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ABSTRACT: MYC assembles and stimulates topoisomerases 1 & 2 in a "topisome"

PROVIDER: PRJNA667145 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12767541.fastq.gz	Fastqsanger.gz
	SRR12767542.fastq.gz	Fastqsanger.gz
	SRR13426398.fastq.gz	Fastqsanger.gz
	SRR13426399.fastq.gz	Fastqsanger.gz

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Similar Datasets

MYC assembles and stimulates topoisomerases 1 & 2 in a “topisome”

Project description:MYC assembles and stimulates topoisomerases 1 & 2 in a “topisome”

| PRJNA752089 | ENA

MYC assembles and stimulates topoisomerases 1 & 2 in a “topisome” [ChIP-seq]

Project description:MYC assembles and stimulates topoisomerases 1 & 2 in a “topisome” [ChIP-seq]

| PRJNA752097 | ENA

MYC assembles and stimulates topoisomerases 1 & 2 in a “topisome” [CAD-seq]

Project description:MYC assembles and stimulates topoisomerases 1 & 2 in a “topisome” [CAD-seq]

| PRJNA752096 | ENA

MYC assembles and stimulates topoisomerases 1 & 2 in a “topisome” [cross-CAD-seq]

Project description:MYC assembles and stimulates topoisomerases 1 & 2 in a “topisome” [cross-CAD-seq]

| PRJNA752095 | ENA

MYC assembles and stimulates topoisomerases 1 & 2 in a “topisome” [cross-CAD-seq]

Project description:High-intensity transcription and replication supercoil DNA to levels that can impede or halt these processes. As a potent transcription amplifier and replication accelerator, the proto-oncogene MYC must somehow manage these high levels of torsional stress. By comparing gene expression with the recruitment of topoisomerases and MYC to promoters, we surmised a direct association of MYC with Topoisomerases 1 (TOP1) and 2A (TOP2A) that was confirmed in vitro and in vivo. Beyond recruiting topoisomerases, MYC directly stimulates their activities in vitro and in vivo. We identify a MYC-nucleated “topoisome” complex that unites and increases the levels of both both TOP1 and TOP2, as well as their activities at promoters and enhancers. Whether TOP2A or TOP2B is included in the topoisome, is dictated by the presence of c-MYC or MYCN, respectively. Thus, in vivo and in vitro, MYC assembles tools that simplify DNA topology and promote genome function under high output conditions.

2021-12-09 | GSE181449 | GEO

MYC assembles and stimulates topoisomerases 1 & 2 in a “topisome” [CAD-seq]

2021-12-09 | GSE181448 | GEO

MYC assembles and stimulates topoisomerases 1 & 2 in a “topisome” [ChIP-seq]

2021-12-09 | GSE181447 | GEO

Analysis of MYC in murine lymphoma cell lines

Project description:This SuperSeries is composed of the following subset Series: GSE12278: MYC stimulates EZH2 expression by repression of its negative regulator miR-26a GSE12394: murine MYC-dependent lymphoma cells: Dox vs. NoDox treatment Refer to individual Series

2010-05-25 | E-GEOD-12400 | biostudies-arrayexpress

A p53-topoisome replaces the acutely genotoxic MYC- topoisome to empower DNA-damage repair in cells

Project description:Hyperproliferation driven by the protooncogene MYC has been presumed to elicit a chain of event that leads to DNA damage and activates the tumor suppressor p53 response. This DNA damage has been presumed to derive from hypertranscription and overreplication. Here, we report that MYC-topoisome (MYC/Topoisomerase 1/Topoisomerase 2) formation is genotoxic within minutes of its formation. Topoisome mediated damage activates pATM and p53, that in turn shuts off MYC and dissociates the topoisome in vitro and in vivo. To manage topological and torsional stress generated at its targets, p53 assembles its own topoisome. Because topoisomerase activity is intrinsically DNA-damaging, the p53-topoisome creates initial burst of DNA damage but, because p53 (unlike MYC) upregulates the DNA damage response and activates TDP1 and TDP2, this damage is quickly suppressed. The novel coupling of TOP1 and TOP2 sponsored by p53, creates a tool to support the expression of p53 targets while braking MYC-accelerated cell growth.

2024-10-30 | GSE243792 | GEO

Ubiquitin-dependent turnover of MYC promotes loading of the PAF complex on RNA Polymerase II to drive transcriptional elongation (ChIP-seq)

Project description:The MYC transcription factor is an unstable protein and its turnover is controlled by the ubiquitin system. Ubiquitination enhances MYC-dependent transactivation, but the underlying mechanism remains unresolved. Here we show that proteasomal turnover of MYC is dispensable for recruitment of RNA polymerase II (RNAPII), but is required to promote transcriptional elongation at MYC target genes. Degradation of MYC stimulates histone acetylation and recruitment of BRD4 and P-TEFb to target promoters, leading to phosphorylation of RNAPII CTD and the release of elongating RNAPII. In the absence of degradation, the RNA polymerase II-associated factor (PAF) complex associates with MYC via interaction of its CDC73 subunit with a conserved domain in the amino-terminus of MYC ("MYC box I"), suggesting that a MYC/PAF complex is an intermediate in transcriptional activation. Since histone acetylation depends on a second highly conserved domain in MYCs amino-terminus ("MYC box II"), we propose that both domains co-operate to transfer elongation factors onto paused RNAPII. ChIP-Seq experiments for MYC-HA (HA-IP) and RNAPII (total,Ser2p,Ser5p) performed in IMEC primary breast epithelial cells. Input-samples were sequenced as controls. The following antibodies were used: HA (Abcam; ab 9110)/ total RNAPII (Santa Cruz; sc-899x)/ Ser2p RNAPII (Abcam; ab 5095)/ Ser5p RNAPII (Covance; MMS-128P)

2016-01-04 | E-GEOD-70001 | biostudies-arrayexpress

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