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decreased expression of miR (Montrer MLXIP Protéines)-122 and increased expression of TRIM29 was significantly associated with poor prognosis in patients with NPC (Montrer NPC1 Protéines).
Ectopic expression of TRIM29 potentially contributes to metastasis and poor prognosis in patients with osteosarcoma.
Knockdown of tripartite motif-containing 29 protein (TRIM29) enhanced the production of type I interferon (Montrer IFNA Protéines) in human and mouse dendritic cells by up to fourfold in response to intracellular herpes simplex virus.
the current study demonstrated that TRIM29 upregulates cyclin (Montrer PCNA Protéines) and Bcl family proteins level to facilitate malignant cell growth and inhibit drug-induced apoptosis in bladder cancer, possibly through PKC (Montrer PRRT2 Protéines)-NF-kappaB (Montrer NFKB1 Protéines) signaling pathways.
High TRIM29 expression is associated with metastasis of nasopharyngeal carcinoma.
Data show that TRIM29 promotes tumor progression by activating Wnt (Montrer WNT2 Protéines)/beta-Catenin (Montrer CTNNB1 Protéines) signaling.
This study establishes TRIM29 as a hypoxia-induced tumor suppressor gene and provides a novel molecular mechanism for ATM (Montrer ATM Protéines)-dependent breast cancer suppression.
Upregulation of TRIM29 is associated with thyroid cancer.
miR (Montrer MLXIP Protéines)-761 acts as an oncogene (Montrer RAB1A Protéines) in triple-negative breast cancer. This mode of action can, at least partially, be ascribed to the down-regulation of its target TRIM29.
Silencing of TRIM29 significantly inhibited the migration and invasion ability of CRC (Montrer CALR Protéines) cells.
this study shows that deletion of TRIM29 enhanced macrophage production of type I interferons and protected mice from infection with influenza virus, while challenge of Trim29-/- mice with Haemophilus influenzae resulted in lethal lung inflammation due to massive production of proinflammatory cytokines by macrophages
Findings established a role for ATDC/TRIM29 as a robust pathogenic driver of bladder cancer development, identified downstream effector pathways, and implicated ATDC as a candidate biomarker and therapeutic target.
ATDC up-regulates CD44 (Montrer CD44 Protéines) in mouse and human PanIN lesions via activation of beta-catenin (Montrer CTNNB1 Protéines) signaling, leading to the induction of an epithelial-to-mesenchymal transition (EMT (Montrer ITK Protéines)) phenotype characterized by expression of Zeb1 and Snail1 (Montrer SNAI1 Protéines).
Histone deacetylase 9 (HDAC9 (Montrer HDAC9 Protéines)) regulates the functions of the ATDC (TRIM29) protein
ATDC increases cell proliferation via inhibition of p53 (Montrer TP53 Protéines) nuclear activities.
The protein encoded by this gene belongs to the TRIM protein family. It has multiple zinc finger motifs and a leucine zipper motif. It has been proposed to form homo- or heterodimers which are involved in nucleic acid binding. Thus, it may act as a transcriptional regulatory factor involved in carcinogenesis and/or differentiation. It may also function in the suppression of radiosensitivity since it is associated with ataxia telangiectasia phenotype.
ataxia telangiectasia group D-associated protein
, ataxia-telangiectasia group D-associated protein
, tripartite motif protein TRIM29
, tripartite motif-containing 29
, tripartite motif-containing protein 29
, tripartite motif protein 29
, tripartite motif-containing protein 29-like