| General information | Literature | Expression | Regulation | Mutation | Interaction |
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Basic Information |
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|---|---|
Gene ID | 8805 |
Name | TRIM24 |
Synonymous | PTC6|RNF82|TF1A|TIF1|TIF1A|TIF1ALPHA|hTIF1;tripartite motif containing 24;TRIM24;tripartite motif containing 24 |
Definition | E3 ubiquitin-protein ligase TRIM24|RING finger protein 82|TIF1-alpha|transcription intermediary factor 1-alpha|transcriptional intermediary factor 1|tripartite motif-containing 24 |
Position | 7q32-q34 |
Gene type | protein-coding |
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Title |
Abstract |
| Tripartite motif 24 (Trim24/Tif1alpha) tumor suppressor protein is a novel negative regulator of interferon (IFN)/signal transducers and activators of transcription (STAT) signaling pathway acting through retinoic acid receptor alpha (Raralpha) inhibition. | Recent genetic studies in mice have established that the nuclear receptor coregulator Trim24/Tif1alpha suppresses hepatocarcinogenesis by inhibiting retinoic acid receptor alpha (Rara)-dependent transcription and cell proliferation. However, Rara targets regulated by Trim24 remain unknown. We report that the loss of Trim24 resulted in interferon (IFN)/STAT pathway overactivation soon after birth (week 5). Despite a transient attenuation of this pathway by the induction of several IFN/STAT pathway repressors later in the disease, this phenomenon became more pronounced in tumors. Remarkably, Rara haplodeficiency, which suppresses tumorigenesis in Trim24(-/-) mice, prevented IFN/STAT overactivation. Moreover, together with Rara, Trim24 bound to the retinoic acid-responsive element of the Stat1 promoter and repressed its retinoic acid-induced transcription. Altogether, these results identify Trim24 as a novel negative regulator of the IFN/STAT pathway and suggest that this repression through Rara inhibition may prevent liver cancer. |