Tripartite motif-containing 24 (TRIM24) also known as transcriptional intermediary factor 1α (TIF1α) is a protein that, in humans, is encoded by the TRIM24 gene. [5] [6] [7]

Mar 30, 2025 · TRIM24 (Tripartite Motif Containing 24) is a Protein Coding gene. Diseases associated with TRIM24 include Differentiated Thyroid Carcinoma and Aortic Malignant Tumor. Among its related pathways are FGFR1 mutant receptor …

Jul 8, 2022 · Here we show that the E3-ligase TRIM24 is a critical factor linking insulin signalling to P-bodies. Upon insulin stimulation, protein kinase B (PKB, also known as Akt) phosphorylates TRIM24 and...

Tripartite motif-containing 24 (TRIM24), also known as transcriptional intermediary factor 1α (TIF1α), is the founding member of TIF1 family. Recent evidence indicates that aberrant expression of TRIM24, functions as an oncogene, is associated with poor prognosis across various cancer types.

Nov 13, 2017 · Here, we determine that non-canonical histone signature acetylated H3 lysine 23 (H3K23ac)-binding protein tripartite motif-containing 24 (TRIM24) is upregulated in clinical GBM specimens and...

TRIM24 regulate resistance to Gefitinib via Akt pathway in non-small cell lung cancer cells. TRIM24 is overexpressed in human bladder cancer and facilitates bladder cancer growth and invasion, possibly through NF-kappaB and AKT signaling pathways. functions as an oncogene in colorectal carcinogenesis

Jun 13, 2016 · We show that recurrent PC-driver mutations in speckle-type POZ protein (SPOP) stabilize the TRIM24 protein, which promotes proliferation under low androgen conditions. TRIM24 augments AR signaling, and AR and TRIM24 co-activated genes are significantly upregulated in CRPC.

Jul 8, 2022 · Here we show that the E3-ligase TRIM24 is a critical factor linking insulin signalling to P-bodies. Upon insulin stimulation, protein kinase B (PKB, also known as Akt) phosphorylates TRIM24 and stimulates its shuttling from the nucleus into the cytoplasm.

Zhu et al. identify TRIM24 as a critical regulator for defending RNA virus infection through ubiquitinating TRAF3 and show that virus-activated IRF3 suppresses TRIM24 expression, forming a negative feedback loop to restrain overactivation of antiviral signaling.

We show that recurrent PC-driver mutations in speckle-type POZ protein (SPOP) stabilize the TRIM24 protein, which promotes proliferation under low androgen conditions. TRIM24 augments AR signaling, and AR and TRIM24 co-activated genes are significantly upregulated in CRPC.