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A commonly inactivated tumor suppressor silences endogenous retroelements in somatic cells

ABSTRACT: A commonly inactivated tumor suppressor silences endogenous retroelements in somatic cells

PROVIDER: PRJNA338982 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1596430_1.fastq.gz	Fastqsanger.gz
	SRR1596430_2.fastq.gz	Fastqsanger.gz
	SRR1596440_1.fastq.gz	Fastqsanger.gz
	SRR1596440_2.fastq.gz	Fastqsanger.gz
	SRR1596431_1.fastq.gz	Fastqsanger.gz

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A commonly inactivated tumor suppressor silences endogenous retroelements in somatic cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-10-31 | GSE85640 | GEO

A commonly inactivated tumor suppressor silences endogenous retroelements in somatic cells [ChIP-Seq]

Project description:Upon G1-S transition, cyclin-dependent kinases (CDKs) phosphorylate the retinoblastoma tumor suppressor protein (pRB) to release E2F transcription factors, which activate transcriptional programs, required for S-phase entry. Beyond the G1-S transition, pRB activity remains poorly understood. Our lab has discovered that hyperphosphorylated pRB (ppRB), found beyond G1, retains exclusive binding to E2F1 through an alternate E2F1-‘specific’ binding site at the pRB c-terminus. We have developed a gene-targeted mouse model that is defective for the E2F1-‘specific’ interaction. We are exploring the function of this complex through genome-wide expression profiling. Overall, this work suggests an alternate pRB-E2F1 complex persists beyond the G1-S transition to establish regions of constitutive heterochromatin

2016-10-31 | GSE77993 | GEO

A commonly inactivated tumor suppressor silences endogenous retroelements in somatic cells [Affymetrix expression]

Project description:Upon G1-S transition, cyclin-dependent kinases (CDKs) phosphorylate the retinoblastoma tumor suppressor protein (pRB) to release E2F transcription factors, which activate transcriptional programs, required for S-phase entry. Beyond the G1-S transition, pRB activity remains poorly understood. Our lab has discovered that pRB retains exclusive binding to E2F1 through an alternate E2F1-‘specific’ binding site at the pRB c-terminus independent of CDK phosphorylation. We have developed a gene-targeted mouse model that is defective for the E2F1-‘specific’ interaction. We are exploring the function of this complex through genome-wide binding and expression profiling. Overall, this work suggests an alternate pRB-E2F1 complex persists independent of CDK phosphorylation to establish regions of constitutive heterochromatin

2016-10-31 | GSE85638 | GEO

A commonly inactivated tumor suppressor silences endogenous retroelements in somatic cells [ChIP-Seq]

Project description:Upon G1-S transition, cyclin-dependent kinases (CDKs) phosphorylate the retinoblastoma tumor suppressor protein (pRB) to release E2F transcription factors, which activate transcriptional programs, required for S-phase entry. Beyond the G1-S transition, pRB activity remains poorly understood. Our lab has discovered that pRB retains exclusive binding to E2F1 through an alternate E2F1-‘specific’ binding site at the pRB c-terminus independent of CDK phosphorylation. We have developed a gene-targeted mouse model that is defective for the E2F1-‘specific’ interaction. We are exploring the function of this complex through genome-wide binding and expression profiling. Overall, this work suggests an alternate pRB-E2F1 complex persists independent of CDK phosphorylation to establish regions of constitutive heterochromatin.

2016-10-31 | GSE85639 | GEO

Interplay of TRIM28 and DNA methylation in controlling human endogenous retroelements

Project description:Reverse transcription-derived sequences account for at least half of the human genome. Although these retroelements are formidable motors of evolution, they can occasionally cause disease, and accordingly are inactivated during early embryogenesis through epigenetic mechanisms. In the mouse, at least for endogenous retroviruses, important mediators of this process are the tetrapod-specific KRAB-containing zinc finger proteins (KRAB-ZFPs) and their cofactor TRIM28. The present study demonstrates that KRAB/TRIM28-mediated regulation is responsible for controlling a very broad range of human-specific endogenous retroelements (EREs) in human embryonic stem (ES) cells and that it exerts, as a consequence, a marked effect on the transcriptional dynamics of these cells. It further reveals reciprocal dependence between TRIM28 recruitment at specific families of EREs and DNA methylation. It finally points to the importance of persistent TRIM28-mediated control of ERE transcriptional impact beyond their presumed inactivation by DNA methylation. Analyses of epigentic effectors and marks in KAP1 WT and KD human embryonic stem cells

2014-05-29 | E-GEOD-57989 | biostudies-arrayexpress

Mus musculus

Project description:A commonly inactivated tumor suppressor silences endogenous retroelements in somatic cells [ChIP-Seq]

| PRJNA338977 | ENA

Mus musculus

Project description:A commonly inactivated tumor suppressor silences endogenous retroelements in somatic cells [ChIP-Seq]

| PRJNA312307 | ENA

Mus musculus

Project description:A commonly inactivated tumor suppressor silences endogenous retroelements in somatic cells [Affymetrix expression]

| PRJNA338976 | ENA

Interplay of TRIM28 and DNA methylation in controlling human endogenous retroelements

2014-05-29 | GSE57989 | GEO

TRIM28 silences endogenous retroviruses in neural progenitor cells

Project description:Here we show that in neural progenitor cells (NPCs) TRIM28 silences transcription of two groups of endogenous retroviruses (ERVs): IAP1 and MMERVK10C. Derepression of ERVs in Trim28-deficient NPCs was associated with a loss of H3K9me3 and resulted in transcriptional upregulation and reverse transcription. These findings demonstrate a unique dynamic transcriptional regulation of ERVs in NPCs. Analysis of upregulation of ERVs in Trim28-deficient NPCs

2015-01-07 | E-GEOD-45930 | biostudies-arrayexpress

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