Emily Noonan

Summary

Publications

  1. ncbi request reprint HDAC inhibition prevents NF-kappa B activation by suppressing proteasome activity: down-regulation of proteasome subunit expression stabilizes I kappa B alpha
    Robert F Place
    Department of Molecular and Cellular Biology, University of Connecticut, 91 North Eagleville Road, U 3125, Storrs, CT 06269 3125, USA
    Biochem Pharmacol 70:394-406. 2005
  2. pmc miR-449a causes Rb-dependent cell cycle arrest and senescence in prostate cancer cells
    Emily J Noonan
    Center for Molecular Biology in Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA
    Oncotarget 1:349-58. 2010
  3. doi request reprint miR-449a targets HDAC-1 and induces growth arrest in prostate cancer
    E J Noonan
    Department of Urology, Veterans Affairs Medical Center and University of California, San Francisco, CA 94121, USA
    Oncogene 28:1714-24. 2009
  4. doi request reprint Hsp70B' and Hsp72 form a complex in stressed human colon cells and each contributes to cytoprotection
    Emily Noonan
    Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06269, USA
    Exp Cell Res 314:2468-76. 2008
  5. pmc Surface expression of Hsp70B' in response to proteasome inhibition in human colon cells
    Emily J Noonan
    Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06269 3125, USA
    Cell Stress Chaperones 13:105-10. 2008
  6. pmc Hsp70B' regulation and function
    Emily J Noonan
    Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06269 3125, USA
    Cell Stress Chaperones 12:393-402. 2007
  7. pmc Hsp70B' regulation and function
    Emily J Noonan
    Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06269 3125, USA
    Cell Stress Chaperones 12:219-29. 2007
  8. pmc MicroRNA-373 induces expression of genes with complementary promoter sequences
    Robert F Place
    Department of Urology, Veterans Affairs Medical Center and University of California, San Francisco, CA 94121, USA
    Proc Natl Acad Sci U S A 105:1608-13. 2008
  9. pmc Defining features and exploring chemical modifications to manipulate RNAa activity
    Robert F Place
    Helen Diller Comprehensive Cancer Center, Department of Urology, University of California, PO Box 589001, San Francisco, CA 94158 9001, USA
    Curr Pharm Biotechnol 11:518-26. 2010
  10. pmc HDACs and the senescent phenotype of WI-38 cells
    Robert F Place
    Department of Molecular and Cell Biology, University of Connecticut, Storrs, Connecticut 06269, USA
    BMC Cell Biol 6:37. 2005

Collaborators

Detail Information

Publications16

  1. ncbi request reprint HDAC inhibition prevents NF-kappa B activation by suppressing proteasome activity: down-regulation of proteasome subunit expression stabilizes I kappa B alpha
    Robert F Place
    Department of Molecular and Cellular Biology, University of Connecticut, 91 North Eagleville Road, U 3125, Storrs, CT 06269 3125, USA
    Biochem Pharmacol 70:394-406. 2005
    ..This information may be useful for the further development and targeting of HDAC inhibitors as anti-neoplastic and anti-inflammatory agents...
  2. pmc miR-449a causes Rb-dependent cell cycle arrest and senescence in prostate cancer cells
    Emily J Noonan
    Center for Molecular Biology in Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA
    Oncotarget 1:349-58. 2010
    ..These data indicate that miR-449a is a miRNA component of the Rb pathway and its tumor suppressor-like effects, in part, depends on Rb status in prostate cancer cells...
  3. doi request reprint miR-449a targets HDAC-1 and induces growth arrest in prostate cancer
    E J Noonan
    Department of Urology, Veterans Affairs Medical Center and University of California, San Francisco, CA 94121, USA
    Oncogene 28:1714-24. 2009
    ..Our findings provide new insight into the function of miRNA in regulating HDAC expression in normal versus cancerous tissue...
  4. doi request reprint Hsp70B' and Hsp72 form a complex in stressed human colon cells and each contributes to cytoprotection
    Emily Noonan
    Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06269, USA
    Exp Cell Res 314:2468-76. 2008
    ..In addition there are implications for chemotherapy protocols and for pathological conditions in which the contributions to cytoprotection of both Hsp70B' and Hsp72 are modulated by cell numbers or density...
  5. pmc Surface expression of Hsp70B' in response to proteasome inhibition in human colon cells
    Emily J Noonan
    Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06269 3125, USA
    Cell Stress Chaperones 13:105-10. 2008
    ..Amino acid sequence differences were concentrated in the lid regions and the C-terminal domains raising the possibility that Hsp72 and Hsp70B' bind different co-chaperones or cell surface receptors...
  6. pmc Hsp70B' regulation and function
    Emily J Noonan
    Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06269 3125, USA
    Cell Stress Chaperones 12:393-402. 2007
    ..These findings are likely to be important in pathological conditions in which Hsp70B' contributes to cell survival...
  7. pmc Hsp70B' regulation and function
    Emily J Noonan
    Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT 06269 3125, USA
    Cell Stress Chaperones 12:219-29. 2007
    ..These findings are likely to be important in pathological conditions in which Hsp70B' contributes to cell survival...
  8. pmc MicroRNA-373 induces expression of genes with complementary promoter sequences
    Robert F Place
    Department of Urology, Veterans Affairs Medical Center and University of California, San Francisco, CA 94121, USA
    Proc Natl Acad Sci U S A 105:1608-13. 2008
    ..In conclusion, we have identified a miRNA that targets promoter sequences and induces gene expression. These findings reveal a new mode by which miRNAs may regulate gene expression...
  9. pmc Defining features and exploring chemical modifications to manipulate RNAa activity
    Robert F Place
    Helen Diller Comprehensive Cancer Center, Department of Urology, University of California, PO Box 589001, San Francisco, CA 94158 9001, USA
    Curr Pharm Biotechnol 11:518-26. 2010
    ..These findings reveal functional features of RNAa that may be utilized to augment saRNA function for mechanistic studies or the development of RNAa-based drugs...
  10. pmc HDACs and the senescent phenotype of WI-38 cells
    Robert F Place
    Department of Molecular and Cell Biology, University of Connecticut, Storrs, Connecticut 06269, USA
    BMC Cell Biol 6:37. 2005
    ..Here we examine the influence of HDAC inhibitors on the expression of senescent markers in pre- and post-senescent WI-38 cells...
  11. ncbi request reprint Cell number-dependent regulation of Hsp70B' expression: evidence of an extracellular regulator
    Emily J Noonan
    Department of Molecular and Cell Biology, University of Connecticut, Storrs, Connecticut 06269, USA
    J Cell Physiol 210:201-11. 2007
    ....
  12. doi request reprint Genistein induces the p21WAF1/CIP1 and p16INK4a tumor suppressor genes in prostate cancer cells by epigenetic mechanisms involving active chromatin modification
    Shahana Majid
    Department of Urology, Veterans Affairs Medical Center, University of California, San Francisco, California 94121, USA
    Cancer Res 68:2736-44. 2008
    ..Altogether, our data provide new insights into the epigenetic mechanism of the action of genistein that may contribute to the chemopreventive activity of this dietary isoflavone and have important implications for epigenetic therapy...
  13. ncbi request reprint HDAC3 overexpression and colon cancer cell proliferation and differentiation
    Colleen C Spurling
    Department of Molecular and Cell Biology, University of Connecticut, Storrs, Connecticut, USA
    Mol Carcinog 47:137-47. 2008
    ..Our data support a central role for HDAC3 in regulating the cell proliferation and differentiation of colon cancer cells and suggest a potential mechanism by which colon cancers may become resistant to luminal butyrate...
  14. ncbi request reprint Circumvention and reactivation of the p53 oncogene checkpoint in mouse colon tumors
    Wataru Aizu
    Department of Molecular and Cell Biology, 91 North Eagleville Road, University of Connecticut, Storrs, CT 06269 3125, USA
    Biochem Pharmacol 72:981-91. 2006
    ....
  15. pmc Double stranded-RNA-mediated activation of P21 gene induced apoptosis and cell cycle arrest in renal cell carcinoma
    Jared M Whitson
    University of California San Francisco, Department of Urology, San Francisco, CA 94121, USA
    Int J Cancer 125:446-52. 2009
    ..This is the first report that demonstrates dsRNA mediated gene activation in renal cell carcinoma and suggests that forced over-expression of p21 may lead to an increase in apoptosis through a survivin dependent mechanism...
  16. doi request reprint Genistein down-regulates androgen receptor by modulating HDAC6-Hsp90 chaperone function
    Shashwati Basak
    Department of Urology, San Francisco Veterans Affairs Medical Center, San Francisco, CA 94121, USA
    Mol Cancer Ther 7:3195-202. 2008
    ..Our results suggest that genistein could be used as a potential chemopreventive agent for prostate cancers along with known inhibitors of HDAC6 and Hsp90...