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TRIM37 augments AP-2γ transcriptional activity and cellular localization via K63-linked polyubiquitination to drive breast cancer progression [RNA-seq]

ABSTRACT: TRIM37 augments AP-2γ transcriptional activity and cellular localization via K63-linked polyubiquitination to drive breast cancer progression [RNA-seq]

PROVIDER: PRJNA756730 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15560034_1.fastq.gz	Fastqsanger.gz
	SRR15560034_2.fastq.gz	Fastqsanger.gz
	SRR15560035_1.fastq.gz	Fastqsanger.gz
	SRR15560035_2.fastq.gz	Fastqsanger.gz
	SRR15560036_1.fastq.gz	Fastqsanger.gz

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TRIM37 augments AP-2γ transcriptional activity and cellular localization via K63-linked polyubiquitination to drive breast cancer progression [ChIP-seq]

Project description:Using a proteomics approach, we identified the Tripartite Motif Containing 37 (TRIM37) as a novel transcriptional coactivator of AP-2γ. We demonstrate TRIM37 facilitates AP-2γ chromatin binding to regulate the AP-2γ mediated transcriptional program directly. We provide evidence that TRIM37 achieves this by stimulating K63-chain-linked polyubiquitination of AP-2γ, promoting protein localization from the cytoplasm to the nucleus. In clinical analyses, we find TRIM37 is upregulated in multiple breast cancer datasets, supporting our findings that TRIM37-AP-2γ interaction is essential for breast cancer tumor growth. Overall, our work revealed that TRIM37 is an oncogenic coactivator of AP-2γ in breast cancer and provides a novel therapeutic target for treating the disease.

2022-07-25 | GSE182546 | GEO

TRIM37 augments AP-2γ transcriptional activity and cellular localization via K63-linked polyubiquitination to drive breast cancer progression [RNA-seq]

2022-07-25 | GSE182545 | GEO

TRIM37 augments AP-2γ transcriptional activity and cellular localization via K63-linked polyubiquitination to drive breast cancer progression.

Project description:TRIM37 augments AP-2γ transcriptional activity and cellular localization via K63-linked polyubiquitination to drive breast cancer progression.

| PRJNA756728 | ENA

TRIM37 augments AP-2γ transcriptional activity and cellular localization via K63-linked polyubiquitination to drive breast cancer progression [ChIP-seq]

Project description:TRIM37 augments AP-2γ transcriptional activity and cellular localization via K63-linked polyubiquitination to drive breast cancer progression [ChIP-seq]

| PRJNA756731 | ENA

TRIM37 augments AP-2γ transcriptional activity and cellular localization via K63-linked polyubiquitination to drive breast cancer progression.

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

2022-07-25 | GSE182547 | GEO

TRIM37 Augments AP-2γ Transcriptional Activity and Cellular Localization via K63-linked Ubiquitination to Drive Breast Cancer Progression.

Project description:Activator Protein 2 gamma (AP-2γ) is a master transcription factor that plays a critical role in the development and progression of breast cancer. However, the underlying mechanism is still unclear. Herein, using a proteomics approach, we identified Tripartite motif-containing 37 (TRIM37) as a novel coactivator of AP-2γ-mediated transcription in breast cancer cells. We demonstrate that TRIM37 facilitates AP-2γ chromatin binding to directly regulate the AP-2γ mediated transcriptional program. We also show that TRIM37 achieves this by stimulating K63 chain-linked ubiquitination of AP-2γ, promoting protein localization from the cytoplasm to the nucleus. In clinical analyses, we find TRIM37 is upregulated in multiple breast cancer datasets, supporting our findings that the TRIM37-AP-2γ interaction is essential for breast cancer tumor growth. Overall, our work reveals that TRIM37 is an oncogenic coactivator of AP-2γ in breast cancer and provides a novel therapeutic target for treating the disease.

| S-EPMC9295074 | biostudies-literature

FBXO42 facilitates Notch signaling activation and global chromatin relaxation by promoting K63-linked polyubiquitination of RBPJ

Project description:Dysregulation of the Notch-RBPJ signaling pathway has been found associated with various human diseases including cancers; however, precisely how this key signaling pathway is fine-tuned via its interactors and modifications is still largely unknown. In this study, using a proteomic approach, we identified FBXO42 as a novel RBPJ interactor. FBXO42 promotes RBPJ polyubiquitination on lysine (K) 175 via K63 linkage, which enhances the association of RBPJ with chromatin remodeling complexes and induces a global chromatin relaxation. Genetically depleting FBXO42 or pharmacologically targeting its E3 ligase activity attenuates the Notch signaling-related leukemia development in vivo. Taken together, our findings not only revealed FBXO42 as a critical regulator of the Notch pathway by modulating RBPJ-dependent global chromatin landscape changes, but also provide insights into the therapeutic intervention of the Notch pathway for leukemia treatment.

2022-07-31 | GSE206985 | GEO

Sex differences in the role of K63 polyubiquitination in the amygdala during fear memory formation

Project description:This project examined sex differences in the role of K63 polyubiquitination in the amygdala during context fear memory formation in male and female rats.

2023-05-18 | PXD036369 | Pride

FBXO42 facilitates Notch signaling activation and global chromatin relaxation by promoting K63-linked polyubiquitination of RBPJ

Project description:FBXO42 facilitates Notch signaling activation and global chromatin relaxation by promoting K63-linked polyubiquitination of RBPJ

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TRIM37 is a novel H2A ubiquitin ligase and a Breast Cancer Oncogene

Project description:The TRIM37 gene is mutatedin Mulbery nanism, a rare autosomal recessive disorder, and is in the 17q23 chromosomal region that is amplified in up to ~40% of breast cancers. Trim37 contains a RING finger domain, a hallmark of E3 ubiquitin ligases, but the protein substrate(s) of Trim37 is unknown. Mono-ubiquitination of histone H2A is a chromatin modification associated with transcriptional repression and here we report that Trim37 is an H2A ubiquitin ligase. Genome-wide Chip-CHIP experiments indicate that in human breast cancer cells containing amplified 17q23, Trim37 is bound to the promoters of many tumor suppressor genes. RNA interference (RNAi)-mediated knockdown of Trim37 results in loss of ubiquitinated H2A, dissociation of PRC1 and PRC2, and transcriptional reactivation of silenced genes. Knockdown of Trim37 in human breast cancer cells containing amplified 17q23 substantially decreases tumor growth in mouse xenografts. Collectively, our results reveal Trim37 as a new H2A ubiquitin ligase that is overexpressed in a subset of breast cancers and redirects PRC2 to silence tumor suppressors and other genes resulting in oncogenesis. Identification of TRIM37 Binding targets in MCF7 cells from the two replicate experiments

2014-10-06 | E-GEOD-48196 | biostudies-arrayexpress

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