Tripartite Motif Containing 11 Proteine (TRIM11)

Human Tripartite Motif Containing 11 (TRIM11) Interaktionspartner

1. CRTC1-TRIM11 fusion appears to be specific of an unpigmented nodular tumor combining a melanocytic phenotype and low-grade tumor behavior.

2. TRIM11 was upregulated in prostate cancer tissue and was associated with reduced prognosis. TRIM11 expression increased cell proliferation in vitro and was downregulated by miR-5193.

3. findings identify TRIM11 as an important activator of the proteasome, define a pathway that adjusts proteasome activity, and reveal a mechanism by which tumor cells acquire higher degradative power to support oncogenic growth

4. Data show that miR-24-3p downregulation contributes to tripartite motif-containing protein 11 (TRIM11) upregulation in cancer (CC).

5. TRIM11 promotes the development and progression of HCC through regulating p53 and its downstream signals.

6. data showed that tripartite motif-containing protein 11(TRIM11) expression was significantly elevated in hepatocellular carcinoma(HCC) tissues and overexpression of TRIM11 is closely associated with HCC progression and poor survival

7. Results show that TRIM11 was highly expressed in lung cancer tissues and cell lines and suggest that it acts as an oncogene in lung cancer through promoting cell growth, migration and invasion.

8. TRIM11 suppresses AIM2 inflammasome by degrading AIM2 via p62-dependent selective autophagy.

9. TRIM11 to be overexpressed in HCC tissues and cell lines. Downregulation of TRIM11 inhibited HCC cell proliferation and invasion in vitro and in vivo as well as suppressed the epithelial-mesenchymal transition (EMT) process.

10. study identified TRIM11 as a new HIV-1 capsid binding protein; data also reveal that TRIM11 restricts HIV-1 reverse transcription by accelerating viral uncoating, and microtubule dynamics is implicated in TRIM11-imposed block to early events of HIV-1 replication

11. TRIM11 is a host cellular factor that interferes with the early steps of HIV-1 replication and provides a connection between viral protein and host antiviral factors.

12. TRIM11 is overexpressed in high-grade gliomas and promotes proliferation, invasion, migration and glial tumor growth.

13. TRIM11 negatively regulates IFN-beta production and antiviral activity by targeting TBK1.

14. Study shows that the E3 ubiquitin ligase TRIM11 plays a critical role in the clearance of mutant PHOX2B, which causes congenital central hypoventilation syndrome, through the proteasome.

15. PAX6 interacts with HOMER3, DNCL1, and TRIM11. Three C-terminal PAX6 mutations, previously identified in patients with eye malformations, all reduced or abolished the interactions.

16. These results suggest that TRIM11, with the ubiquitin-proteasome pathway, regulates ARC105 function in TGFbeta signaling.

17. Downregulation of TRIM11 and TRIM15 enhanced virus release suggesting that these proteins contribute to the endogenous restriction of retroviruses in cells.

18. This study suggests a potential role for Trim11 in the specification of NA phenotype by interaction with Phox2b.

Mouse (Murine) Tripartite Motif Containing 11 (TRIM11) Interaktionspartner

1. TRIM11 suppresses AIM2 inflammasome by degrading AIM2 via p62-dependent selective autophagy.

2. The results suggest that TRIM11 plays a role in the regulation of intracellular humanin level through ubiquitin-mediated protein degradation pathways.