Mary Loeken

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc Pax3 stimulates p53 ubiquitination and degradation independent of transcription
    Xiao dan Wang
    Section on Developmental and Stem Cell Biology, Department of Medicine, Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts, USA
    PLoS ONE 6:e29379. 2011
  2. ncbi request reprint Advances in understanding the molecular causes of diabetes-induced birth defects
    Mary R Loeken
    Joslin Diabetes Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
    J Soc Gynecol Investig 13:2-10. 2006
  3. ncbi request reprint Current perspectives on the causes of neural tube defects resulting from diabetic pregnancy
    Mary R Loeken
    Section on Developmental and Stem Cell Biology at Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA
    Am J Med Genet C Semin Med Genet 135:77-87. 2005
  4. ncbi request reprint Hypoxic stress in diabetic pregnancy contributes to impaired embryo gene expression and defective development by inducing oxidative stress
    Rulin Li
    Section of Developmental and Stem Cell Biology, Joslin Diabetes Center, Boston, MA 02215, USA
    Am J Physiol Endocrinol Metab 289:E591-9. 2005
  5. doi request reprint Oxidative stress during diabetic pregnancy disrupts cardiac neural crest migration and causes outflow tract defects
    Sarah C Morgan
    Section on Developmental and Stem Cell Biology, Joslin Diabetes Center, One Joslin Place, Boston, Massachusetts 02215, USA
    Birth Defects Res A Clin Mol Teratol 82:453-63. 2008
  6. doi request reprint Gender differences in research grant applications and funding outcomes for medical school faculty
    Susan E Waisbren
    Children s Hospital, Boston, Massachusetts, USA
    J Womens Health (Larchmt) 17:207-14. 2008
  7. doi request reprint Diabetes and apoptosis: neural crest cells and neural tube
    James H Chappell
    Section on Developmental and Stem Cell Biology, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA
    Apoptosis 14:1472-83. 2009
  8. pmc Rescue of neural tube defects in Pax-3-deficient embryos by p53 loss of function: implications for Pax-3- dependent development and tumorigenesis
    Lydie Pani
    Section on Cellular and Molecular Physiology, Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    Genes Dev 16:676-80. 2002
  9. ncbi request reprint Polymorphic susceptibility to the molecular causes of neural tube defects during diabetic embryopathy
    Lydie Pani
    Section on Cellular and Molecular Physiology, Joslin Diabetes Center, Boston, Massachusetts 02215, USA
    Diabetes 51:2871-4. 2002
  10. ncbi request reprint Activation of the hexosamine pathway causes oxidative stress and abnormal embryo gene expression: involvement in diabetic teratogenesis
    Melissa Horal
    Section on Developmental and Stem Cell Biology, Joslin Diabetes Center, Boston, Massachusetts 02215, USA
    Birth Defects Res A Clin Mol Teratol 70:519-27. 2004

Collaborators

  • Margaret Buckingham
  • George King
  • Deborah Levine
  • James H Chappell
  • Andrew J Copp
  • Frederic Relaix
  • Sarah C Morgan
  • Melissa Horal
  • Lydie Pani
  • Xiao dan Wang
  • Lisa L Sandell
  • Susan E Waisbren
  • Fangnian Wang
  • Rulin Li
  • Yuji Hiramatsu
  • Billy W H Chan
  • Jo M Solet
  • Nicole Ullrich
  • Andrea Farkas Patenaude
  • Janina Longtine
  • Hannah Bowles
  • Ellice Lieberman
  • Rochelle Walensky
  • Hyung Yul Lee
  • Carol Nadelson
  • Patricia Weitzman
  • Carole Goldberg
  • John M Levorse
  • Adrienne G Randolph
  • Kelly H Zou
  • Sandra Gould
  • S Jean Emans
  • Deborah Quinn
  • Tayaba Hasan
  • Helen Christou
  • Shoba Thirumangalathu
  • Sung Kwon Jung
  • Martha Chase
  • Peter J S Smith
  • Antti Virkamäki
  • Robert Stanton
  • Zhiquan Zhang
  • Naotaka Sekiguchi
  • Tsuyoshi Koide
  • Tamotsu Yokota
  • Toshihiko Shiroishi
  • Keiji Isshiki
  • Kwok Siu Chan
  • Maran B W Leung
  • Sau Man Yeung
  • Alisa S W Shum
  • Michio Hayashi

Detail Information

Publications16

  1. pmc Pax3 stimulates p53 ubiquitination and degradation independent of transcription
    Xiao dan Wang
    Section on Developmental and Stem Cell Biology, Department of Medicine, Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts, USA
    PLoS ONE 6:e29379. 2011
    ..This demonstrates that Pax3 regulates these processes by blocking p53 function. Here we investigated the mechanism by which Pax3 blocks p53 function...
  2. ncbi request reprint Advances in understanding the molecular causes of diabetes-induced birth defects
    Mary R Loeken
    Joslin Diabetes Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
    J Soc Gynecol Investig 13:2-10. 2006
    ..To review the current understanding of the molecular causes of birth defects resulting from diabetic pregnancy, with a focus on neural tube defects...
  3. ncbi request reprint Current perspectives on the causes of neural tube defects resulting from diabetic pregnancy
    Mary R Loeken
    Section on Developmental and Stem Cell Biology at Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA
    Am J Med Genet C Semin Med Genet 135:77-87. 2005
    ..Evidence in support of this model, in which excess glucose metabolism inhibits expression of Pax3, thereby derepressing p53-dependent apoptosis of neuroepithelium and leading to NTD will be discussed...
  4. ncbi request reprint Hypoxic stress in diabetic pregnancy contributes to impaired embryo gene expression and defective development by inducing oxidative stress
    Rulin Li
    Section of Developmental and Stem Cell Biology, Joslin Diabetes Center, Boston, MA 02215, USA
    Am J Physiol Endocrinol Metab 289:E591-9. 2005
    ..These observations suggest that maternal hyperglycemia depletes O(2) in the embryo and that this contributes to oxidative stress and the adverse effects of maternal hyperglycemia on embryo development...
  5. doi request reprint Oxidative stress during diabetic pregnancy disrupts cardiac neural crest migration and causes outflow tract defects
    Sarah C Morgan
    Section on Developmental and Stem Cell Biology, Joslin Diabetes Center, One Joslin Place, Boston, Massachusetts 02215, USA
    Birth Defects Res A Clin Mol Teratol 82:453-63. 2008
    ..Here we tested whether maternal diabetes, through hyperglycemia-induced oxidative stress, before the onset of CNC delamination, impairs CNC migration and cardiac outflow tract septation...
  6. doi request reprint Gender differences in research grant applications and funding outcomes for medical school faculty
    Susan E Waisbren
    Children s Hospital, Boston, Massachusetts, USA
    J Womens Health (Larchmt) 17:207-14. 2008
    ..To evaluate whether there were differences in acquisition of research grant support between male and female faculty at eight Harvard Medical School-affiliated institutions...
  7. doi request reprint Diabetes and apoptosis: neural crest cells and neural tube
    James H Chappell
    Section on Developmental and Stem Cell Biology, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA
    Apoptosis 14:1472-83. 2009
    ..This, then provides a cellular explanation for the cardiac outflow tract and neural tube and defects induced by diabetic pregnancy...
  8. pmc Rescue of neural tube defects in Pax-3-deficient embryos by p53 loss of function: implications for Pax-3- dependent development and tumorigenesis
    Lydie Pani
    Section on Cellular and Molecular Physiology, Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts 02215, USA
    Genes Dev 16:676-80. 2002
    ..These results suggest that Pax-3 regulates neural tube closure by inhibiting p53-dependent apoptosis, rather than by inducing neural tube-specific gene expression...
  9. ncbi request reprint Polymorphic susceptibility to the molecular causes of neural tube defects during diabetic embryopathy
    Lydie Pani
    Section on Cellular and Molecular Physiology, Joslin Diabetes Center, Boston, Massachusetts 02215, USA
    Diabetes 51:2871-4. 2002
    ..Moreover, if susceptibility to diabetic embryopathy is variable in humans as well as in mice, it may be possible to screen individuals at increased risk for this complication of diabetes...
  10. ncbi request reprint Activation of the hexosamine pathway causes oxidative stress and abnormal embryo gene expression: involvement in diabetic teratogenesis
    Melissa Horal
    Section on Developmental and Stem Cell Biology, Joslin Diabetes Center, Boston, Massachusetts 02215, USA
    Birth Defects Res A Clin Mol Teratol 70:519-27. 2004
    ..The hexosamine pathway is activated in many tissues during diabetes and could contribute to oxidative stress by inhibiting the pentose shunt pathway, thereby diminishing production of the cellular antioxidant, reduced glutathione (GSH)...
  11. ncbi request reprint Hyperglycemia-induced oxidative stress in diabetic complications
    George L King
    Section on Vascular Cell Biology and Complications, Joslin Diabetes Center, Boston, Massachusetts, USA
    Histochem Cell Biol 122:333-8. 2004
    ..The focus of this review will be on the role of oxidative stress in the etiology of diabetic complications...
  12. ncbi request reprint Diacylglycerol production and protein kinase C activity are increased in a mouse model of diabetic embryopathy
    Yuji Hiramatsu
    Section on Cellular and Molecular Physiology, Joslin Diabetes Center, Boston, Massachusetts 02215, USA
    Diabetes 51:2804-10. 2002
    ..These data indicate that hyperglycemia just before organogenesis activates the DAG-PKC cascade and is correlated with congenital defects...
  13. ncbi request reprint Establishment of new mouse embryonic stem cell lines is improved by physiological glucose and oxygen
    Fangnian Wang
    Section on Developmental and Stem Cell Biology, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA
    Cloning Stem Cells 8:108-16. 2006
    ..These results suggest that culture of cells derived from murine blastocysts in physiological oxygen and glucose reduces oxidant stress, which increases the success of establishing new embryonic stem cell lines...
  14. pmc Cardiac outflow tract septation failure in Pax3-deficient embryos is due to p53-dependent regulation of migrating cardiac neural crest
    Sarah C Morgan
    Section on Developmental and Stem Cell Biology, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA
    Mech Dev 125:757-67. 2008
    ..These results indicate that Pax3 is required for cardiac outflow tract septation because it blocks p53-dependent processes during CNC migration...
  15. ncbi request reprint Maternal diabetes increases the risk of caudal regression caused by retinoic acid
    Billy W H Chan
    Department of Anatomy, The Chinese University of Hong Kong, Hong Kong, People s Republic of China
    Diabetes 51:2811-6. 2002
    ..This positive interaction between RA and maternal diabetes may have implications for humans in suggesting increased susceptibility to environmental teratogens during diabetic pregnancy...

Research Grants20

  1. Embryonic Gene Expression During Diabetic Embryopathy
    Mary Loeken; Fiscal Year: 2006
    ....
  2. MOLECULAR REGULATION: EMBYROGENESIS BY METABOLIC STRESS
    Mary Loeken; Fiscal Year: 2003
    ..Aim 3 will test whether overexpression of factors that regulate both developmental control and stress-responsive genes protects embryos from the altered gene expression, apoptosis, and NTD associated with excess glucose. ..
  3. Embryonic Gene Expression During Diabetic Embryopathy
    Mary R Loeken; Fiscal Year: 2010
    ..abstract_text> ..
  4. SEARCH FOR THE MOLECULAR CAUSES OF DIABETIC EMBRYOPATHY
    Mary Loeken; Fiscal Year: 1999
    ..These experiments will reveal, in a way that has not been done in the past, the molecular mechanisms by which embryonic development is during diabetic pregnancy. ..
  5. Embryonic Gene Expression During Diabetic Embryopathy
    Mary Loeken; Fiscal Year: 2009
    ..abstract_text> ..
  6. SEARCH FOR THE MOLECULAR CAUSES OF DIABETIC EMBRYOPATHY
    Mary R Loeken; Fiscal Year: 2010
    ..This project will investigate how altered expression of a gene that is required during early embryo development, resulting from diabetic pregnancy, leads to birth defects. ..
  7. SEARCH FOR THE MOLECULAR CAUSES OF DIABETIC EMBRYOPATHY
    Mary Loeken; Fiscal Year: 2007
    ..This research will significantly advance our knowledge of how closure and dorsalization of the neural tube is regulated, and provide new information on the molecular mechanisms by which diabetic pregnancy causes NTD. ..
  8. Embryonic Gene Expression During Diabetic Embryopathy
    Mary Loeken; Fiscal Year: 2007
    ....
  9. SEARCH FOR THE MOLECULAR CAUSES OF DIABETIC EMBRYOPATHY
    Mary Loeken; Fiscal Year: 2006
    ..This research will significantly advance our knowledge of how closure and dorsalization of the neural tube is regulated, and provide new information on the molecular mechanisms by which diabetic pregnancy causes NTD. ..
  10. SEARCH FOR THE MOLECULAR CAUSES OF DIABETIC EMBRYOPATHY
    Mary Loeken; Fiscal Year: 2005
    ..This research will significantly advance our knowledge of how closure and dorsalization of the neural tube is regulated, and provide new information on the molecular mechanisms by which diabetic pregnancy causes NTD. ..
  11. SEARCH FOR THE MOLECULAR CAUSES OF DIABETIC EMBRYOPATHY
    Mary Loeken; Fiscal Year: 2004
    ..This research will significantly advance our knowledge of how closure and dorsalization of the neural tube is regulated, and provide new information on the molecular mechanisms by which diabetic pregnancy causes NTD. ..
  12. MOLECULAR REGULATION: EMBYROGENESIS BY METABOLIC STRESS
    Mary Loeken; Fiscal Year: 2002
    ..Aim 3 will test whether overexpression of factors that regulate both developmental control and stress-responsive genes protects embryos from the altered gene expression, apoptosis, and NTD associated with excess glucose. ..
  13. SEARCH FOR THE MOLECULAR CAUSES OF DIABETIC EMBRYOPATHY
    Mary Loeken; Fiscal Year: 2002
    ..These experiments will reveal, in a way that has not been done in the past, the molecular mechanisms by which embryonic development is during diabetic pregnancy. ..
  14. MOLECULAR REGULATION: EMBYROGENESIS BY METABOLIC STRESS
    Mary Loeken; Fiscal Year: 2001
    ..Aim 3 will test whether overexpression of factors that regulate both developmental control and stress-responsive genes protects embryos from the altered gene expression, apoptosis, and NTD associated with excess glucose. ..
  15. SEARCH FOR THE MOLECULAR CAUSES OF DIABETIC EMBRYOPATHY
    Mary Loeken; Fiscal Year: 2001
    ..These experiments will reveal, in a way that has not been done in the past, the molecular mechanisms by which embryonic development is during diabetic pregnancy. ..
  16. SEARCH FOR THE MOLECULAR CAUSES OF DIABETIC EMBRYOPATHY
    Mary Loeken; Fiscal Year: 2000
    ..These experiments will reveal, in a way that has not been done in the past, the molecular mechanisms by which embryonic development is during diabetic pregnancy. ..
  17. Embryonic Gene Expression During Diabetic Embryopathy
    Mary R Loeken; Fiscal Year: 2010
    ..abstract_text> ..