Geraldine Finlay

Summary

Affiliation: Tufts-New England Medical Center
Country: USA

Publications

  1. ncbi request reprint Regulation of PDGF production and ERK activation by estrogen is associated with TSC2 gene expression
    G A Finlay
    Pulmonary and Critical Care Division, Department of Medicine, Tupper Research Institute, New England Medical Center, NEMC 257, 750 Washington St, Boston, MA 02111, USA
    Am J Physiol Cell Physiol 285:C409-18. 2003
  2. ncbi request reprint Estrogen-induced smooth muscle cell growth is regulated by tuberin and associated with altered activation of platelet-derived growth factor receptor-beta and ERK-1/2
    Geraldine A Finlay
    Pulmonary and Critical Care Division, Department of Medicine, Tupper Research Institute, Tufts New England Medical Center, Boston, Massachusetts 02111, USA
    J Biol Chem 279:23114-22. 2004
  3. ncbi request reprint Platelet-derived growth factor-induced p42/44 mitogen-activated protein kinase activation and cellular growth is mediated by reactive oxygen species in the absence of TSC2/tuberin
    Geraldine A Finlay
    Pulmonary and Critical Care Division, Department of Medicine, Tupper Research Institute, New England Medical Center, Boston, Massacusetts 02111, USA
    Cancer Res 65:10881-90. 2005
  4. ncbi request reprint Selective inhibition of growth of tuberous sclerosis complex 2 null cells by atorvastatin is associated with impaired Rheb and Rho GTPase function and reduced mTOR/S6 kinase activity
    Geraldine A Finlay
    Pulmonary and Critical Care Division, Department of Medicine, Tupper Research Institute, Tufts New England Medical Center, Boston, MA 02111, USA
    Cancer Res 67:9878-86. 2007
  5. pmc Renal and liver tumors in Tsc2(+/-) mice, a model of tuberous sclerosis complex, do not respond to treatment with atorvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor
    Geraldine A Finlay
    Pulmonary and Critical Care Division, Tufts Medical Center, Boston, MA 02111, USA
    Mol Cancer Ther 8:1799-807. 2009
  6. ncbi request reprint Estrogen modulates xanthine dehydrogenase/xanthine oxidase activity by a receptor-independent mechanism
    Rohit Budhiraja
    Pulmonary and Critical Care Division, Tupper Research Institute, Tufts New England Medical Center, Tufts University School of Medicine, Boston, MA, USA
    Antioxid Redox Signal 5:705-11. 2003

Detail Information

Publications6

  1. ncbi request reprint Regulation of PDGF production and ERK activation by estrogen is associated with TSC2 gene expression
    G A Finlay
    Pulmonary and Critical Care Division, Department of Medicine, Tupper Research Institute, New England Medical Center, NEMC 257, 750 Washington St, Boston, MA 02111, USA
    Am J Physiol Cell Physiol 285:C409-18. 2003
    ..Understanding the mechanisms that regulate the diverse responses to the steroid hormone estrogen could lead to novel approaches to the treatment of estrogen-related diseases that are characterized by aberrant cell proliferation...
  2. ncbi request reprint Estrogen-induced smooth muscle cell growth is regulated by tuberin and associated with altered activation of platelet-derived growth factor receptor-beta and ERK-1/2
    Geraldine A Finlay
    Pulmonary and Critical Care Division, Department of Medicine, Tupper Research Institute, Tufts New England Medical Center, Boston, Massachusetts 02111, USA
    J Biol Chem 279:23114-22. 2004
    ..Furthermore, the opposing effects of tuberin on estrogen-induced activation of PDGFRbeta and ERK-1/-2 suggest a pivotal role for tuberin in directing the signaling events that dictate the growth response to E2...
  3. ncbi request reprint Platelet-derived growth factor-induced p42/44 mitogen-activated protein kinase activation and cellular growth is mediated by reactive oxygen species in the absence of TSC2/tuberin
    Geraldine A Finlay
    Pulmonary and Critical Care Division, Department of Medicine, Tupper Research Institute, New England Medical Center, Boston, Massacusetts 02111, USA
    Cancer Res 65:10881-90. 2005
    ..Together, our data suggest that loss of tuberin, which causes mTOR activation, leads to a novel cellular growth-promoting pathway involving mitochondrial oxidant-dependent p42/44 MAPK activation and mitogenic growth responses to PDGF...
  4. ncbi request reprint Selective inhibition of growth of tuberous sclerosis complex 2 null cells by atorvastatin is associated with impaired Rheb and Rho GTPase function and reduced mTOR/S6 kinase activity
    Geraldine A Finlay
    Pulmonary and Critical Care Division, Department of Medicine, Tupper Research Institute, Tufts New England Medical Center, Boston, MA 02111, USA
    Cancer Res 67:9878-86. 2007
    ..Atorvastatin may have potential therapeutic benefit in TSC syndromes, including LAM...
  5. pmc Renal and liver tumors in Tsc2(+/-) mice, a model of tuberous sclerosis complex, do not respond to treatment with atorvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor
    Geraldine A Finlay
    Pulmonary and Critical Care Division, Tufts Medical Center, Boston, MA 02111, USA
    Mol Cancer Ther 8:1799-807. 2009
    ....
  6. ncbi request reprint Estrogen modulates xanthine dehydrogenase/xanthine oxidase activity by a receptor-independent mechanism
    Rohit Budhiraja
    Pulmonary and Critical Care Division, Tupper Research Institute, Tufts New England Medical Center, Tufts University School of Medicine, Boston, MA, USA
    Antioxid Redox Signal 5:705-11. 2003
    ..In conclusion, 17alpha- and 17beta-estradiol modulate the hypoxia-induced regulation of XDH/XO activity at a posttranscriptional level by a receptor-independent mechanism...