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C-Myc is a universal amplifier of gene expression [ChIP-Seq]

ABSTRACT: The c-Myc HLH-bZIP protein has been implicated in physiological or pathological growth, proliferation, apoptosis, metabolism and differentiation at the cellular, tissue or organismal levels via regulation of numerous target genes. In part due to the incomplete inventory and functional accounting of Myc’s targets, no principle unifies Myc action. To relate the dynamics of Myc-binding with target expression and function in a system where Myc-levels are temporally and physiologically regulated, the transcriptomes and the genome-wide distributions of Myc, RNA polymerase II and chromatin modifications were compared during lymphocyte activation and in ES cells. A remarkably simple rule emerged from this quantitative analysis: Myc is not an on-off switch, but is a non-linear amplifier of expression, acting universally at active genes, except for immediate early genes that are strongly induced before Myc. This rule of Myc action explains the vast majority of Myc biology observed in literature.

ORGANISM(S): Mus musculus

PROVIDER: GSE37229 | GEO | 2012/09/27

SECONDARY ACCESSION(S): PRJNA159017

REPOSITORIES: GEO

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c-Myc is a universal amplifier of gene expression [Microarray]

Project description:The c-Myc HLH-bZIP protein has been implicated in physiological or pathological growth, proliferation, apoptosis, metabolism and differentiation at the cellular, tissue or organismal levels via regulation of numerous target genes. In part due to the incomplete inventory and functional accounting of Myc’s targets, no principle unifies Myc action. To relate the dynamics of Myc-binding with target expression and function in a system where Myc-levels are temporally and physiologically regulated, the transcriptomes and the genome-wide distributions of Myc, RNA polymerase II and chromatin modifications were compared during lymphocyte activation and in ES cells. A remarkably simple rule emerged from this quantitative analysis: Myc is not an on-off switch, but is a non-linear amplifier of expression, acting universally at active genes, except for immediate early genes that are strongly induced before Myc. This rule of Myc action explains the vast majority of Myc biology observed in literature.

2012-09-27 | GSE37222 | GEO

c-Myc is a universal amplifier of gene expression [Microarray]

2012-09-27 | E-GEOD-37222 | biostudies-arrayexpress

c-Myc is a universal amplifier of gene expression [ChIP-Seq]

2012-09-27 | E-GEOD-37229 | biostudies-arrayexpress

c-Myc is a universal amplifier of gene expression

Project description:This SuperSeries is composed of the following subset Series: GSE37222: c-Myc is a universal amplifier of gene expression [Microarray] GSE37229: c-Myc is a universal amplifier of gene expression [ChIP-Seq] Refer to individual Series

2012-09-27 | E-GEOD-37230 | biostudies-arrayexpress

c-Myc is a universal amplifier of gene expression

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

2012-09-27 | GSE37230 | GEO

RNA clamping by Vasa assembles a piRNA Amplifier complex on transposon transcripts

Project description:Germline-specific Piwi-interacting RNAs (piRNAs) protect the genome against selfish genetic elements and are essential for fertility in animals. piRNAs targeting active transposons are amplified by a feed-forward loop known as the Ping-pong cycle, which links endonucleolytic slicing of target RNAs by Piwi proteins to biogenesis of new piRNAs. However, the biochemical framework for this pathway remains elusive. Here, we describe the identification of a transient Amplifier complex mediating the biogenesis of secondary piRNAs in insect cells. This complex is nucleated by the RNA helicase Vasa and contains the two Piwi proteins participating in the Ping-pong loop, the Tudor protein Qin/Kumo and antisense piRNA guides. These components assemble on the surface of Vasa's helicase domain, which functions as an RNA clamp to anchor Amplifier onto transposon transcripts. We show that ATP-dependent RNP remodelling by Vasa facilitates the transfer of 5'-sliced piRNA precursors between the Ping-pong partners, and failure to achieve this results in Drosophila female sterility. Immunoprecipitated small RNA were purified from untransfected or transfected Bmn4 cells for preparation of high-throughput sequencing libraries.

2014-06-04 | E-GEOD-57420 | biostudies-arrayexpress

RNA clamping by Vasa assembles a piRNA Amplifier complex on transposon transcripts

2014-06-04 | GSE57420 | GEO

Interventional hydrogel microsphere vaccine as an immune amplifier for activated antitumour immunity after ablation therapy

Project description:Current chemotherapy or immunotherapy regimens for pancreatic cancer are limited. Although minimally invasive irreversible electroporation (IRE) ablation is a promising option for unresectable pancreatic cancers, the typical immunosuppressive tumour microenvironment promotes immune evasion and rapid tumour recurrence. Thus, triggering efficient amplification of endogenous adaptive antitumour immunity is critical for improving immunotherapy after ablation therapy. Here, we developed a hydrogel microsphere vaccine as an immune amplifier for post-ablation cancer immunotherapy. The vaccine acts as a general immune amplifier to trigger a rocket-like amplification of the cDC1-mediated antigen cross-presentation cascade, resulting in dramatic amplification of the antitumour immunity of endogenous CD8+ T cells. We also showed that the hydrogel microsphere vaccine promoted the transformation of pancreatic cancer from "cold" to "hot" tumours in a safe and efficient manner, significantly increased the survival of mice bearing orthotopic pancreatic tumours, and induced strong systemic antitumour immunity, which inhibited the growth of distant metastases.

2023-05-22 | GSE215417 | GEO

Project description:c-Myc is a universal amplifier of gene expression

| PRJNA158957 | ENA

The polyamine-hypusine circuit controls an oncogenic translational program necessary for MYC-driven lymphomagenesis

Project description:MYC oncogenes are activated in broad spectrum of human malignancies and transcriptionally reprogram the genome to drive cancer cell growth. Given this it is unclear if targeting a single effector will have a therapeutic benefit. MYC activates the polyaminehypusine circuit, which post-translationally modifies the translation factor eIF5A. The hypusine axis has been proposed to suppress tumorigenesis. Here we report essential roles for hypusinated eIF5A in the development and maintenance of Myc-driven lymphoma, where loss of eIF5A hypusination abolishes malignant transformation. Mechanistically, integrating RNA-seq, Ribo-seq and proteomic analyses revealed that efficient translation of select targets is dependent upon eIF5A hypusination, including key regulators of G1 to S phase cell cycle progression. Notably, this circuit controls Myc’s proliferative response at several levels, and it is activated across multiple tumor types. These findings suggest the hypusine circuit as a therapeutic target for a broad spectrum of malignancies.

2024-01-26 | PXD031361 | Pride

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