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ScRNA-Seq analysis of Trim28-deleted NPp53 mouse prostate tissue

ABSTRACT: scRNA-Seq analysis of Trim28-deleted NPp53 mouse prostate tissue

PROVIDER: PRJNA818014 | ENA |

REPOSITORIES: ENA

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scRNA-Seq analysis of Trim28-deleted NPp53 mouse prostate tissue

Project description:The Tripartite motif-containing 28 (TRIM28) transcription factor is upregulated in high-grade prostate cancers and was recently proposed as a therapeutic target for castration-resistant prostate cancers. To study the role of TRIM28 in prostate cancer progression in vivo, we used a genetically engineered mouse model, combining prostate-specific Trim28 inactivation with inactivation of Trp53 and Pten. We analyzed the prostates using single cell RNA-Seq.

2023-03-03 | GSE199015 | GEO

RNA-seq of gonadal adipose tissue from male and female Trim28-WT and Trim28 adipose specific KO mice

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Single cell RNA-seq from Trim28 ovary knockout and wildtype mice ovaries and testis

Project description:Single cell RNA-seq (scRNA-seq) from Trim28 ovary knockout and wildtype mice ovaries and testis to help elucidate the function of Trim28 in the adult mouse ovaries. The analysis revealed that loss of Trim28 in the adult mouse ovaries lead to a transcriptional repogramming of the Granulosa cells towards the Sertoli cell fate. Therefore, Trim28 has a function to maintain the adult ovarian cell identity

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TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression [microarray]

Project description:In this study, proteomic profiling of TRIM24 interactome in conjunction with shRNA screening of TRIM24 top-interactors nominated that TRIM28 is indispensable for TRIM24 protein stability. We showed that TRIM28 stabilizes TRIM24 against SPOP-mediated ubiquitination and degradation. TRIM28 promotes TRIM24 and AR transcription activity, androgen-dependent and -independent PCa growth. In addition, we demonstrated that TRIM28 level in high in advanced PCa, which drives TRIM24/AR transcription activity in a similar manner to SPOP mutation, which implies that TRIM28 potentially dictates the therapeutic outcome of TRIM24-targeted therapy.

2018-10-05 | GSE108145 | GEO

TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression [ChIP-seq]

2018-10-05 | GSE108144 | GEO

TRIM28 establishes skeletal stem cell identity and safeguards skeletogenesis (scRNA-Seq)

Project description:TRIM28 establishes skeletal stem cell identity and safeguards skeletogenesis (scRNA-Seq)

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RNA seq analysis of AR-deleted luminal prostate epithelial cells during organogenesis

Project description:Transcriptome analysis of lineage marked AR-deleted and wild type luminal prostate epithelial cells from prostates from 4 week old males, and bulk wild-type prostates from 3 week old male mice.

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TRIM28 establishes skeletal stem cell identity and safeguards skeletogenesis (scRNA-Seq)

Project description:The identity, renewal, and multipotency of stem cells are controlled by epigenetic mechanisms. DNA methylation and trimethylation on histone H3K9 (H3K9me3) are two epigenetic marks that coordinate gene silencing in early embryogenesis. Yet whether they also play a role in regulating somatic stem cell activities governing organogenesis, particularly in the skeletal system, is unknown. Here we show that chromatin silencing, established by TRIM28 (aka. KAP1 and TIF1β) via DNA methylation and H3K9me3 during early organogenesis is crucial for skeletal development. Loss of TRIM28 in skeletal stem cells unsilences the promoter and two previously uncharacterized enhancers of the Grem1 gene, leading to GREM1 hyperexpression, which further activates AKT/mTORC1 signaling to promote skeletal stem cell renewal while restricting osteogenesis and chondrogenesis. Notably, loss of Trim28 in the growth plate also leads to the emergence of a novel stem cell cluster with neural crest cell properties and a distinctive neurogenic tendency. These collectively result in a wide range of skeletal abnormalities. Taken together, our data suggest that TRIM28 coordinates methylation of DNA and histone H3K9 to safeguard the identity and fate determination of skeletal stem cells by epigenetically silencing the GREM1/AKT/mTORC1 signaling axis.

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Project description:RNA-seq of gonadal adipose tissue from male and female Trim28-WT and Trim28 adipose specific KO mice

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