Tripartite Motif Containing 33 Proteins (TRIM33)

Human Tripartite Motif Containing 33 (TRIM33) interaction partners

1. Anti-TIF1gamma antibodies are rarely present in patients with solid cancers or paraneoplastic rheumatic syndromes. This finding strengthens the approach to using anti-TIF1gamma IgG as a marker for cancer-associated dermatomyositis.

2. Tumors from paraneoplastic anti-TIF1gamma-positive cancer-associated myositis patients showed an increased number of genetic alterations, such as mutations and loss of heterozygosity, in TIF1 genes.

3. Data show that tripartite motif-containing protein 33 (TRIM33) silencing attenuates down-regulation of MYC and TGF-beta signaling in response to bromodomain and extraterminal domain protein inhibitors (BETi).

4. suggest that SnoN suppresses TGF-betainduced epithelial-mesenchymal transition and invasion of bladder cancer cells in a TIF1gammadependent manner

5. The adenovirus E4-ORF3 protein functions as a SUMO E3 ligase for TIF-1gamma sumoylation and poly-SUMO chain elongation.

6. our findings reveal a new mechanism by which SOX2-mediated transcription repression of TIF1gamma promotes TGF-beta-induced epithelial-mesenchymal transition in non-small-cell lung cancer

7. our work indicates that TIF1gamma exerts its tumor-suppressive functions in part by promoting chromosomal stability.

8. Results show that TRIM33 is significantly downregulated in clear renal cell carcinoma tissues which seems to correlate with pathologic stages and grades.

9. Tumour suppressor TRIM33 targets nuclear beta-catenin degradation

10. Study suggests TRIM33 and NRAS-CSDE1 as candidate genes for autism, and may provide a novel insight into the etiology of autism

11. The dermatomyositis autoantigen TIF1gamma is markedly up-regulated during muscle regeneration in human and mouse muscle cells.

12. Data indicate that tripartite motif containing 33 protein TIF1gamma promotes sumoylation of SKI-like proto-oncogene protein SnoN1 and regulates epithelial-mesenchymal transition (EMT).

13. regulates tumor growth and metastasis through inhibition of TGF-beta/Smad signaling and may serve as a novel prognostic biomarker in hepatocellular carcinoma

14. The ubiquitination of DHX33 by TRIM33 is lysine 63 specific and is required for the formation of the DHX33-NLRP3 inflammasome complex.

15. Results identify a new TGFbeta regulatory layer, whereby sumoylation strengthens the TIF1gamma repressive action on canonical TGFbeta signaling.

16. Case Report: suggest that TIF1gamma expression in neoplasms not only determines the tumour activity but also causes dermatomyositis.

17. mutation and methylation in the promoter region of TIF1gamma in non-small cell lung cancer

18. TRIM33 plays a role in PARP-dependent DNA damage response and regulates ALC1 activity by promoting its timely removal from sites of DNA damage.

19. These studies demonstrate that anti-NXP-2 and anti-TIF-1gamma antibodies are frequent DM specificities (found in 55% of patients) and are present in most patients with cancer-associated dermatomyositis.

20. TIF1gamma is an APC/C-interacting protein that regulates APC/C function. It is not a substrate for APC/C-dependent ubiquitylation but associates specifically with the APC/C holoenzyme & Cdc20 to affect APC/C activity & progression through mitosis.

Xenopus laevis Tripartite Motif Containing 33 (TRIM33) interaction partners

1. Ectodermin is a key switch in the control of TGF-beta gene responses during early embryonic development and cell proliferation.

Mouse (Murine) Tripartite Motif Containing 33 (TRIM33) interaction partners

1. Data show that tripartite motif 33 (TRIM33) mediates Wnt signaling by directly regulating the expression of a specific subset of Wnt target genes.

2. Trim33 is thus revealed as being essential for the navigation of macrophages and neutrophils towards developmental or inflammatory cues within vertebrate tissues.

3. Study reveals new important functions of TRIM33 in macrophage production and activation by LPS and pinpoints TRIM33 as an important transcriptional actor of monocyte/macrophage mediated inflammation.

4. TRIM33 is necessary for osteoblast proliferation by regulating cell cycle and for differentiation via bone morphogenetic protein signaling pathway.

5. these results indicate that Trim33 deficiency leads to the expansion of a subset of myeloid cells characterizing the myelodysplastic/myeloproliferative neoplasm.

6. Trim33 altered expression of a small group of genes in the testis and the gene with the most significant increase was transcribed from an upstream RLTR10B.

7. TRIM33 deficiency results in high expression of Ifnb1 at late stages of macrophages activation.

8. our work indicates that TIF1gamma exerts its tumor-suppressive functions in part by promoting chromosomal stability.

9. The findings reveal an essential role for TRIM33 in preventing apoptosis in B lymphoblastic leukemia by interfering with enhancer-mediated Bim activation.

10. This study demonistrated that Smad4 and Trim33 regulate neural stem cells in the developing cortex in mice.

11. Epithelium-specific Tak1:Smad4- and Trim33:Smad4-double mutants display reduced expression of Mmp13 in palatal medial edge epithelial cells.

12. The dermatomyositis autoantigen TIF1gamma is markedly up-regulated during muscle regeneration in human and mouse muscle cells.

13. reduces invasion and metastasis of hepatocellular carcinoma cells

14. These data provide a new paradigm for Tif1gamma in regulating the balance between lymphoid- and myeloid-derived hematopoietic stem cells (HSC) through TGF-beta signaling, leading to HSC aging.

15. TRIM33 plays a role in PARP-dependent DNA damage response and regulates ALC1 activity by promoting its timely removal from sites of DNA damage.

16. TIF1gamma plays essential roles in multiple murine blood lineages and that its function in transcription elongation is evolutionally conserved.

17. Tif1gamma suppresses murine pancreatic tumoral transformation by a Smad4-independent pathway.

18. Study reports an essential role for TRIM33 in the activation of Gsc and Mixl1 by nodal signals, and delineate how Smads gain access to poised promoters of master regulators under the command of nodal TGF-beta signals.

19. Loss of Tif1g in mouse HSCs favored the expansion of the granulo-monocytic progenitor compartment & induced the age-dependent appearance of a cell-autonomous myeloproliferative disorder resembling human CMML.

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

Zebrafish Tripartite Motif Containing 33 (TRIM33) interaction partners

1. The authors show that tif1gamma modulates the erythroid versus myeloid fate outcomes from HSCs by differentially controlling the levels of gata1 and pu.1.

2. TIF1gamma couples the blood-specific transcriptional complex with Pol II elongation machinery to promote the transcription elongation of erythroid genes by counteracting Pol II pausing.

3. transcriptional intermediary factor has a major role in the differentiation of hematopoietic cells