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Articles by M. J Tsai
Total Records ( 4 ) for M. J Tsai
  M. J TSAI and H. C. CHEN
 

A plain chest radiograph reveals multiple calcified cysts in the upper abdomen of a man who has been on dialysis for 15 years. What is the most plausible diagnosis?

  N. J McKenna , A. J Cooney , F. J DeMayo , M Downes , C. K Glass , R. B Lanz , M. A Lazar , D. J Mangelsdorf , D. D Moore , J Qin , D. L Steffen , M. J Tsai , S. Y Tsai , R Yu , R. N Margolis , R. M Evans and B. W. O`Malley
 

Nuclear receptors and coregulators are multifaceted players in normal metabolic and homeostatic processes in addition to a variety of disease states including cancer, inflammation, diabetes, obesity, and atherosclerosis. Over the past 7 yr, the Nuclear Receptor Signaling Atlas (NURSA) research consortium has worked toward establishing a discovery-driven platform designed to address key questions concerning the expression, organization, and function of these molecules in a variety of experimental model systems. By applying powerful technologies such as quantitative PCR, high-throughput mass spectrometry, and embryonic stem cell manipulation, we are pursuing these questions in a series of transcriptomics-, proteomics-, and metabolomics-based research projects and resources. The consortium’s web site (www.nursa.org) integrates NURSA datasets and existing public datasets with the ultimate goal of furnishing the bench scientist with a comprehensive framework for hypothesis generation, modeling, and testing. We place a strong emphasis on community input into the development of this resource and to this end have published datasets from academic and industrial laboratories, established strategic alliances with Endocrine Society journals, and are developing tools to allow web site users to act as data curators. With the ongoing support of the nuclear receptor and coregulator signaling communities, we believe that NURSA can make a lasting contribution to research in this dynamic field.

  D. K Lee , I Kurihara , J. W Jeong , J. P Lydon , F. J DeMayo , M. J Tsai and S. Y. Tsai
 

Synchrony between embryo competency and uterine receptivity is essential for successful implantation. Mice with ablation of chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) in the uterus (PRCre/+;COUP-TFIIflox/flox) exhibit implantation defects and increased estrogen receptor (ER) activity in the luminal epithelium, suggesting high ER activity may disrupt the window of uterine receptivity. To determine whether increased ER activity in the PRCre/+;COUP-TFIIflox/flox uterus is the cause of defective implantation, we assessed whether inhibition of ER activity could rescue the PRCre/+;COUP-TFIIflox/flox uterine implantation defect. ICI 182,780 (ICI), a pure ER antagonist, was administered to PRCre/+;COUP-TFIIflox/flox mutant and COUP-TFIIflox/flox control mice during the receptive period, and the number of implantation sites was examined. COUP-TFIIflox/flox control mice treated with oil or ICI showed the normal number of implantation sites. As expected, no implantation sites were observed in PRCre/+;COUP-TFIIflox/flox mutant mice treated with oil, consistent with previous observations. In contrast, implantation sites were greatly increased in ICI-treated PRCre/+;COUP-TFIIflox/flox mutant mice, albeit at a reduced number in comparison with the control mice. ICI treatment was also able to restore the expression of Wnt4 and bone morphogenetic protein 2, important for endometrial decidualization in the PRCre/+;COUP-TFIIflox/flox mutant mice. To confirm that the rescue of embryo attachment and decidualization is a consequence of a reduced ER activity upon ICI treatment, we showed a reduction of the expression of ER target genes in PRCre/+;COUP-TFIIflox/flox mutant mice. Because COUP-TFII was also shown in our laboratory to be important for placentation during pregnancy, we asked whether ICI treatment could also rescue the placentation defect to allow full-term pregnancy in these mice. We found that whereas mice were born in COUP-TFIIflox/flox control mice given ICI, no pups were born in the PRCre/+;COUP-TFIIflox/flox mutant mice, suggesting that the increased ER activity is not the reason for placentation defects. These results demonstrate that during the periimplantation period, COUP-TFII regulates embryo attachment and decidualization through controlling ER activity. However, COUP-TFII expression is still required in the postimplantation period to facilitate placentation.

  C. E Foulds , A Tsimelzon , W Long , A Le , S. Y Tsai , M. J Tsai and B. W. O'Malley
 

The human steroid receptor RNA activator (SRA) gene encodes both noncoding RNAs (ncRNAs) and protein-generating isoforms. In reporter assays, SRA ncRNA enhances nuclear receptor and myogenic differentiation 1 (MyoD)-mediated transcription but also participates in specific corepressor complexes, serving as a distinct scaffold. That SRA RNA levels might affect some biological functions, such as proliferation, apoptosis, steroidogenesis, and myogenesis, has been reported. However, the breadth of endogenous target genes that might be regulated by SRA RNAs remains largely unknown. To address this, we depleted SRA RNA in two human cancer cell lines with small interfering RNAs and then assayed for changes in gene expression by microarray analyses. The majority of significantly changed genes were reduced upon SRA knockdown, implicating SRA RNAs as endogenous coactivators. Unexpectedly, only a small subset of direct estrogen receptor- target genes was affected in estradiol-treated MCF-7 cells. Eight bona fide SRA downstream target genes were identified (SLC2A3, SLC2A12, CCL20, TGFB2, DIO2, TMEM65, TBL1X, and TMPRSS2), representing entirely novel SRA targets, except for TMPRSS2. These data suggest unanticipated roles for SRA in glucose uptake, cellular signaling, T3 hormone generation, and invasion/metastasis. SRA depletion in MDA-MB-231 cells reduced invasiveness and expression of some genes critical for this process. Consistent with the knockdown data, overexpressed SRA ncRNA coactivates certain target promoters and may enhance the activity of some coregulatory proteins. This study is a valuable resource because it represents the first genome-wide analysis of a mammalian RNA coregulator.

 
 
 
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