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Hi-C of fibroblasts and germ cells from wild mice with Rb fusions

ABSTRACT: Hi-C of fibroblasts and germ cells from wild mice with Rb fusions

PROVIDER: PRJNA608908 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11186520_1.fastq.gz	Fastqsanger.gz
	SRR11186520_2.fastq.gz	Fastqsanger.gz
	SRR11186521_1.fastq.gz	Fastqsanger.gz
	SRR11186521_2.fastq.gz	Fastqsanger.gz
	SRR11186522_1.fastq.gz	Fastqsanger.gz

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Hi-C of fibroblasts and germ cells from wild mice with Rb fusions

Project description:Structural data of genome organization in somatic cells (fibroblasts) and germ cells (primary spermatocytes and round spermatids) from wild mice with Rb fusions from the Barcelona Rb System.

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Transcription profiling of mouse embryonic fibroblasts Rb-/- MEF (ME3) and Rb+/+ MEF (MEFA) during adipocyte differentiation

Project description:Gene expression of Retinoblastoma deficient mouse embryonic fibroblasts (Rb-/- MEF, ME3) and wildtype mouse embryonic fibroblasts (Rb+/+ MEF,MEFA) during adipocyte differentiation were studied by cDNA microarray analysis. 2-day postconfluent cells (day 0) were treated with a hormonal cocktail including Rosiglitzone for differentiation into adipocytes. Gene expression at day 1, day 3, and day 8 after hormonal induction were compared to that before induction (day 0).

2010-01-20 | E-MARS-12 | biostudies-arrayexpress

Expression data from mouse adult fibroblasts with Rb deletion and/or p53DD expression exposed to cisplatin (CDDP)

Project description:The RB and p53 tumor suppressor pathways regulate the transcription of genes involved in cell cycle progression, DNA replication, DNA repair, and apoptosis. These tumor suppressors are critical modulators of the response to genotoxic damage and both pathways are frequently inactivated in human cancers. We used microarrays to monitor gene expression patterns upon exposure to cisplatin treatment in fibroblasts harboring loss/inactivation of RB and/or p53. We generated mouse adult fibroblasts harboring loss/inactivation of RB and/or p53 and subjected these cell populations to cisplatin treatment for 24 hours. Treated cell populations were allowed to recover from cisplatin exposure, generating a recurred cell popuation. Untreated and recurred cell populations were then subjected to RNA extraction and hybridization on Affymetrix microarrays.

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Characterization of cancer-associated fibroblasts from ex vivo germ cell tumors

Project description:Cancer-associated fibroblasts (CAF) as one abundant cell type of the tumor microenvironment are known to have tumor supporting abilities by promoting tumor proliferation and modulating the immunal landscape. In this study, germ cell tumor-derived CAF were molecular and epigenetically characterized to identify CAF secreted signal molecules which play a pivotal role in the GCT-CAF interaction.

2024-11-15 | PXD049249 | Pride

Tissue-specific ChIP-seq of C. elegans Rb/E2F

Project description:The Rb/E2F tumor suppressor regulates gene expression to control the onset and timing of differentiation in many different cell types during development. This critical function makes Rb/E2F a frequent target for inactivation in tumors of diverse tissue origin. However, the mechanisms by which Rb/E2F governs tissue-specific gene regulation in vivo are poorly understood. We have determined the genome-wide binding profiles for components of the C. elegans Rb/E2F transcriptional regulatory pathway in the germ line, the intestine, and broadly in somatic tissues. Rb/E2F exhibits highly tissue-specific regulation, with unique sets of target genes that are activated or repressed depending on whether cells are in a progenitor (germ line) or terminally differentiated (somatic) state. In particular, LIN-35 binding is impaired in the germ line relative to the soma. Moreover, in the intestine, LIN-35 binds independently of EFL-1/DPL-1 at broad intergenic sites at which the heterochromatin protein HPL-2 also binds. Finally, recently defined âHOTâ sites, which are non-specifically bound by many unrelated factors, appear to be restricted primarily to somatic tissues, suggesting that germ line chromatin is in a state that globally restricts promiscuous association of regulatory factors. In sum, these tissue-specific binding profiles led to significant mechanistic insights into tissue-specific properties of Rb/E2F function in C. elegans that are likely relevant to other organisms.

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Expression data from mouse adult fibroblasts with Rb deletion and/or p53DD expression exposed to cisplatin (CDDP)

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Amycolatopsis mediterranei RB strain:RB

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Rickettsia honei RB strain:RB

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Pseudomonas aeruginosa RB strain:RB

Project description:Pseudomonas aeruginosa RB

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Localization of the Rb tumor suppressor in MEFs during reprogramming to iPS and the consequence of Rb loss on the transcriptional profile and histone landscape in these cells

Project description:The reprogramming of differentiated cells to an embryonic stem cell-like state provides a powerful system to explore fundamental mechanisms of development, including how mammalian cells establish and maintain pluripotency and long-term self-renewal capability. Based on the similarities between embryonic stem cells and cancer cells, we investigated the potential role of the retinoblastoma tumor suppressor and cell cycle regulator RB in the reprogramming of fibroblasts into induced pluripotent stem cells (iPS cells). Herein we demonstrate that loss of RB function leads to both an acceleration of the reprogramming process and the generation of more iPS clones from fibroblasts. This effect is largely due to a restrictive role for RB at the early stages of reprogramming. Surprisingly, however, RB inactivation does not enhance the formation of iPS clones by accelerating the proliferation of cells undergoing reprogramming. Rather, a genome-wide investigation of RB targets indicates that RB binds to regulatory regions of pluripotency genes such as Sox2 and Oct4 and contributes to their full repression in differentiated cells. This effect correlates with the maintenance of a repressive chromatin structure at these loci. Accordingly, Rb-deficient fibroblasts can be reprogrammed into iPS cells even in the absence of exogenous Sox2, which is normally required to initiate reprogramming from fibroblasts. These experiments identify a novel barrier in the reprogramming process, mainly the repression of certain pluripotency genes such as Sox2 by RB, which provides a new link between tumor suppressor mechanisms and cellular reprogramming.

2014-11-13 | GSE40594 | GEO

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