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High TRIM16 expression is associated with drug resistance in Non-Small Cell Lung Cancer.
TRIM16 inhibits the migration and invasion via suppressing the Sonic hedgehog signaling pathway in ovarian cancer cells.
The cooperation between TRIM16 and Galectin-3 in targeting and activation of selective autophagy protects cells from lysosomal damage and Mycobacterium tuberculosis invasion.
TRIM16 expression is decreased in prostate cancer tissues and overexpression of TRIM16 inhibits cell migration, invasion and the EMT process in vitro in prostate cancer through the transcription factor Snail.
Results found that the expression of TRIM16 was significantly downregulated in hepatocellular carcinoma cell (HCC) lesions and define TRIM16 as an inhibitor of epithelial-mesenchymal transition and metastasis in HCC.
TRIM16 directly regulated the degradation of Gli1 protein via the ubiquitinproteasome pathway. TRIM16 expression was low in breast cancer. It negatively correlated with metastasis and suppressed stem-cell properties in breast cancer cells.
Data suggest that TRIM16 and TDP43 are both good prognosis indicators; data shows that TRIM16 inhibits cancer cell viability by a novel mechanism involving interaction and stabilisation of TDP43 with consequent effects on E2F1 and pRb proteins.
Expression of SDMGC and TRIM16 was upregulated in the distant metastasis tissues
Chromatin immunoprecipitation assays revealed TRIM16 directly bound the IFNbeta1 gene promoter. Low level TRIM16 expression in 91 melanoma patient samples, strongly correlated with lymph node metastasis, and, predicted poor patient prognosis.
results suggest that TRIM16 is a potential pharmacologic target for the treatment of NSCLC and promotion TRIM16 expression might represent a novel strategy to NSCLC metastasis
TRIM16 can promote apoptosis by directly modulating caspase-2 activity in cancer cells.
data suggest that TRIM16 acts as a novel regulator of both neuroblastoma G 1/S progression and cell differentiation
via its unique structure, TRIM16 possesses both heterodimerization function with other TRIM proteins and also has E3 ubiquitin ligase activity.
TRIM16 acts as a tumour suppressor, affecting neuritic differentiation, cell migration and replication through interactions with cytoplasmic vimentin and nuclear E2F1 in neuroblastoma cells.
role in regulating keratinocyte differentiation
These results provide evidence for a role of EBBP in innate immunity by enhancing the alternative secretion pathway of IL-1beta.
EBBP increased betaRARE-transactivating function through its coiled-coil domain
The estrogen-responsive B box protein (EBBP) restores retinoid sensitivity in retinoid-resistant cancer cells via effects on histone acetylation.
This gene was identified as an estrogen and anti-estrogen regulated gene in epithelial cells stably expressing estrogen receptor. The protein encoded by this gene contains two B box domains and a coiled-coiled region that are characteristic of the B box zinc finger protein family. The proteins of this family have been reported to be involved in a variety of biological processes including cell growth, differentiation and pathogenesis. Expression of this gene was detected in most tissues. Its function, however, has not yet been determined.
tripartite motif protein 16
, tripartite motif-containing 16
, tripartite motif-containing protein 16
, estrogen-responsive B box protein