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...

Research Grants3

  1. The Role of Tuberin in Smooth Muscle Cell Proliferation
    Geraldine Finlay; Fiscal Year: 2007
    This is an application for a Mentored Clinical Scientist Development Award for Dr. Geraldine Finlay to pursue research on the influence of tuberin on the control of smooth muscle cell growth in response to estrogen...
  2. Tuberin and hamartin in rapamycin-sensitive & rapamycin-insensitive smooth muscle
    Geraldine Finlay; Fiscal Year: 2009
    ..The purpose of the proposed studies is to improve our understanding of the mechanisms that lead to uncontrolled growth in smooth muscle and to develop new targets for the treatment of pulmonary hypertension. ..
  3. Tuberin and hamartin in rapamycin-sensitive & rapamycin-insensitive smooth muscle
    Geraldine A Finlay; Fiscal Year: 2010
    ..The purpose of the proposed studies is to improve our understanding of the mechanisms that lead to uncontrolled growth in smooth muscle and to develop new targets for the treatment of pulmonary hypertension. ..