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Tripartite motif containing 16

EBBP, estrogen-responsive B box protein, TRIM16
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Trim, ACID, CAN, V1a, IL-8
Papers using EBBP antibodies
Regulation of the transition from vimentin to neurofilaments during neuronal differentiation
Supplier
Cheung B B et al., In Oncogene, 2002
... The TRIM16-GFP deletion mutants were produced by OriGene (Rockville, MD, USA) ...
Papers on EBBP
Tripartite motif 16 suppresses breast cancer stem cell properties through regulation of Gli-1 degradation via the ubiquitin-proteasome pathway.
New
Yao et al., Xi'an, China. In Oncol Rep, Feb 2016
Tripartite motif 16 (TRIM16) is a proteasome coactivator that regulates proteolytic activity in eukaryotic cells.
Long noncoding ribonucleic acid specific for distant metastasis of gastric cancer is associated with TRIM16 expression and facilitates tumor cell invasion in vitro.
New
Wang et al., Beijing, China. In J Gastroenterol Hepatol, Sep 2015
Expression of lncRNA special for distant metastasis of GC (SDMGC) and target gene TRIM16 were tested in GC tissues and cell lines.
Tripartite motif 16 inhibits epithelial-mesenchymal transition and metastasis by down-regulating sonic hedgehog pathway in non-small cell lung cancer cells.
New
Yao et al., Xi'an, China. In Biochem Biophys Res Commun, Jun 2015
The present study was to examine the effect of Tripartite motif 16 (TRIM16) on epithelial-mesenchymal transition (EMT) and metastasis in non-small cell lung cancer (NSCLC) cells, and its clinical significance in NSCLC.
TRIM59 Promotes the Proliferation and Migration of Non-Small Cell Lung Cancer Cells by Upregulating Cell Cycle Related Proteins.
Wang et al., Nanchang, China. In Plos One, 2014
In an effort to profile the expression patterns of TRIM superfamily in several non-small cell lung cancer (NSCLC) cell lines, we found that the expression of 10 TRIM genes including TRIM3, TRIM7, TRIM14, TRIM16, TRIM21, TRIM22, TRIM29, TRIM59, TRIM66 and TRIM70 was significantly upregulated in NSCLC cell lines compared with the normal human bronchial epithelial (HBE) cell line, whereas the expression of 7 other TRIM genes including TRIM4, TRIM9, TRIM36, TRIM46, TRIM54, TRIM67 and TRIM76 was significantly down-regulated in NSCLC cell lines compared with that in HBE cells.
TRIM16 inhibits proliferation and migration through regulation of interferon beta 1 in melanoma cells.
Marshall et al., Sydney, Australia. In Oncotarget, 2014
High basal or induced expression of the tripartite motif protein, TRIM16, leads to reduce cell growth and migration of neuroblastoma and skin squamous cell carcinoma cells.
Microarray analysis of retroviral restriction factor gene expression in response to porcine endogenous retrovirus infection.
Twardoch et al., In Pol J Microbiol, 2013
The up-regulated transcripts were recorded for two differentially expressed genes (TRIM1, TRIM16) with the use of GeneSpring platform and Significance Analysis of Microarrays.
Differential expression of tripartite motif-containing family in normal human dermal fibroblasts in response to porcine endogenous retrovirus infection.
Twardoch et al., Sosnowiec, Poland. In Folia Biol (praha), 2013
Nine (TRIM1, TRIM2, TRIM5, TRIM14, TRIM16, TRIM18, TRIM22, TRIM27 and TRIM31) statistically significantly differentially expressed genes were found (P < 0.05, one-way ANOVA).
TRIM16 overexpression induces apoptosis through activation of caspase-2 in cancer cells.
Cheung et al., Australia. In Apoptosis, 2013
TRIM16 exhibits tumour suppressor functions by interacting with cytoplasmic vimentin and nuclear E2F1 proteins in neuroblastoma and squamous cell carcinoma cells, reducing cell migration and replication.
TRIM16 inhibits neuroblastoma cell proliferation through cell cycle regulation and dynamic nuclear localization.
Cheung et al., Australia. In Cell Cycle, 2013
We have previously demonstrated that tripartite motif 16 (TRIM16), a member of the RING B-box coiled-coil (RBCC)/tripartite totif (TRIM) protein family, has significant effects on neuroblastoma proliferation and migration in vitro and tumorigenicity in vivo.
Evaluation of the sensitizing potential of antibiotics in vitro using the human cell lines THP-1 and MUTZ-LC and primary monocyte-derived dendritic cells.
Baron et al., Aachen, Germany. In Toxicol Appl Pharmacol, 2012
To find out whether these novel in vitro assays are also capable to predict the sensitizing potential of small molecular weight drugs, model compounds such as beta-lactams and sulfonamides - which are the most frequent cause of adverse drug reactions - were co-incubated with THP-1, MUTZ-LC, or primary monocyte-derived dendritic cells for 48 h and subsequent expression of selected marker genes (IL-8, IL-1β, CES1, NQO1, GCLM, PIR and TRIM16) was studied by real time PCR.
The retinoid signalling molecule, TRIM16, is repressed during squamous cell carcinoma skin carcinogenesis in vivo and reduces skin cancer cell migration in vitro.
Marshall et al., Australia. In J Pathol, 2012
The retinoid signalling molecule, tripartite motif protein 16 (TRIM16), is a regulator of keratinocyte differentiation and a tumour suppressor in retinoid-sensitive neuroblastoma.
TRIM16 acts as an E3 ubiquitin ligase and can heterodimerize with other TRIM family members.
Cheung et al., Australia. In Plos One, 2011
TRIM16 does not have a RING domain but does harbour two B-box domains.
Active transport of contact allergens in human monocyte-derived dendritic cells is mediated by multidrug resistance related proteins.
Baron et al., Aachen, Germany. In Arch Biochem Biophys, 2011
Hence, to survey the functionality of indomethacin after stimulation with contact allergens IL-8 and TRIM16 regulation was measured by a DC-based in vitro assay.
TRIM16 acts as a tumour suppressor by inhibitory effects on cytoplasmic vimentin and nuclear E2F1 in neuroblastoma cells.
GeneRIF
Cheung et al., Australia. In Oncogene, 2010
TRIM16 acts as a tumour suppressor, affecting neuritic differentiation, cell migration and replication through interactions with cytoplasmic vimentin and nuclear E2F1 in neuroblastoma cells.
High-resolution transcriptional profiling of chemical-stimulated dendritic cells identifies immunogenic contact allergens, but not prohaptens.
Baron et al., Aachen, Germany. In Skin Pharmacol Physiol, 2009
Whole-genome screening and consecutive PCR analysis of differential gene expression in moDCs stimulated with either CAld or the obligatory sensitizer revealed coregulation of 11 marker genes which were related to immunological reactions (IL-8, CD1e, CD200R1, PLA2G5, TNFRSF11A), oxidative or metabolic stress responses (AKR1C3, SLC7A11, GCLM) or other processes (DPYLS3, TFPI, TRIM16).
The estrogen-responsive B box protein (EBBP) restores retinoid sensitivity in retinoid-resistant cancer cells via effects on histone acetylation.
GeneRIF
Cheung et al., Australia. In Cancer Lett, 2009
The estrogen-responsive B box protein (EBBP) restores retinoid sensitivity in retinoid-resistant cancer cells via effects on histone acetylation.
The estrogen-responsive B box protein: a novel enhancer of interleukin-1beta secretion.
GeneRIF
Beer et al., Zürich, Switzerland. In Cell Death Differ, 2006
These results provide evidence for a role of EBBP in innate immunity by enhancing the alternative secretion pathway of IL-1beta.
The estrogen-responsive B box protein is a novel regulator of the retinoid signal.
GeneRIF
Marshall et al., Australia. In J Biol Chem, 2006
EBBP increased betaRARE-transactivating function through its coiled-coil domain
The estrogen-responsive B box protein: a novel regulator of keratinocyte differentiation.
GeneRIF
Werner et al., Zürich, Switzerland. In J Biol Chem, 2002
role in regulating keratinocyte differentiation
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