TRIP11

Gene Summary

Gene:TRIP11; thyroid hormone receptor interactor 11
Aliases: ACG1A, CEV14, TRIP-11, TRIP230, GMAP-210
Location:14q31-q32
Summary:This gene was identified based on the interaction of its protein product with thyroid hormone receptor beta. This protein is associated with the Golgi apparatus. The N-terminal region of the protein binds Golgi membranes and the C-terminal region binds the minus ends of microtubules; thus, the protein is thought to play a role in assembly and maintenance of the Golgi ribbon structure around the centrosome. Mutations in this gene cause achondrogenesis type IA.[provided by RefSeq, Mar 2010]
Databases:OMIM, VEGA, HGNC, Ensembl, GeneCard, Gene
Protein:thyroid receptor-interacting protein 11
HPRD
Source:NCBIAccessed: 17 March, 2015

Ontology:

What does this gene/protein do?
Show (9)

Cancer Overview

Research Indicators

Publications Per Year (1990-2015)
Graph generated 17 March 2015 using data from PubMed using criteria.

Literature Analysis

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Tag cloud generated 17 March, 2015 using data from PubMed, MeSH and CancerIndex

Latest Publications: TRIP11 (cancer-related)

Kulkarni S, Heath C, Parker S, et al.
Fusion of H4/D10S170 to the platelet-derived growth factor receptor beta in BCR-ABL-negative myeloproliferative disorders with a t(5;10)(q33;q21).
Cancer Res. 2000; 60(13):3592-8 [PubMed] Related Publications
We have studied a patient who presented with clinical features suggestive of chronic myeloid leukemia in accelerated phase. BCR-ABL transcripts were undetectable by reverse transcription-PCR, but a novel reciprocal translocation, t(5;10)(q33;q21.2), was seen by standard cytogenetic analysis. Chromosome band 5q33 contains the gene encoding the platelet-derived growth factor beta receptor (PDGFbetaR), the receptor tyrosine kinase that is disrupted by the t(5;7), t(5;12), and t(5;14) in myeloid disorders, resulting in the fusion of PDGFbetaR to HIP1, TEL/ETV6, and CEV14, respectively. Southern analysis with PDGFbetaR cDNA revealed novel bands in patient but not control DNA after digestion with several restriction enzymes, indicating that this gene is also targeted by the t(5;10). Fluorescence in situ hybridization analysis of chromosome 5 indicated that a small inversion at 5q33 had taken place in addition to the interchromosomal translocation. The site of the chromosome 10 breakpoint fell within YAC 940e4. Because all PDGFbetaR fusions described thus far result in splicing to a common exon of this gene, we performed 5'-rapid amplification of cDNA ends PCR on patient RNA. Several clones were isolated in which PDGFbetaR fused in frame to H4/D10S170, a previously described ubiquitously expressed gene that is fused to the ret protein tyrosine kinase to form the PTC-1 oncogene in approximately 20% of papillary thyroid carcinomas. The presence of H4-PDGFbetaR chimeric mRNA in the patient was confirmed by reverse transcription-PCR; reciprocal PDGFbeta1R-H4 transcripts were not detected. We conclude that t(5;10)(q33;q21.2) is a novel translocation in BCR-ABL-negative chronic myeloid leukemia and that this abnormality results in an H4-PDGFbetaR fusion gene. This finding further strengthens the association between myeloproliferative disorders and deregulated tyrosine kinases.

Chen Y, Chen PL, Chen CF, et al.
Thyroid hormone, T3-dependent phosphorylation and translocation of Trip230 from the Golgi complex to the nucleus.
Proc Natl Acad Sci U S A. 1999; 96(8):4443-8 [PubMed] Free Access to Full Article Related Publications
Trip230 is a novel coactivator of the thyroid hormone receptor that is negatively regulated by the retinoblastoma tumor-suppressor protein. In an examination of its subcellular distribution, Trip230 localized predominantly to the vicinity of the Golgi instead of the nucleus, as other nuclear hormone receptor coactivators. Using a series of deletion mutants, a critical region identified for Golgi area targeting coincided with a previously defined thyroid hormone receptor-binding domain of Trip230. During cell cycle progression, the expression level of Trip230 is constant and a significant portion is imported into the nucleus at S phase. Within an hour of treating cells with T3, Trip230 immunofluorescence transiently colocalized with TR in prominent subnuclear structures. T3-dependent nuclear import of Trip230 does not require new protein synthesis. Coincident with T3 treatment and nuclear import, newly phosphorylated residue(s) appeared in Trip230, suggesting that phosphorylation may be involved in its nuclear import. These findings provided a novel mechanism for the regulation of nuclear hormone transcription factors by hormone-responsive phosphorylation and nuclear import of cytoplasmically located coactivators.

Abe A, Emi N, Tanimoto M, et al.
Fusion of the platelet-derived growth factor receptor beta to a novel gene CEV14 in acute myelogenous leukemia after clonal evolution.
Blood. 1997; 90(11):4271-7 [PubMed] Related Publications
Chromosomal translocations involving band 5q31-35 occur in several hematologic disorders. A clone with a t(5; 14)(q33; q32) translocation appeared at the relapse phase in a patient with acute myelogenous leukemia who exhibited a sole chromosomal translocation, t(7; 11), at initial diagnosis. After the appearance of this clone, the leukemia progressed with marked eosinophilia, and combination chemotherapy was ineffective. Southern blot analysis showed a rearrangement of the platelet-derived growth factor receptor beta (PDGFRbeta) gene at 5q33 which was not observed at initial diagnosis. This translocation resulted in a chimeric transcript fusing the PDGFRbeta gene on 5q33 with a novel gene, CEV14, located at 14q32. Expression of the 5' region of the PDGFRbeta cDNA, upstream of the breakpoint, was not detected. However, the 3' region of PDGFRbeta, which was transcribed as part of the CEV14-PDGFRbeta fusion gene, was detected. A partial cDNA for a novel gene, CEV14, includes a leucine zipper motif and putative thyroid hormone receptor interacting domain and is expressed in a wide range of tissues. The expression of a CEV14-PDGFRbeta fusion gene in association with aggressive leukemia progression suggests that this protein has oncogenic potential.

Bardi G, Pandis N, Arsenis P, et al.
Mixed lineage leukemia with cytogenetically unrelated abnormal clones.
Cancer Genet Cytogenet. 1989; 40(1):83-7 [PubMed] Related Publications
We present a case of acute leukemia with morphologic, cytochemical, and immunophenotypic markers indicating that the population of blasts have characteristics of lymphoid and myelomonocytic origin. The cytogenetic study revealed the following mosaic abnormal karyotype: 46XX,dup(1)(q21----32)/46,XX,dup(11)(q13----25)/47,XX,trip(11) (q13----25),+der(17)t(17;?) (q24;?). The two clones involving #11 are obviously related. It is reasonable to assume that the third clone is an evolutionary result of the second one. Because no cytogenetic similarities were found among the first clone and the other two, we suggest that this mixed leukemia was of biclonal origin. To our knowledge, acute leukemia with mixed lineage characteristics and with the simultaneous presence of cytogenetically unrelated clones has not previously been reported.

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Cite this page: Cotterill SJ. TRIP11 gene, Cancer Genetics Web: http://www.cancer-genetics.org/TRIP11.htm Accessed:

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