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Studies show that endogenous MAGEC2 interacts with TRIM28 in melanoma cells, and indicate that its regulatory role on MAGEC2 protein expression in many tumor cells type depends on proteasome-mediated pathway.
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TRIM24 and AR coactivated gene signature of SPOP-mutant prostate cancer (PCa) is similarly activated in human PCa with high TRIM28 expression.
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a null mutation in TRIM28 causes significant alterations in transposable element expression in both the naive and primed states of human pluripotency, and phenotypically this has limited effects on self-renewal, instead causing a loss of germline competency.
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Data suggest that retention of SMARCAD1 in nucleus is dependent on interaction of CUE1 domain of SMARCAD1 with RBCC domain of KAP1; these studies were conducted with recombinant proteins expressed in mouse embryonic stem cell line and human somatic cell line. (SMARCAD1 = ATP-dependent helicase-1; KAP1 = KRAB-interacting protein-1)
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Comparison of chromatin immunoprecipitation and high throughput nucleotide sequencing data and a reference motif set for human KRAB C2H2 zinc finger proteins has been reported.
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Genes co-repressed by TRIM28 and FAM208A are evolutionarily young, or exhibit tissue-specific expression, are enriched in young L1s, and display evidence for regulation through LTR promoters. Finally, we demonstrate that the HUSH complex is also required to repress L1 elements in human cells.
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Authors identify a viral mechanism for the counteraction of KAP1 in which interference with the KAP1 phosphatase protein phosphatase 1 (PP1) by the AAV2 Rep proteins mediates enhanced phosphorylation of KAP1-S824 and thus relief from KAP1 repression.
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Evaluation of the potential mechanism demonstrated that TRIM28 promoted cervical cancer cell growth by activating the mammalian target of rapamycin (mTOR) signaling pathway. In support of this finding, TRIM28-induced cell proliferation was abolished by treatment with everolimus, a specific mTOR inhibitor
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TRIM28 employs KRAB-ZNFs to evoke epigenetic silencing of its target differentiation genes via H3K9me3 and DNA methylation.
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Study describes germline mutations and loss of function of TRIM28 in familial Wilms tumours, along with somatic loss of function in a non-familial Wilms tumour. Inactivation of TRIM28 provides the molecular basis for defining a previously described subtype of Wilms tumour, that has early age of onset and excellent prognosis.
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Study identified TRIM28 among REST-interacting proteins, and suggested functional links between REST and TRIM28 during neuronal development and differentiation via induction of CTNND2 expression.
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Data indicate a mechanism in breast cancer cells that tripartite motif-containing 28 protein (TRIM28) enhances metastasis by stabilizing TWIST1, suggesting that targeting TRIM28 could be an efficacious strategy in breast cancer treatment.
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Gamma-H2AX, phosphorylated KAP-1 and 53BP1 play an important role in the repair of heterochromatic radon-induced DNA double-strand breaks.
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Our data demonstrate that the downregulation of TRIM28 gene expression reduced the ability of CSCs to self-renew that resulted in significant reduction of tumor growth. Loss of function of TRIM28 leads to dysregulation of cell cycle, cellular response to stress, cancer cell metabolism, and inhibition of oxidative phosphorylation.
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Cell proliferation and apoptosis were almost completely abolished in the PAa cells cotreated with TRIM28 siRNA and etoposide following knockdown of E2F1. The results of our study demonstrated that the combination of TRIM28 siRNA and etoposide may be effective against nonsmall cell lung cancer (NSCLC)and has the potential of being a new therapeutic tool for future treatment.
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The authors found that TRIM28 regulates alpha-Synuclein and tau nuclear levels and that its reduction rescues toxicity in animal models of tau- and alpha-Synuclein-mediated degeneration.
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TRIM28 represses Endogenous retroviruses and consequently regulates the expression of neighboring genes.
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it is primarily peroxide-induced p38 MAPK that mediates Ser473 phosphorylation and activation of TIF1beta to enable more efficient DNA repair to assist in tumor cell survival against exogenous ROS
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TRIM28 acts as a central factor in controlling endothelial inflammatory responses and angiogenic activities by retaining expression of TNFR-1 and -2 and VEGF receptor 2 in endothelial cells
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TRIM28 depletion repressed EZH2 recruitment to chromatin and expression of this gene set, in parallel with decreased CD44(hi)/CD24(lo) mammosphere formation.