Tripartite Motif Containing 24 Proteins (TRIM24)

Human Tripartite Motif Containing 24 (TRIM24) interaction partners

1. in response to RA, TRIM24 serves as an adapter linking RARalpha to the proteasome for its degradation. In addition, TRIM24 and the proteasome are recruited with RARalpha to the promoters of target genes and thus are inherently linked to RARalpha transcriptional activity.

2. findings establish a new link between histone H3 acetylation and SUMOylation of the reader protein TRIM24, a functional connection that may bear on TRIM24's oncogenic function and may inform future studies of PTM cross-talk between histones and epigenetic regulators

3. TRIM24 and AR coactivated gene signature of SPOP-mutant prostate cancer (PCa) is similarly activated in human PCa with high TRIM28 expression.

4. these results suggested that TRIM24 has an important role in the growth of Nasopharyngeal carcinoma (NPC). Additionally, silenced TRIM24 may lead to inhibited cell proliferation and induced cell apoptosis in NPC cells.

5. TRIM24 is upregulated in HNSCC and promotes HNSCC cell growth and invasion through modulation of cell cycle, glucose metabolism, and GLUT3, making TRIM24 a potential oncoprotein in HNSCC.

6. The findings identify TRIM24 as an oncogenic transcriptional co-activator in epidermal growth factor receptor-driven glioblastoma and also demonstrate a previously unknown signal relay by which H3K23ac/TRIM24 mediates epidermal growth factor receptor stimulation of STAT3 activation, thereby enhancing the oncogenic activity of the epidermal growth factor receptor/STAT3 pathway in human cancers.

7. Results suggest that TRIM24 is a novel coactivator of the CAR that is involved in cell- and/or promoter- selective transactivation.

8. TRIM24 expression was increased in human colorectal cancer and might be a novel prognostic biomarker.

9. Study showed that TRIM24 was upregulated during gastric carcinogenesis and demonstrated that TRIM24 was a functional target gene of miR-511, and miR-511 inactivated PI3K/AKT and Wnt/beta-catenin pathways by suppressing TRIM24.

10. Overexpression of KAT6A or TRIM24 promoted PIK3CA expression, AKT phosphorylation, and cell proliferation.

11. we identified altered glucose metabolism in the progression of head and neck squamous cell carcinoma and showed that it could be partially attributed to the novel link between GLUT4 and TRIM24

12. This study concluded that reduced TRIM24 protein is associated with poor survival in esophageal squamous cell cancer (ESCC) patients, suggesting TRIM24 protein is a potential prognostic biomarker for ESCC.

13. Data suggest that, in cardiomyocytes, TRIM32 attenuates activation of SRF signaling and hypertrophy due to dysbindin; TRIM24 promotes these effects. TRIM32 promotes dysbindin degradation; TRIM24 protects dysbindin from degradation. (TRIM = tripartite motif-containing protein; SRF = serum response factor)

14. hypothesis of "synergistic modification induced recognition" is then proposed to link histone modification and TRIM24 binding

15. Report provides evidence for an oncogenic role for TRIM24 as a transcriptional activator and mediator of hormone-refractory prostate cancer cell growth in SPOP mutant and castration-resistant prostate cells.

16. TRIM24 expression is positively correlated with Acetylated H3 lysine 23 levels, and high levels of both TRIM24 and Acetylated H3 lysine 23 predict shorter overall survival of breast cancer patients.

17. TRIM24 regulate resistance to Gefitinib via Akt pathway in non-small cell lung cancer cells.

18. TRIM24 is overexpressed in human bladder cancer and facilitates bladder cancer growth and invasion, possibly through NF-kappaB and AKT signaling pathways.

19. functions as an oncogene in colorectal carcinogenesis

20. A role for TRIM24 in breast tumorigenesis through reprogramming of glucose metabolism in human mammary epithelial cells, further supporting TRIM24 as a viable therapeutic target in breast cancer.

Mouse (Murine) Tripartite Motif Containing 24 (TRIM24) interaction partners

1. Maintenance of pluripotency is regulated by a network of transcription factors coordinated by Oct4, Sox2, and Nanog; Trim24 significantly improved efficiency of cellular reprogramming, demonstrating its direct functionality in establishing pluripotency.

2. data identify a previously unappreciated Trim24-dependent requirement for IL-1R expression on TH2 cells and an important nonredundant role for T-cell-intrinsic Trim24 in TH2-mediated allergy and antihelminth immunity

3. Trim24 repressed VL30-class endogenous retroviruses retrotransposons

4. 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.

5. Somatic hepatocyte-specific inactivation of TRIM24, TRIM28, or TRIM33 all promote hepatocellular carcinoma in a cell-autonomous manner in mice.

6. TRIM24 regulates AR-mediated transcription in collaboration with TIP60 and BRD7.

7. TIF1alpha-chromatin association is direct and involves DNA and nucleosome interactions mediated by the bromodomain

8. These studies indicate that TIF1alpha is a factor that modulates the expression of a set of genes during the first wave of genome activation in the mouse embryo.

9. The results not only provide genetic evidence that Trim24 and Rara co-regulate hepatocarcinogenesis in an antagonistic manner but also suggest that aberrant activation of Rara is deleterious to liver homeostasis.

10. TIF1alpha-null mutant pathological phenotype supports the hypothesis that aging is promoted by increased activity of the vitamin D signaling pathway