Sang Oh Yoon

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Isoginkgetin inhibits tumor cell invasion by regulating phosphatidylinositol 3-kinase/Akt-dependent matrix metalloproteinase-9 expression
    Sang Oh Yoon
    Department of Cell Biology, Harvard Medical School, LHRRB 606, 240 Longwood Avenue, Boston, MA 02115, USA
    Mol Cancer Ther 5:2666-75. 2006
  2. ncbi request reprint A novel mechanism for integrin-mediated ras activation in breast carcinoma cells: the alpha6beta4 integrin regulates ErbB2 translation and transactivates epidermal growth factor receptor/ErbB2 signaling
    Sang Oh Yoon
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Res 66:2732-9. 2006
  3. ncbi request reprint Hypoxia stimulates carcinoma invasion by stabilizing microtubules and promoting the Rab11 trafficking of the alpha6beta4 integrin
    Sang Oh Yoon
    Division of Cancer Biology and Angiogenesis, Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
    Cancer Res 65:2761-9. 2005
  4. pmc Ran-binding protein 3 phosphorylation links the Ras and PI3-kinase pathways to nucleocytoplasmic transport
    Sang Oh Yoon
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA
    Mol Cell 29:362-75. 2008
  5. pmc Phosphoproteomic analysis identifies Grb10 as an mTORC1 substrate that negatively regulates insulin signaling
    Yonghao Yu
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Science 332:1322-6. 2011
  6. pmc ERK2 but not ERK1 induces epithelial-to-mesenchymal transformation via DEF motif-dependent signaling events
    Sejeong Shin
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA
    Mol Cell 38:114-27. 2010
  7. ncbi request reprint Ras stimulation of E2F activity and a consequent E2F regulation of integrin alpha6beta4 promote the invasion of breast carcinoma cells
    Sang Oh Yoon
    Division of Cancer Biology and Angiogenesis, Department of Pathology Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA
    Cancer Res 66:6288-95. 2006
  8. ncbi request reprint The Met receptor and alpha 6 beta 4 integrin can function independently to promote carcinoma invasion
    Jun Chung
    Division of Cancer Biology and Angiogenesis, Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
    J Biol Chem 279:32287-93. 2004
  9. pmc Glucose addiction of TSC null cells is caused by failed mTORC1-dependent balancing of metabolic demand with supply
    Andrew Y Choo
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Mol Cell 38:487-99. 2010
  10. doi request reprint SKAR links pre-mRNA splicing to mTOR/S6K1-mediated enhanced translation efficiency of spliced mRNAs
    Xiaoju Max Ma
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA
    Cell 133:303-13. 2008

Collaborators

Detail Information

Publications20

  1. ncbi request reprint Isoginkgetin inhibits tumor cell invasion by regulating phosphatidylinositol 3-kinase/Akt-dependent matrix metalloproteinase-9 expression
    Sang Oh Yoon
    Department of Cell Biology, Harvard Medical School, LHRRB 606, 240 Longwood Avenue, Boston, MA 02115, USA
    Mol Cancer Ther 5:2666-75. 2006
    ..This suggests that isoginkgetin could be a potential candidate as a therapeutic agent against tumor invasion...
  2. ncbi request reprint A novel mechanism for integrin-mediated ras activation in breast carcinoma cells: the alpha6beta4 integrin regulates ErbB2 translation and transactivates epidermal growth factor receptor/ErbB2 signaling
    Sang Oh Yoon
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Cancer Res 66:2732-9. 2006
    ..These findings provide a mechanism that substantiates the reported role of alpha(6)beta(4) in carcinoma invasion...
  3. ncbi request reprint Hypoxia stimulates carcinoma invasion by stabilizing microtubules and promoting the Rab11 trafficking of the alpha6beta4 integrin
    Sang Oh Yoon
    Division of Cancer Biology and Angiogenesis, Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
    Cancer Res 65:2761-9. 2005
    ..This increase is dependent on Rab11 and stable microtubules. In summary, we identify vesicle trafficking as a novel target of hypoxic stimulation that is important for tumor invasion...
  4. pmc Ran-binding protein 3 phosphorylation links the Ras and PI3-kinase pathways to nucleocytoplasmic transport
    Sang Oh Yoon
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA
    Mol Cell 29:362-75. 2008
    ..Our findings highlight an important link between two major cell-fate determinants: nuclear transport and the Ras/ERK/RSK and PI3K/Akt signaling pathways...
  5. pmc Phosphoproteomic analysis identifies Grb10 as an mTORC1 substrate that negatively regulates insulin signaling
    Yonghao Yu
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Science 332:1322-6. 2011
    ....
  6. pmc ERK2 but not ERK1 induces epithelial-to-mesenchymal transformation via DEF motif-dependent signaling events
    Sejeong Shin
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA
    Mol Cell 38:114-27. 2010
    ..Thus, an apparent critical role for ERK2 DEF motif signaling during tumorigenesis is the regulation of Fra1 and the subsequent induction of ZEB1/2, suggesting a potential therapeutic target for Ras-regulated tumorigenesis...
  7. ncbi request reprint Ras stimulation of E2F activity and a consequent E2F regulation of integrin alpha6beta4 promote the invasion of breast carcinoma cells
    Sang Oh Yoon
    Division of Cancer Biology and Angiogenesis, Department of Pathology Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA
    Cancer Res 66:6288-95. 2006
    ..This mechanism links active H-Ras, transcriptionally active E2F, and the alpha6beta4 integrin in a common pathway that culminates in enhanced alpha6beta4-dependent invasion...
  8. ncbi request reprint The Met receptor and alpha 6 beta 4 integrin can function independently to promote carcinoma invasion
    Jun Chung
    Division of Cancer Biology and Angiogenesis, Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
    J Biol Chem 279:32287-93. 2004
    ..These data argue that the invasive function of Met can be independent of alpha(6)beta(4) and that alpha(6)beta(4) has a generic influence on the invasion of carcinoma cells that is not specific to Met...
  9. pmc Glucose addiction of TSC null cells is caused by failed mTORC1-dependent balancing of metabolic demand with supply
    Andrew Y Choo
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Mol Cell 38:487-99. 2010
    ..Therefore, mTORC1 inhibition during energetic stress is primarily to balance metabolic demand with supply...
  10. doi request reprint SKAR links pre-mRNA splicing to mTOR/S6K1-mediated enhanced translation efficiency of spliced mRNAs
    Xiaoju Max Ma
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA
    Cell 133:303-13. 2008
    ..Thus, SKAR-mediated recruitment of activated S6K1 to newly processed mRNPs serves as a conduit between mTOR checkpoint signaling and the pioneer round of translation when cells exist in conditions supportive of protein synthesis...
  11. pmc Glycogen synthase kinase-3 is an endogenous inhibitor of Snail transcription: implications for the epithelial-mesenchymal transition
    Robin E Bachelder
    Department of Pathology, Division of Cancer Biology and Angiogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    J Cell Biol 168:29-33. 2005
    ..These findings indicate that epithelial cells must sustain activation of a specific kinase to impede a mesenchymal transition...
  12. pmc p90 ribosomal S6 kinase and p70 ribosomal S6 kinase link phosphorylation of the eukaryotic chaperonin containing TCP-1 to growth factor, insulin, and nutrient signaling
    Yuki Abe
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 284:14939-48. 2009
    ..Although the molecular mechanism of CCTbeta regulation remains unclear, our findings demonstrate a link between oncogene and growth factor signaling and chaperonin CCT-mediated cellular activities...
  13. pmc Rapamycin differentially inhibits S6Ks and 4E-BP1 to mediate cell-type-specific repression of mRNA translation
    Andrew Y Choo
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 105:17414-9. 2008
    ..Finally, we show that mTOR catalytic inhibitors are effective inhibitors of the rapamycin-resistant phenotype...
  14. ncbi request reprint Selenite inhibits apoptosis via activation of the PI3-K/Akt pathway
    Sang Oh Yoon
    Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Taejon 305 701, South Korea
    Ann N Y Acad Sci 973:221-3. 2002
  15. ncbi request reprint Pro-MMP-2 activation by the PPARgamma agonist, ciglitazone, induces cell invasion through the generation of ROS and the activation of ERK
    Kyu Han Kim
    Department of Biological Science, Biochemical Toxicology Lab, Korea Advanced Institute of Science and Technology, 373 1 Gusong Dong, Yusong gu, Taejon, Republic of Korea
    FEBS Lett 581:3303-10. 2007
    ..This study suggests that ciglitazone-induced pro-MMP-2 activation increases PPARgamma-independent tumor cell invasion through ROS production and ERK activation in some types of cancer cells...
  16. ncbi request reprint Roles of matrix metalloproteinases in tumor metastasis and angiogenesis
    Sang Oh Yoon
    Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305 701, Korea
    J Biochem Mol Biol 36:128-37. 2003
    ..The detailed regulations of MMPs are described in this review...
  17. ncbi request reprint Cell proliferation induced by reactive oxygen species is mediated via mitogen-activated protein kinase in Chinese hamster lung fibroblast (V79) cells
    Min Joon Han
    Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305 701, Korea
    Mol Cells 15:94-101. 2003
    ..At the transcriptional level, the phosphorylation of c-Jun and ATF-2, which are mediated by JNK and p38 MAPK, were also increased by treatment with PMS...
  18. ncbi request reprint Sustained production of H(2)O(2) activates pro-matrix metalloproteinase-2 through receptor tyrosine kinases/phosphatidylinositol 3-kinase/NF-kappa B pathway
    Sang Oh Yoon
    Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Taejon 305 701, South Korea
    J Biol Chem 277:30271-82. 2002
    ..Furthermore, PMS increased cell motility and invasion but decreased cell-cell interaction. Cell-matrix interaction was not affected by PMS...
  19. ncbi request reprint Histone deacetylases, HDAC1 and HSIR2, act as a negative regulator of ageing through p53 in human gingival fibroblast
    Moon Moo Kim
    Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305 701, South Korea
    Mech Ageing Dev 125:351-7. 2004
    ..These results suggest that primary HGFs can be a useful human ageing model, and HDAC1, HSIR2, p53 and p21 may play an important role in ageing process of human beings...
  20. ncbi request reprint Selenite suppresses hydrogen peroxide-induced cell apoptosis through inhibition of ASK1/JNK and activation of PI3-K/Akt pathways
    Sang Oh Yoon
    Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Taejon 305 701, South Korea
    FASEB J 16:111-3. 2002
    ..These observations demonstrate that selenite increases cell proliferation and maintains cell survival by activating the antiapoptotic signal and blocking the apoptotic signal...