Roles for c-Myc in Self-renewal of Hematopoietic Stem Cells

Satoh, Yusuke; Matsumura, Itaru; Tanaka, Hirokazu; Ezoe, Sachiko; Sugahara, Hiroyuki; Mizuki, Masao; Shibayama, Hirohiko; Ishiko, Eri; Ishiko, Jun; Nakajima, Kōichi; Kanakura, Yuzuru

doi:10.1074/jbc.m400407200

Cited by 138 publications

(106 citation statements)

References 54 publications

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“…Two other Notch target genes, NRARP and Deltex-1 were shown to be potent negative regulators of Notch signaling [23,24]. Furthermore, Notch target genes implicated in cancer are c-myc [16,25,26], cyclinD1 [27] and p21/Waf1 [28]. Other Notch target genes are NFkB2 [29], Ifi-202, Ifi-204, Ifi-D3, and ADAM19 [19].…”

Section: Notch Target Genesmentioning

confidence: 99%

The Notch signaling pathway: Transcriptional regulation at Notch target genes

Borggrefe

Oswald

2009

Cell. Mol. Life Sci.

575

499

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. The Notch gene encodes a transmembrane receptor that gave the name to the evolutionary highly conserved Notch signaling cascade. It plays a pivotal role in the regulation of many fundamental cellular processes such as proliferation, stem cell maintenance and differentiation during embryonic and adult development. After specific ligand binding, the intracellular part of the Notch receptor is cleaved off and translocates to the nucleus, where it binds to the transcription factor RBP-J. In the absence of activated Notch, RBP-J represses Notch target genes by recruiting a corepressor complex. Here, we review Notch signaling with a focus on gene regulatory events at Notch target genes. This is of utmost importance to understand Notch signaling since certain RBP-J associated cofactors and particular epigenetic marks determine the specificity of Notch target gene expression in different cell types. We subsequently summarize the current knowledge about Notch target genes and the physiological significance of Notch signaling in development and cancer.

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Section: Notch Target Genesmentioning

confidence: 99%

The Notch signaling pathway: Transcriptional regulation at Notch target genes

Borggrefe

Oswald

2009

Cell. Mol. Life Sci.

575

499

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“…Specifically, retroviral transduction of MLL-ENL into wild type or Hoxa9 À/À primary myeloid progenitors revealed the necessity of Hoxa9 in MLL-ENL-mediated leukemogenesis . Moreover, MLL-ENL immortalization of myeloid progenitor cells could be substituted for by overexpression of HoxA9 and Meis1 (Zeisig et al, 2004), and was dependent on the activity of the oncoprotein c-Myc (Schreiner et al, 2001), a downstream effector of Hoxb4 that is sufficient to induce HSC self-renewal (Satoh et al, 2004). By contrast, analogous studies in a germline mouse model of Mll-AF9-mediated leukemogenesis suggest that Hoxa9 is not necessary for leukemia but does influence the phenotype of the leukemia (Kumar et al, 2004).…”

Section: Mll Fusion Genesmentioning

confidence: 99%

Hox genes in hematopoiesis and leukemogenesis

2007

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“…Many factors that regulate cell-cycle progression are mutated in cancer resulting in deregulated cellular growth. It has been demonstrated that Notch is involved in driving cell-cycle progression by regulating genes involved in the G 1 to S-phase transition (Ronchini and Capobianco, 2000;Satoh et al, 2004;Murata et al, 2005;Sharma et al, 2006;Weng et al, 2006). Notch directly regulates D-type cyclins, which, in conjunction with cyclin-dependent kinase (cdk) 4 and cdk6 facilitate progression through the G 1 phase (Ronchini and Capobianco, 2000).…”

Section: Notch Regulates Cell-cycle Progressionmentioning

confidence: 99%

“…Notch induces cell-cycle progression also through direct transactivation of c-myc (Satoh et al, 2004;Sharma et al, 2006;Weng et al, 2006). Normally, c-myc is only expressed in dividing cells and induces cell-cycle progression through induction of D-type cyclins, cyclin E, cdk4 and cdc25A, as well as repression of p27 expression (reviewed in Amati et al, 1998).…”

Section: Notch Regulates Cell-cycle Progressionmentioning

confidence: 99%