition of zinc to transfectants containing MAIR cDNA as part of a heavy metalinducible vector caused apoptosis of the cells characterized by cell fragmentation; a reduction in mitochondrial membrane potential; activation of caspase-7, -8, and -9, but not caspase-3; and DNA degradation. We also found that the RING finger and coiled-coil domains were required for MAIR activity by analysis with deletion mutants.

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Cloning and Characterization of a Gene (RFN22) Encoding a Novel Brain Expressed Ring Finger Protein (BERP) That Maps to Human Chromosome 11p15.5

Cited by 23 publications

References 15 publications

Human Brat Ortholog TRIM3 Is a Tumor Suppressor That Regulates Asymmetric Cell Division in Glioblastoma

Human Brat Ortholog TRIM3 Is a Tumor Suppressor That Regulates Asymmetric Cell Division in Glioblastoma

Transcriptional signature of an adult brain tumor in Drosophila

Cloning and Characterization of a Novel RING-B-box-Coiled-coil Protein with Apoptotic Function

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