Dataset Information

Comparative proteomic profiling of neonatal rat ventricular cardiomyocytes (NRVCMs) following TRIM24 downregulation

ABSTRACT: TRIM24 (Tripartite Motif-Containing 24) is a key transcriptional co-regulator involved in various cellular processes, including chromatin remodeling and gene expression. However, its role in cardiomyocytes remains largely unexplored. In this study, we investigated the global proteomic changes associated with TRIM24 downregulation in neonatal rat ventricular cardiomyocytes (NRVCMs) to better understand its function in cardiac biology. NRVCMs were transduced by an Adenovirus with a synthetic microRNA targeting TRIM24. Protein isolated from the NRVCMs transduced with a scrambled microRNA was used as control.

INSTRUMENT(S): Synapt MS

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Fetal Cardiomyocyte

SUBMITTER: Elke Hammer

LAB HEAD: Elke Hammer

PROVIDER: PXD062686 | Pride | 2025-07-14

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	190326_RefSeq_rat_TRIM24.fasta	Fasta
	20191024_S1M1_DI_EH_DZHKi_Ctrl_KD_1.raw.7z	Raw
	20191024_S1M1_DI_EH_DZHKi_Ctrl_KD_2.raw.7z	Raw
	20191024_S1M1_DI_EH_DZHKi_Ctrl_KD_3.raw.7z	Raw
	20191024_S1M1_DI_EH_DZHKi_Ctrl_KD_4.raw.7z	Raw

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Publications

TRIM24 regulates chromatin remodeling and calcium dynamics in cardiomyocytes.

Neu Marco M Deshpande Anushka A Borlepawar Ankush A Hammer Elke E Alameldeen Ahmed A Vöcking Phillipp P Seeger Timon T Hausmann Michael M Frey Norbert N Rangrez Ashraf Yusuf AY

Cell communication and signaling : CCS 20250701 1

<h4>Background</h4>Cardiomyocyte proteostasis and calcium homeostasis are critical for maintaining cardiac function, with their dysregulation contributing to cardiac hypertrophy and heart failure. The Tripartite Motif Protein 24 (TRIM24), a well-characterized chromatin reader and transcriptional regulator in cancer, has recently emerged as a potential player in cardiac biology. However, its precise role in cardiomyocytes remains unclear. Using molecular, structural and functional approaches, thi ...[more]

PMID: 40598158

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Project description:Recent genetic studies in mice have established a key role for the nuclear receptor coregulator Trim24 in liver tumor suppression and provided evidence that Trim24 suppresses hepatocarcinogenesis by inhibiting retinoic acid receptor alpha (Rara)-dependent transcription and cell proliferation. However, it is unknown which downstream targets of Rara regulated by Trim24 are critical for tumorigenesis. We report here that loss of Trim24 results in the overexpression of interferon (IFN)/STAT pathway genes in the liver, a process that occurs early in tumorigenesis and is more pronounced in tumors, despite the enhanced expression, late in the disease, of negative regulators such as Usp18, Socs1 and Socs2. Remarkably, Rara haplodeficiency, which was previously shown to suppress tumor development in Trim24-/- mice, also suppresses overexpression of the IFN/STAT pathway, thus providing evidence for a cross-pathway control that may be relevant to the transformation process. Biochemical studies revealed that Trim24 binds to the retinoic acid (RA)-responsive element in the Stat1 promoter in a RA-dependent manner and represses RA-induced transcription from this promoter. Together, these results identify Trim24 as a novel regulator of the IFN/STAT pathway and indicate that Trim24-mediated repression of the IFN/STAT signaling through Rara inhibition may play a critical role in preventing liver cancer. Generation of Trim24-/- mice has been described previously (Khetchoumian et al., 2007) by gene disruption. To generate compound mutant mice with a single allele of Rara deleted in the Trim24 -/- mutant background, we crossed Trim24 -/- mice with Rara+/- mice. The resulting Trim24+/- Rara+/- mice were generated in the hybrid (C57BL/6 (60%), 129/Sv (40%)) genetic background. These double heterozygous Trim24+/- Rara+/- mice were intercrossed to generate Trim24 -/-, Trim24 -/- Rara+/- and wild-type mice. Transcriptional profiling of mice at 5-weeks and 14-weeks of age.