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MYC S146L is a context-dependent activating substitution in cancer development [CUT&TAG]

ABSTRACT: MYC S146L is a context-dependent activating substitution in cancer development [CUT&TAG]

PROVIDER: PRJNA809749 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18116710_1.fastq.gz	Fastqsanger.gz
	SRR18116710_2.fastq.gz	Fastqsanger.gz
	SRR18116711_1.fastq.gz	Fastqsanger.gz
	SRR18116711_2.fastq.gz	Fastqsanger.gz
	SRR18116712_1.fastq.gz	Fastqsanger.gz

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MYC S146L is a context-dependent activating substitution in cancer development

Project description:MYC S146L is a context-dependent activating substitution in cancer development

| PRJNA809750 | ENA

MYC S146L is a context-dependent activating substitution in cancer development [RNA-seq]

Project description:MYC S146L is a context-dependent activating substitution in cancer development [RNA-seq]

| PRJNA809740 | ENA

MYC S146L is a context-dependent activating substitution in cancer development [CUT&TAG]

Project description:MYC is one of the most dysregulated oncogenes and is thought to be fundamental to tumor formation and/or maintenance in many cancer types. This dominant pro-tumor activity makes MYC an attractive target for cancer therapy. However, MYC is a transcription factor lacking enzymatic activity, and the structure of one of its two domains is unknown e.g., its transactivation domain. Consequently, few direct MYC-targeting therapies have been developed, and none have been successful in the clinic. Nevertheless, significant effort has been devoted to understanding the mechanisms of oncogenic MYC activity with the objective of uncovering novel vulnerabilities of MYC-dependent cancers. These extensive investigations have revealed in detail how MYC translocation, amplification, and other upstream perturbations contribute to MYC activity in cancer. However, missense mutations of the MYC gene have remained relatively understudied for their potential role in MYC-mediated oncogenesis. While the function of several low-frequency mutations in MYC have been described, our understanding of other equally or more frequent mutations is incomplete. Herein, we define the function of a recurrent missense mutation in MYC resulting in the substitution S146L. This mutation reinforces the interaction between MYC and its cofactor TRRAP and may enhance oncogenic MYC activity in certain cellular contexts. Implication: our results fortify the mechanistic understanding of oncogenic MYC and may indicate a novel prognostic marker for patients whose tumors harbor the somatic mutation resulting in MYC S146L.

2022-07-31 | GSE197327 | GEO

MYC S146L is a context-dependent activating substitution in cancer development [RNA-seq]

2022-07-31 | GSE197323 | GEO

Mediator Subunit 30 Directs Myc Oncogenesis [Cut&Tag]

Project description:Mediator Subunit 30 Directs Myc Oncogenesis [Cut&Tag]

2023-11-08 | GSE217545 | GEO

S146L in MYC is a context-dependent activating substitution in cancer development.

Project description:MYC is one of the most dysregulated oncogenes and is thought to be fundamental to tumor formation and/or maintenance in many cancer types. This dominant pro-tumor activity makes MYC an attractive target for cancer therapy. However, MYC is a transcription factor lacking enzymatic activity, and the structure of one of its two domains is unknown e.g., its transactivation domain. Consequently, few direct MYC-targeting therapies have been developed, and none have been successful in the clinic. Nevertheless, significant effort has been devoted to understanding the mechanisms of oncogenic MYC activity with the objective of uncovering novel vulnerabilities of MYC-dependent cancers. These extensive investigations have revealed in detail how MYC translocation, amplification, and other upstream perturbations contribute to MYC activity in cancer. However, missense mutations of the MYC gene have remained relatively understudied for their potential role in MYC-mediated oncogenesis. While the function of several low-frequency mutations in MYC have been described, our understanding of other equally or more frequent mutations is incomplete. Herein, we define the function of a recurrent missense mutation in MYC resulting in the substitution S146L. This mutation enhances the interaction between MYC and its cofactor TRRAP and may enhance oncogenic MYC activity in certain cellular contexts.

| S-EPMC9417018 | biostudies-literature

POH1 regulates MYC in pancreatic cancer cells [CUT&TAG]

Project description:CUT&Tag experiments were used to analyze DNA-binding of MYC protein in the vector or POH1-Flag expressed mouse pancreatic cancer cells.

2024-11-01 | GSE217221 | GEO

MYC S146L is a context-dependent activating substitution in cancer development

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

2022-07-31 | GSE197330 | GEO

HCT116_SMARCA4 CUT&Tag

Project description:HCT116_SMARCA4 CUT&Tag

| PRJNA875063 | ENA

scNanoSeq-CUT&Tag: a long-read single-cell CUT&Tag sequencing method for efficient chromatin modification profiling within individual cells

Project description:We developed scNanoSeq-CUT&Tag, a streamlined method by adapting a modified CUT&Tag protocol to Oxford Nanopore sequencing platform for efficient chromatin modification profiling at single-cell resolution. We firstly tested the performance of scNanoSeq-CUT&Tag on six human cell lines: K562, 293T, GM12878, HG002, H9, HFF1 and adult mouse blood cells, it showed that scNanoSeq-CUT&Tag can accurately distinguish different cell types in vitro and in vivo. Moreover, scNanoSeq-CUT&Tag enables to effectively map the allele-specific epigenomic modifications in the human genome andallows to analyze co-occupancy of histone modifications. Taking advantage of long-read sequencing,scNanoSeq-CUT&Tag can sensitively detect epigenomic state of repetitive elements. In addition, by applying scNanoSeq-CUT&Tag to testicular cells of adult mouse B6D2F1, we demonstrated that scNanoSeq-CUT&Tag maps dynamic epigenetic state changes during mouse spermatogenesis. Finally, we exploited the epigenetic changes of human leukemia cell line K562 during DNA demethylation, it showed that NanoSeq-CUT&Tag can capture H3K27ac signals changes along DNA demethylation. Overall, we prove that scNanoSeq-CUT&Tag is a valuable tool for efficiently probing chromatin state changes within individual cells.

2024-09-06 | GSE249799 | GEO

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