Browse our Tripartite Motif Containing 28 Proteins (TRIM28)

Human Tripartite Motif Containing 28 (TRIM28) interaction partners

1. 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.

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

3. 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.

4. 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)

5. 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.

6. 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.

7. 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.

8. 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

9. TRIM28 employs KRAB-ZNFs to evoke epigenetic silencing of its target differentiation genes via H3K9me3 and DNA methylation.

10. 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.

11. 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.

12. 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.

13. Gamma-H2AX, phosphorylated KAP-1 and 53BP1 play an important role in the repair of heterochromatic radon-induced DNA double-strand breaks.

14. 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.

15. 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.

16. 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.

17. TRIM28 represses Endogenous retroviruses and consequently regulates the expression of neighboring genes.

18. 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

19. 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

20. TRIM28 depletion repressed EZH2 recruitment to chromatin and expression of this gene set, in parallel with decreased CD44(hi)/CD24(lo) mammosphere formation.

Mouse (Murine) Tripartite Motif Containing 28 (TRIM28) interaction partners

1. Paupar and Kap1 loss-of-function is associated with disruption in olfactory bulb neurogenesis.

2. IL-6-STAT3 signaling facilitates TRIM28 binding to the Il17-Il17f locus, and this process is required for epigenetic activation and high-order chromosomal interaction in autoimmune experimental encephalomyelitis.

3. Results show that KAP1 maintains H3K9me3 at imprinting control regions and transposable elements and protects them from TETdependent hydroxymethylation.

4. regulation of epigenetic modifications coordinated by TRIM28 plays a crucial role in reprogramming process.

5. The interaction of repressor proteins Trim28 and YY1 are involved in the silencing of Moloney murine leukemia virus.

6. an important role for TRIM28 in cells resisting transition between somatic and pluripotent states, is reported.

7. Nuclear factors that bind to genomic regions with "Sertoli Cell Signature" could functionally interact with SOX9; TRIM28 is a new SOX9 partner in fetal testes.

8. TRIM28 safeguards germline-to-soma inheritance of epigenetic features at other genomic regions in an exquisitely stage-dependent manner.

9. Data suggest that TRIM28 regulates the expression of a subset of lncRNAs.

10. Zygotic TRIM28 is essential for genomic imprinting. Secondary imprints were hypomethylated in TRIM28 mutants.

11. Trim28(+/D9) mutant mice exhibit a bi-modal body-weight distribution, with isogenic animals randomly emerging as either normal or obese and few intermediates.

12. Data suggest that interaction between KAP1 and the KRAB A box of zinc finger protein 809 (ZFP809) is critical in KAP1-dependent control of gene silencing for ZFP809 targets.

13. We find that NPCs use TRIM28-mediated histone modifications to dynamically regulate transcription and silencing of ERVs, which is in contrast to other somatic cell types using DNA methylation

14. WTX stabilized chromatin binding by TRIM28 and contributed to transcriptional repression of repetitive sequences by TRIM28 in mouse embryonic stem cells.

15. KAP-1 may contribute to the repression of Ey and beta-major globin gene transcription through recruitment to the promoters of these two genes, mediated by the interaction of KAP-1 with either Zfp445 or MafK, respectively

16. the TIF1beta-HP1 system functions as a critical repressive machinery that targets genes not normally activated in the hematopoietic compartment, thereby maintaining the transcriptional signature specific to HSCs.

17. KAP1 as a previously unappreciated interpreter of cell signaling, which modulates the ability of MyoD to drive myogenesis.

18. TRIM24, an epigenetic co-regulator of transcription, directly and indirectly represses hepatic lipid accumulation, inflammation, fibrosis and damage in the murine liver.

19. KAP1 and PRC1 bound cooperatively at the promoters of differentiation-inducible genes and repressed their transcription.

20. in the absence of TRIM28, we observed increased apoptosis as well as diminished expression of multiple erythroid transcription factors and heme biosynthetic enzymes in immature erythroid cells

Cow (Bovine) Tripartite Motif Containing 28 (TRIM28) interaction partners

1. Nuclear factors that bind to genomic regions with "Sertoli Cell Signature" could functionally interact with SOX9; TRIM28 is a new SOX9 partner in fetal testes.