Structure, Chromosomal Locus, and Promoter of MouseHes2Gene, a Homologue ofDrosophila hairyandEnhancer of split

Nishimura, Masataka; Isaka, Fumiaki; Ishibashi, Mākoto; Tomita, Koichi; Tsuda, Hiroshi; Nakanishi, Shigetada; Kageyama, Ryoichiro

doi:10.1006/geno.1998.5213

Cited by 120 publications

(124 citation statements)

References 32 publications

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“…Like other members of the human family, HES2 contains a bHLH domain, suggesting the ability to act as a transcription factor. The mouse ortholog of HES2 has been shown to bind to E-box and, with lower affinity, N-box regulatory sequences (Ishibashi et al, 1993); however, unlike other HES family members, mouse HES2 is not upregulated by the cellular differentiation factor Notch (Nishimura et al, 1998). Our studies found HES2 to be transcribed in most tissues surveyed, including brain and adrenal gland.…”

Section: Discussionmentioning

confidence: 51%

Definition and characterization of a region of 1p36.3 consistently deleted in neuroblastoma

et al. 2004

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Substantial genomic and functional evidence from primary tumors and cell lines indicates that a consistent region of distal chromosome 1p is deleted in a sizable proportion of human neuroblastomas, suggesting that this region contains one or more tumor suppressor genes. To determine systematically and precisely the location and extent of 1p deletion in neuroblastomas, we performed allelic loss studies of 737 primary neuroblastomas and genotype analysis of 46 neuroblastoma cell lines. Together, the results defined a single region within 1p36.3 that was consistently deleted in 25% of tumors and 87% of cell lines. Two neuroblastoma patients had constitutional deletions of distal 1p36 that overlapped the tumor-defined region. The tumor-and constitutionally-derived deletions together defined a smallest region of consistent deletion (SRD) between D1S2795 and D1S253. The 1p36.3 SRD was deleted in all but one of the 184 tumors with 1p deletion. Physical mapping and DNA sequencing determined that the SRD minimally spans an estimated 729 kb. Genomic content and sequence analysis of the SRD identified 15 characterized, nine uncharacterized, and six predicted genes in the region. The RNA expression profiles of 21 of the genes were investigated in a variety of normal tissues. The SHREW1 and KCNAB2 genes both had tissue-restricted expression patterns, including expression in the nervous system. In addition, a novel gene (CHD5) with strong homology to proteins involved in chromatin remodeling was expressed mainly in neural tissues. Together, these results suggest that one or more genes involved in neuroblastoma tumorigenesis or tumor progression are likely contained within this region.

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Section: Discussionmentioning

confidence: 51%

Definition and characterization of a region of 1p36.3 consistently deleted in neuroblastoma

et al. 2004

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“…Activation of RBP-J dependent promoters by Notch-IC: role of the TAD and the RAMANK domain HES-1 and HES-5 are well characterized target genes of Notch-IC (Takebayashi et al, 1994(Takebayashi et al, , 1995Nishimura et al, 1998). The promoters of both genes carry RBP-J recognition sites and are activated by Notch-IC signi®cantly, although to di erent degrees.…”

Section: Resultsmentioning

confidence: 99%

“…The Notch-IC/RBP-J interaction abolishes the repressor function of RBP-J and activates transcription. RBP-J response elements have been described in the promoter region of the mammalian HES-1 and HES-5 genes, which encode for mammalian helix ± loop ± helix factors structurally related to the Drosophila hairy and Enhancer of split proteins (Jarriault et al, 1995;Nishimura, 1998).…”

Section: Introductionmentioning

confidence: 99%

Neoplastic transformation by Notch is independent of transcriptional activation by RBP-J signalling

et al. 2000

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“…The cells were then transfected with 20 or 40 ng wildtype Hes-1 promoter construct (kindly provided by Dr Kageyama, Kyoto University, Japan) (Nishimura et al, 1998) using Lipofectamine 2000 (Life Technologies). After transfection the cells were treated with either 2.5 mM L-685,458, 1 or 2 mM VPA, or 50 or 100 nM TSA for 24 h where after cells were lysed and assayed for luciferase activity using the Dual-Luciferase Reporter Assay System according to the manufacturer's instructions (Promega).…”

Section: Luciferase Reporter Assaymentioning

confidence: 99%

Effects of the histone deacetylase inhibitor valproic acid on Notch signalling in human neuroblastoma cells

et al. 2005

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Neuroblastoma (NB), a sympathetically derived childhood tumour, shows characteristics of neuronal precursor cells, suggesting a halted differentiation process. We have previously shown that the Notch signalling cascade, a key player during normal neurogenesis, also might be involved in NB differentiation. Valproic acid (VPA), a well-tolerated antiepileptic drug, has been shown to induce differentiation and cell death of NB cells, possibly associated with its recently described HDAC inhibiting activity. Stimulation of NB cells with VPA led to increased cell death and phenotypic changes associated with differentiation, that is, neurite extension and upregulation of neuronal markers. VPA treatment also led to an activated Notch signalling cascade as shown by increased levels of intracellular Notch-1 and Hes-1, mimicking the initial phase of induced differentiation. These results reinforce that VPA potentially could be used in differentiation therapy of NB and that the effects in part could be a consequence of interference with the Notch signalling cascade.

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Structure, Chromosomal Locus, and Promoter of MouseHes2Gene, a Homologue ofDrosophila hairyandEnhancer of split

Cited by 120 publications

References 32 publications

Definition and characterization of a region of 1p36.3 consistently deleted in neuroblastoma

Definition and characterization of a region of 1p36.3 consistently deleted in neuroblastoma

Neoplastic transformation by Notch is independent of transcriptional activation by RBP-J signalling

Effects of the histone deacetylase inhibitor valproic acid on Notch signalling in human neuroblastoma cells

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