GABP, HCF‐1 and YY1 are involved in Rb gene expression during myogenesis

Deléhouzée, Sophie; Yoshikawa, Tatsufumi; Sawa, Chika; Sawada, Jun Ichi; Ito, Takumi; Omori, Masashi; Yamaguchi, Yuki; Kabe, Yoshio; Handa, Hiroshi

doi:10.1111/j.1365-2443.2005.00873.x

Cited by 43 publications

(44 citation statements)

References 31 publications

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“…In their study, they demonstrate before differentiation GABP and YY1 are present on the Rb promoter limiting the level of Rb expression. As cells advance through myogenesis, HCF-1 is recruited to, and YY1 is removed from, the promoter resulting in a sharp upregulation of Rb gene expression observed at day 2 of myogenesis (Delehouzee et al, 2005). This model for RB regulated myogenic differentiation is further supported by earlier studies investigating the effect of Rb deletion before and after myogenic differentiation (Huh et al, 2004).…”

Section: Rb and Neurogenesissupporting

confidence: 56%

RB, the conductor that orchestrates life, death and differentiation

Khidr

2006

Oncogene

104

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The retinoblastoma susceptibility gene was the first tumor suppressor gene identified in humans and the first tumor suppressor gene knocked out by targeted deletion in mice. RB serves as a transducer between the cell cycle machinery and promoter-specific transcription factors, its most documented activity being the repression of the E2F family of transcription factors, which regulate the expression of genes involved in cell proliferation and survival. Recent investigations of RB function suggest that it works as a fundamental regulator to coordinate pathways of cellular growth and differentiation. In this review, we unravel the novel role of an equally important aspect of RB in downregulating the differentiation inhibitor EID-1 during cellular differentiation by teasing apart the signal, which elicit differentiation and limit cell cycle progression, since the molecular mechanisms relating to RB activation of differentiation is much less understood. We review the various roles for RB in differentiation of neurons, muscle, adipose tissue, and the retina. In addition, we provide an update for the current models of the role of RB in cell cycle to entry and exit, extending the view toward chromatin remodeling and expose the dichotomies in the regulation of RB family members. We conclude with a discussion of a novel RB regulatory network, incorporating the dynamic contribution of EID family proteins.

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Section: Rb and Neurogenesissupporting

confidence: 56%

RB, the conductor that orchestrates life, death and differentiation

Khidr

2006

Oncogene

104

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“…YY1 has been functionally associated with multiple components of cell cycle signaling pathways, such as c-Myc (5,49,56), retinoblastoma protein (Rb) (12,46), and p53 (57), implicating YY1 in tumor development (19,23). Previous studies from our laboratory have also reported that YY1 is involved in cell cycle regulation, showing differential cellular localization and complex formation with DNA across the cell cycle (18,45).…”

mentioning

confidence: 77%

Phosphorylation of the Transcription Factor YY1 by CK2α Prevents Cleavage by Caspase 7 during Apoptosis

Riman

Rizkallah

Kassardjian

et al. 2012

Molecular and Cellular Biology

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In this report, we describe the phosphorylation of Yin Yang 1 (YY1) in vitro and in vivo by CK2␣ (casein kinase II), a multifunctional serine/threonine protein kinase. YY1 is a ubiquitously expressed multifunctional zinc finger transcription factor implicated in regulation of many cellular and viral genes. The products of these genes are associated with cell growth, the cell cycle, development, and differentiation. Numerous studies have linked YY1 to tumorigenesis and apoptosis. YY1 is a target for cleavage by caspases in vitro and in vivo as well, but very little is known about the mechanisms that regulate its cleavage during apoptosis. Here, we identify serine 118 in the transactivation domain of YY1 as the site of CK2␣ phosphorylation, proximal to a caspase 7 cleavage site. CK2␣ inhibitors, as well as knockdown of CK2␣ by small interfering RNA, reduce S118 phosphorylation in vivo and enhance YY1 cleavage under apoptotic conditions, whereas increased CK2␣ activity by overexpression in vivo elevates S118 phosphorylation. A serine-to-alanine substitution at serine 118 also increases the cleavage of YY1 during apoptosis compared to wild-type YY1. Taken together, we have discovered a regulatory link between YY1 phosphorylation at serine 118 and regulation of its cleavage during programmed cell death.

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“…Rb promoter binding was assessed through quantitative PCR using SYBR GreenER master mix (Invitrogen). Mouse Rb primers, described previously (14), were as follows: forward primer, 5Ј-CGCCGCGGGCGGAAGTG-3Ј; reverse primer, 5Ј-CTCA CCCGACTCCCGTTAC-3Ј; actin forward primer, 5Ј-GCTTCTTTGCAGCTC CTTCGTTG-3Ј; and actin reverse primer, 5Ј-TTTGCACATGCCGGAGCCGT TGT-3Ј. In the T98G cells, the mouse Rb primers were used to amplify the human promoter, due to sufficient conservation.…”

Section: Rosa26mentioning

confidence: 99%

Regulation of RB Transcription In Vivo by RB Family Members

Burkhart¹,

Ngai²,

Roake³

et al. 2010

Molecular and Cellular Biology

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In cancer cells, the retinoblastoma tumor suppressor RB is directly inactivated by mutation in the RB gene or functionally inhibited by abnormal activation of cyclin-dependent kinase activity. While variations in RB levels may also provide an important means of controlling RB function in both normal and cancer cells, little is known about the mechanisms regulating RB transcription. Here we show that members of the RB and E2F families bind directly to the RB promoter. To investigate how the RB/E2F pathway may regulate Rb transcription, we generated reporter mice carrying an eGFP transgene inserted into a bacterial artificial chromosome containing most of the Rb gene. Expression of eGFP largely parallels that of Rb in transgenic embryos and adult mice. Using these reporter mice and mutant alleles for Rb, p107, and p130, we found that RB family members modulate Rb transcription in specific cell populations in vivo and in culture. Interestingly, while Rb is a target of the RB/E2F pathway in mouse and human cells, Rb expression does not strictly correlate with the cell cycle status of these cells. These experiments identify novel regulatory feedback mechanisms within the RB pathway in mammalian cells.The RB tumor suppressor gene was first identified through its direct mutation or deletion in human retinoblastoma. The RB protein is thought to function largely as a transcriptional cofactor that can repress or potentiate the functions of numerous transcription factors, affecting the expression of a broad number of target genes. Since its initial discovery, RB function has been demonstrated to be inactivated in virtually all human cancers through a variety of mechanisms. In particular, in addition to direct mutation events in the RB gene, the RB protein is often functionally inactivated by phosphorylation in tumor cells with constitutive activation of cyclin/Cdk complexes (44,55). RB inactivation through reduced transcription may also participate in the development of cancer (4, 41); surprisingly, however, little is known about the mechanisms regulating RB transcription in normal and tumor cells.Interestingly, the RB promoter contains a conserved binding site for the E2F transcription factors, some of which are direct partners of RB and key downstream mediators of RB (9). Increasing evidence suggests that this site may contribute to the regulation of RB transcription. For instance, overexpression of E2F1 can activate RB transcription, which may contribute to the variations in RB mRNA levels during cell cycle progression that are observed in some contexts (30, 43) but not in others (5,13,20). In addition, methylation of the E2F site in the RB promoter is sufficient to recruit repressor complexes to inhibit RB transcription (15). Accordingly, reporter assays show that mutation of the E2F site in the RB promoter leads to an absence of RB repression (33). Furthermore, mutation of the E2F (and Sp1) sites in the mouse Rb promoter in transgenic mice has revealed the importance of these sites for Rb expression in vivo (1).Togeth...

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GABP, HCF‐1 and YY1 are involved in Rb gene expression during myogenesis

Cited by 43 publications

References 31 publications

RB, the conductor that orchestrates life, death and differentiation

RB, the conductor that orchestrates life, death and differentiation

Phosphorylation of the Transcription Factor YY1 by CK2α Prevents Cleavage by Caspase 7 during Apoptosis

Regulation of RB Transcription In Vivo by RB Family Members

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