Cyclin D1 Represses the Basic Helix-Loop-Helix Transcription Factor, BETA2/NeuroD

Ratineau, Christelle; Petry, Mary; Mutoh, Hiroyuki; Leiter, Andrew B.

doi:10.1074/jbc.m110747200

Cited by 76 publications

(60 citation statements)

References 31 publications

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“…In contrast to its canonical role in the cell cycle as a cofactor for certain cyclin-dependent kinases (CDKs), in other models (58,59), in some cases cyclin D1 acts as a transcriptional coactivator promoting or suppressing gene expression, apparently independently of CDKs (60). Furthermore, certain cyclin-CDK complexes participate in splicing as well as transcription (61) and thus may alter gene expression in cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Monoallelic loss of tumor suppressor GRIM-19 promotes tumorigenesis in mice

Kalakonda¹,

Nallar²,

Jaber

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Significance Gene-associated with retinoid-interferon induced mortality-19 (GRIM-19) is an interferon-retinoid–regulated growth suppressor that inhibits cell growth by targeting the transcription factor STAT3 for inhibition. In primary human tumors GRIM-19 is suppressed or mutated, leading to constitutive STAT3 activity and indicating the tumor-suppressive function of GRIM-19. To understand the in vivo role of Grim-19 in tumor development, we generated a Grim-19 conditional knockout mouse. We found that deletion of even a single Grim-19 allele is sufficient to augment skin tumorigenesis in mice, thus establishing a critical role for Grim-19 as a tumor suppressor. Tumors that developed in the absence of Grim-19 exhibited mitochondrial respiratory chain dysfunction, elevated glycolysis, and Stat3-responsive gene expression.

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Section: Discussionmentioning

confidence: 99%

Monoallelic loss of tumor suppressor GRIM-19 promotes tumorigenesis in mice

Kalakonda¹,

Nallar²,

Jaber

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…Subsequent studies strikingly demonstrated that cyclin D1 is a modifier of gene transcription, and that this function of cyclin D1 has important implications in tumor biology. Specifically, cyclin D1 has been shown to regulate a number of sequence-specific transcription factors, including C/EBPb (Lamb et al, 2003), STAT3 (Bienvenu et al, 2001), DMP1 (Inoue and Sherr, 1998), and BETA2/NeuroD (Ratineau et al, 2002). The largest class of transcription factors regulated by cyclin D1 belong to the nuclear receptor superfamily, and include the estrogen receptor (Zwijsen et al, 1998;Lamb et al, 2000), androgen receptor (Knudsen et al, 1999;Reutens et al, 2001;Petre et al, 2002;Burd et al, 2005), thyroid hormone receptor (Pibiri et al, 2001), and peroxisome proliferator activated receptor-g (Qin et al, 2003).…”

Section: Cell Cyclementioning

confidence: 99%

Cyclin D1: polymorphism, aberrant splicing and cancer risk

et al. 2006

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The cyclin D1 proto-oncogene exercises powerful control over the mechanisms that regulate the mitotic cell cycle, and excessive cyclin D1 expression and/or activity is common in human cancers. Although somatic mutations of the cyclin D1 locus are rarely observed, mounting evidence demonstrates that a specific polymorphism of cyclin D1 (G/A870) and a protein product of a potentially related alternate splicing event (cyclin D1b) may influence cancer risk and outcome. Herein, we review the epidemiological and functional literatures that link these alterations of cyclin D1 to human tumor development and progression.

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“…There are many other reports showing that cell cycle regulators may function as cell fate determinants by a role independent of cell cycle regulation. 20,21,43,44 Furthermore, another detailed analysis suggests that not only G 1 -phase but also S-phase is correlated with the differentiation state of NSPCs. 38 Thus, the physiological functions of cyclin D2 in aspects of fate determination in vivo still remain to be elucidated.…”

Section: Cyclin D2 and Mammalianmentioning

confidence: 99%

How to keep proliferative neural stem/progenitor cells

Tsunekawa

Osumi

2012

Cell Cycle

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I t has long been argued that cell cycle regulators such as cyclins, cyclindependent kinases and their inhibitors affect the fate of neuronal progenitor cells. Recently, we identified that cyclin D2, which localizes at the basal tip of the radial glial cell (i.e., the neural progenitor in the developing neocortex), functions to give differential cell fates to its daughter cells just after cell division. This basally biased localization is due to transportation of cyclin D2 mRNA via its unique cis-regulatory sequence and local translation into cyclin D2 protein at the basal endfoot. During division of the neural progenitor cells, cyclin D2 protein is inherited by the daughter cell that retain the basal process, resulting in asymmetric distribution of cyclin D2 protein between the two daughter cells. Cyclin D2 is similarly localized in the human fetal cortical primordium, suggesting a common mechanism for the maintenance of neural progenitors and a possible scenario in evolution of primate brains. Here we introduce our recent findings and discuss how cyclin D2 functions in mammalian brain development and evolution.

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Cyclin D1 Represses the Basic Helix-Loop-Helix Transcription Factor, BETA2/NeuroD

Cited by 76 publications

References 31 publications

Monoallelic loss of tumor suppressor GRIM-19 promotes tumorigenesis in mice

Monoallelic loss of tumor suppressor GRIM-19 promotes tumorigenesis in mice

Cyclin D1: polymorphism, aberrant splicing and cancer risk

How to keep proliferative neural stem/progenitor cells

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