• 제목/요약/키워드: Orphan Cells

검색결과 26건 처리시간 0.019초

중첩격자에 대한 이동최소자승법 적용 연구 (APPLICATION OF MOVING LEAST SQUARE METHOD IN CHIMERA GRID METHOD)

  • 이관중;이승수;조진연
    • 한국전산유체공학회지
    • /
    • 제13권1호
    • /
    • pp.49-56
    • /
    • 2008
  • Chimera grid methods have been widely used in Computational Fluid Dynamics due to its simplicity in constructing grid systems over complex bodies, and suitability for unsteady flow computations with bodies in relative motion. However, the interpolation procedure for ensuring the continuity of the solution over overlapped regions fails when the so-called orphan cells are present. We have adopted the MLS(Moving Least Squares) method to replace commonly used linear interpolations in order to alleviate the difficulty associated with the orphan cells. MLS is one of the interpolation methods used in mesh-less methods. A number of examples with MLS are presented to show the validity and the accuracy of the method.

중첩격자에 대한 이동최소자승법 적용 연구 (APPLICATION OF MOVING LEAST SQUARE METHOD IN CHIMERA GRID METHOD)

  • 이관중;이승수
    • 한국전산유체공학회:학술대회논문집
    • /
    • 한국전산유체공학회 2007년도 춘계 학술대회논문집
    • /
    • pp.17-22
    • /
    • 2007
  • Chimera grid Method is widely used in Computational Fluid Dynamics due to its simplicity in constructing grid system over complex bodies. Especially, Chimera grid method is suitable for unsteady flow computations with bodies in relative motions. However, interpolation procedure for ensuring continuity of solution over overlapped region fails when so-call orphan cells are present. We have adopted MLS(Moving Least Squares) method to replace commonly used linear interpolations in order to alleviate the difficulty associated with orphan cells. MSL is one of interpolation methods used in mesh-less methods. A number of examples with MLS are presented to show the validity and the accuracy of the method.

  • PDF

Distinct Repressive Properties of the Mammalian and Fish Orphan Nuclear Receptors SHP and DAX-1

  • Park, Yun-Yong;Teyssier, Catherine;Vanacker, Jean-Marc;Choi, Hueng-Sik
    • Molecules and Cells
    • /
    • 제23권3호
    • /
    • pp.331-339
    • /
    • 2007
  • It has been suggested that the structure and function of nuclear receptors are evolutionally conserved. Here, we compare the molecular functions of the nile tilapia (Oreochromis niloticus) small heterodimer partner (nSHP/NR0B2) and the Dosage-sensitive sex reversal AHC critical region on X chromosome gene 1 (nDAX-1/NR0B1) with those of human SHP and DAX-1 (hSHP and hDAX-1, respectively). We found that, upon transient cotransfection of human cells, nDAX-1 repressed the activity of tilapia SF-1 (nSF-1) but not that of human SF-1, although the physical interaction with human SF-1 was retained. Similarly, nSHP repressed the activity of nSF-1, whereas hSHP did not, pointing to divergent evolution of SHP/SF-1 in fish and human. We thus propose that the repressive functions of SHP and DAX-1 have been conserved in fish and mammals although with different transcriptional targets and mechanisms. These differences provide new insights into the physiological diversification of atypical orphan nuclear receptors during vertebrate evolution.

EID-1 Interacts with Orphan Nuclear Receptor SF-1 and Represses Its Transactivation

  • Park, Yun-Yong;Park, Ki Cheol;Shong, Minho;Lee, Soon-Jung;Lee, Young-Ho;Choi, Hueng-Sik
    • Molecules and Cells
    • /
    • 제24권3호
    • /
    • pp.372-377
    • /
    • 2007
  • The orphan nuclear receptor, SF-1, plays a pivotal role in the development and differentiation of the endocrine and reproductive systems, and also regulates the transcription of a host of genes, including those encoding several steroidogenic enzymes and gonadotropins. We found that a previously unidentified repressor, EID-1, is an SF-1-interacting protein that inhibits the transactivation of SF-1. A transient transfection assay revealed that EID-1 inhibits SF-1, but not LRH-1, $ERR{\gamma}$, or mCAR. Using the yeast two hybrid and GST pull-down assays, we determined that EID-1 interacted strongly with SF-1. In addition, it colocalized with SF-1 in mammalian cells and interacted specifically with the AF-2 domain of SF-1, competing with SRC-1 to inhibit SF-1 transactivation. EID-1 is expressed in the mouse testis, and its expression decreases during testis development. The results of the present study suggest that EID-1 can act as a repressor, regulating the function of SF-1.

Bisphenol A Bis(2,3-dihydroxypropyl) ether (BADGE.2H2O) Induces Orphan Nuclear Receptor Nur77 Gene Expression and Increases Steroidogenesis in Mouse Testicular Leydig Cells

  • Ahn, Seung-Won;Nedumaran, Balachandar;Xie, Yuanbin;Kim, Don-Kyu;Kim, Yong Deuk;Choi, Hueng-Sik
    • Molecules and Cells
    • /
    • 제26권1호
    • /
    • pp.74-80
    • /
    • 2008
  • Bisphenol A bis (2,3-dihydroxypropyl) ether ($BADGE.2H_2O$) is a component of commercial liquid epoxy resins commonly used in the food-packing industry and in dental sealants. There is evidence that it has significant estrogenic activity. Nur77 plays a crucial role in the regulation of certain genes involved in LH-mediated steroidogenesis in testicular Leydig cells. It was previously demonstrated that Bisphenol A (BPA) stimulates Nur77 gene induction and steroidogenesis. In this study, we investigated the effects of $BADGE.2H_2O$ on Nur77 gene expression and steroidogenesis. Northern blot analysis showed that it increased the expression of Nur77 mRNA and protein, and transient transfection assays demonstrated that it increased the promoter activity and transactivation of Nur77. It also increased the expression of certain steroidogenic genes, such as StAR and $3{\beta}$-HSD. Finally, over-expression of a dominant negative Nur77 cDNA via adenoviral infection reduced $BADGE.2H_2O$-mediated progesterone biosynthesis. These results indicate that $BADGE.2H_2O$ disrupts testicular steroidogenesis by increasing Nur77 gene expression.

Orphan Nuclear Receptor Nurr1 as a Potential Novel Marker for Progression in Human Prostate Cancer

  • Wang, Jian;Yang, Jing;Zou, Ying;Huang, Guo-Liang;He, Zhi-Wei
    • Asian Pacific Journal of Cancer Prevention
    • /
    • 제14권3호
    • /
    • pp.2023-2028
    • /
    • 2013
  • A number of studies have indicated that Nurr1, which belongs to a novel class of orphan nuclear receptors (the NR4A family), is important for carcinogenesis. Here we investigated expression of Nurr1 protein in benign and malignant human prostate tissues and association with clinicopathologic features using immunohistochemical techniques. Moreover, we also investigated the ability of Nurr1 to influence proliferation, migration, invasion and apoptosis of human prostate cancer cells using small interfering RNA silencing. Immunohistochemical analysis revealed that the expression of Nurr1 protein was higher in prostate cancer tissues than in benign prostate tissue (P<0.001), levels being positively correlated with tumor T classification (P = 0.003), N classification (P = 0.017), M classification (P = 0.011) and the Gleason score (P = 0.020) of prostate cancer patients. In vitro, silencing of endogenous Nurr1 attenuated cell proliferation, migration and invasion, and induced apoptosis of prostate cancer cells. These results suggest that Nurr1 may be used as an indicator for prostate cancer progression and be useful for novel potential therapeutic strategies.

IL-17-Producing Cells in Tumor Immunity: Friends or Foes?

  • Da-Sol Kuen;Byung-Seok Kim;Yeonseok Chung
    • IMMUNE NETWORK
    • /
    • 제20권1호
    • /
    • pp.6.1-6.20
    • /
    • 2020
  • IL-17 is produced by RAR-related orphan receptor gamma t (RORγt)-expressing cells including Th17 cells, subsets of γδT cells and innate lymphoid cells (ILCs). The biological significance of IL-17-producing cells is well-studied in contexts of inflammation, autoimmunity and host defense against infection. While most of available studies in tumor immunity mainly focused on the role of T-bet-expressing cells, including cytotoxic CD8+ T cells and NK cells, and their exhaustion status, the role of IL-17-producing cells remains poorly understood. While IL-17-producing T-cells were shown to be anti-tumorigenic in adoptive T-cell therapy settings, mice deficient in type 17 genes suggest a protumorigenic potential of IL-17-producing cells. This review discusses the features of IL-17-producing cells, of both lymphocytic and myeloid origins, as well as their suggested pro- and/or anti-tumorigenic functions in an organ-dependent context. Potential therapeutic approaches targeting these cells in the tumor microenvironment will also be discussed.

The Nuclear Orphan Receptor NR4A1 is Involved in the Apoptotic Pathway Induced by LPS and Simvastatin in RAW 264.7 Macrophages

  • Kim, Yong Chan;Song, Seok Bean;Lee, Sang Kyu;Park, Sang Min;Kim, Young Sang
    • IMMUNE NETWORK
    • /
    • 제14권2호
    • /
    • pp.116-122
    • /
    • 2014
  • Macrophage death plays a role in several physiological and inflammatory pathologies such as sepsis and arthritis. In our previous work, we showed that simvastatin triggers cell death in LPS-activated RAW 264.7 mouse macrophage cells through both caspase-dependent and independent apoptotic pathways. Here, we show that the nuclear orphan receptor NR4A1 is involved in a caspase-independent apoptotic process induced by LPS and simvastatin. Simvastatin-induced NR4A1 expression in RAW 264.7 macrophages and ectopic expression of a dominant-negative mutant form of NR4A1 effectively suppressed both DNA fragmentation and the disruption of mitochondrial membrane potential (MMP) during LPS- and simvastatin-induced apoptosis. Furthermore, apoptosis was accompanied by Bcl-2-associated X protein (Bax) translocation to the mitochondria. Our findings suggest that NR4A1 expression and mitochondrial translocation of Bax are related to simvastatin-induced apoptosis in LPS-activated RAW 264.7 macrophages.

GPR78 promotes lung cancer cell migration and metastasis by activation of Gαq-Rho GTPase pathway

  • Dong, Dan-Dan;Zhou, Hui;Li, Gao
    • BMB Reports
    • /
    • 제49권11호
    • /
    • pp.623-628
    • /
    • 2016
  • GPR78 is an orphan G-protein coupled receptor (GPCR) that is predominantly expressed in human brain tissues. Currently, the function of GPR78 is unknown. This study revealed that GPR78 was expressed in lung cancer cells and functioned as a novel regulator of lung cancer cell migration and metastasis. We found that knockdown of GPR78 in lung cancer cells suppressed cell migration. Moreover, GPR78 modulated the formation of actin stress fibers in A549 cells, in a RhoA- and Rac1-dependent manner. At the molecular level, GPR78 regulated cell motility through the activation of $G{\alpha}q$-RhoA/Rac1 pathway. We further demonstrated that in vivo, the knockdown of GPR78 inhibited lung cancer cell metastasis. These findings suggest that GPR78 is a novel regulator for lung cancer metastasis and may serve as a potential drug target against metastatic human lung cancer.