Roles of pRB in the Regulation of Nucleosome and Chromatin Structures

Uchida, Chiharu

doi:10.1155/2016/5959721

Cited by 32 publications

(27 citation statements)

References 128 publications

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“…Passage of the restriction point requires activation of E2F-DP, which transcribes many cell cycle genes [58][59][60][61][62][63]. Rb binding to the E2F-DP heterodimer is known to convert E2F-DP from a potent transcription activator to a potent transcription repressor [64][65][66]. Only hypophosphorylated Rb binds to the E2F-DP heterodimer [67][68][69][70].…”

Section: Discussionmentioning

confidence: 99%

EDMD-Causing Emerin Mutant Myogenic Progenitors Exhibit Impaired Differentiation Using Similar Mechanisms

Iyer

Holaska

2020

Cells

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Mutations in the gene encoding emerin (EMD) cause Emery–Dreifuss muscular dystrophy (EDMD1), an inherited disorder characterized by progressive skeletal muscle wasting, irregular heart rhythms and contractures of major tendons. The skeletal muscle defects seen in EDMD are caused by failure of muscle stem cells to differentiate and regenerate the damaged muscle. However, the underlying mechanisms remain poorly understood. Most EDMD1 patients harbor nonsense mutations and have no detectable emerin protein. There are three EDMD-causing emerin mutants (S54F, Q133H, and Δ95–99) that localize correctly to the nuclear envelope and are expressed at wildtype levels. We hypothesized these emerin mutants would share in the disruption of key molecular pathways involved in myogenic differentiation. We generated myogenic progenitors expressing wildtype emerin and each EDMD1-causing emerin mutation (S54F, Q133H, Δ95–99) in an emerin-null (EMD−/y) background. S54F, Q133H, and Δ95–99 failed to rescue EMD−/y myogenic differentiation, while wildtype emerin efficiently rescued differentiation. RNA sequencing was done to identify pathways and networks important for emerin regulation of myogenic differentiation. This analysis significantly reduced the number of pathways implicated in EDMD1 muscle pathogenesis.

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Section: Discussionmentioning

confidence: 99%

EDMD-Causing Emerin Mutant Myogenic Progenitors Exhibit Impaired Differentiation Using Similar Mechanisms

Iyer

Holaska

2020

Cells

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“…Consequently, its dysregulation is directly linked to uncontrolled cell growth and carcinogenesis. 61 de Oliveira et al 62 evaluated the expression of p53 and pRb in oral malignant and premalignant lesions. They showed that compared with premalignant lesions, OSCC presented higher expression of the pRb, whereas the former presented higher expression of p53 compared with OSCC lesions.…”

Section: Cell Cycle Proliferation and Apoptosis-related Moleculesmentioning

confidence: 99%

Molecular markers associated with development and progression of potentially premalignant oral epithelial lesions: Current knowledge and future implications

Nikitakis

Pentenero

Georgaki

et al. 2018

Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology

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Identification and management of potentially premalignant oral epithelial lesions (PPOELs) at highest risk of malignant transformation holds great promise for successful secondary prevention of oral squamous cell carcinoma, potentially reducing oral cancer morbidity and mortality. However, to date, neither clinical nor histopathologic validated risk predictors that can reliably predict which PPOELs will definitively progress to malignancy have been identified. In addition, the management of PPOELs remains a major challenge. Arguably, progress in the prevention and treatment of oral premalignancy and cancer will require improved understanding of the underlying molecular mechanisms, facilitating the discovery of diagnostic, prognostic, and predictive markers, as well as the identification of novel targeted therapeutics. This review provides a synopsis of the molecular biomarkers that have been studied in PPOELs and have been correlated with the presence and grade of dysplasia and/or their propensity to undergo malignant transformation to oral squamous cell carcinoma. The emphasis is on highlighting new emerging research fields, particularly epigenetic events, including methylation and micro-RNA regulation. Several promising biomarkers are highlighted. Current limitations and challenges are discussed. Recommendations for future focused research areas, to validate and promote clinically useful applications, are offered.

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“…More than 1000 cell cycle-dependent genes have been identified in genome-wide screens (Whitfield et al 2002, Bar-Joseph et al 2008, Sadasivam et al 2012, Grant et al 2013, Peña-Diaz et al 2013, Macosko et al 2015, Dominguez et al 2016, Fischer et al 2016a, Liu et al 2017, and expression of most of these is nearly absent in G0 cells. For the most part, expression of cell cycle-dependent genes is regulated by the RB (retinoblastoma) pocket protein family (van den Heuvel and Dyson 2008), the E2F (adenovirus early gene 2 binding factor) transcription factor family (Rowland andBernards 2006, Chen et al 2009), and MuvB (multi-vulva class B) complexes (Sadasivam and DeCaprio 2013). In recent years, it has become evident that distinct combinations of these transcription factors promote the expression of the two major classes of cell cycle genes that show peak expression either in G1/S or in G2/M.…”

Section: Introductionmentioning

confidence: 99%

Cell cycle transcription control: DREAM/MuvB and RB-E2F complexes

Fischer

Müller

2017

Critical Reviews in Biochemistry and Molecular Biology

190

250

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The precise timing of cell cycle gene expression is critical for the control of cell proliferation; de-regulation of this timing promotes the formation of cancer and leads to defects during differentiation and development. Entry into and progression through S phase requires expression of genes coding for proteins that function in DNA replication. Expression of a distinct set of genes is essential to pass through mitosis and cytokinesis. Expression of these groups of cell cycle-dependent genes is regulated by the RB pocket protein family, the E2F transcription factor family, and MuvB complexes together with B-MYB and FOXM1. Distinct combinations of these transcription factors promote the transcription of the two major groups of cell cycle genes that are maximally expressed either in S phase (G1/S) or in mitosis (G2/M). In this review, we discuss recent work that has started to uncover the molecular mechanisms controlling the precisely timed expression of these genes at specific cell cycle phases, as well as the repression of the genes when a cell exits the cell cycle.

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Roles of pRB in the Regulation of Nucleosome and Chromatin Structures

Cited by 32 publications

References 128 publications

EDMD-Causing Emerin Mutant Myogenic Progenitors Exhibit Impaired Differentiation Using Similar Mechanisms

EDMD-Causing Emerin Mutant Myogenic Progenitors Exhibit Impaired Differentiation Using Similar Mechanisms

Molecular markers associated with development and progression of potentially premalignant oral epithelial lesions: Current knowledge and future implications

Cell cycle transcription control: DREAM/MuvB and RB-E2F complexes

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