Estrogen Prevents Bone Loss via Estrogen Receptor α and Induction of Fas Ligand in Osteoclasts

[1]  J. Lloyd,et al.  Osteopetrosis , 1972 .

[2]  T. Noguchi,et al.  Effects of brefeldin A on the synthesis and secretion of egg white proteins in primary cultured oviduct cells of laying Japanese quail (Coturnix coturnix japonica). , 1989, Biochimica et biophysica acta.

[3]  AC Tose.  Cell , 1993, Cell.

[4]  K. Korach,et al.  Estrogen resistance caused by a mutation in the estrogen-receptor gene in a man. , 1994, The New England journal of medicine.

[5]  R. Kimble,et al.  Simultaneous block of interleukin-1 and tumor necrosis factor is required to completely prevent bone loss in the early postovariectomy period. , 1995, Endocrinology.

[6]  K. Umesono,et al.  The nuclear receptor superfamily: The second decade , 1995, Cell.

[7]  Tatsuya Yoshizawa,et al.  Mice lacking the vitamin D receptor exhibit impaired bone formation, uterine hypoplasia and growth retardation after weaning , 1997, Nature Genetics.

[8]  J. Miyazaki,et al.  A transgenic mouse line that retains Cre recombinase activity in mature oocytes irrespective of the cre transgene transmission. , 1997, Biochemical and biophysical research communications.

[9]  M. Kumegawa,et al.  Estrogen Inhibits Bone Resorption by Directly Inducing Apoptosis of the Bone-resorbing Osteoclasts , 1997, The Journal of experimental medicine.

[10]  Sheila J. Jones,et al.  Impaired osteoclastic bone resorption leads to osteopetrosis in cathepsin-K-deficient mice. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[11]  I. Kola,et al.  Cathepsin K Knockout Mice Develop Osteopetrosis Due to a Deficit in Matrix Degradation but Not Demineralization , 1999, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[12]  K. Korach,et al.  Estrogen receptor null mice: what have we learned and where will they lead us? , 1999, Endocrine reviews.

[13]  P. Chambon,et al.  Effect of single and compound knockouts of estrogen receptors alpha (ERalpha) and beta (ERbeta) on mouse reproductive phenotypes. , 2000, Development.

[14]  T. Martin,et al.  Therapeutic approaches to bone diseases. , 2000, Science.

[15]  R. Bland.  Steroid hormone receptor expression and action in bone. , 2000, Clinical science.

[16]  T. Nakashima,et al.  Force‐Induced Osteoclast Apoptosis In Vivo Is Accompanied by Elevation in Transforming Growth Factor β and Osteoprotegerin Expression , 2000, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[17]  S. O. Mueller,et al.  Estrogen receptors and endocrine diseases: lessons from estrogen receptor knockout mice. , 2001, Current opinion in pharmacology.

[18]  S. Davis,et al.  Minireview: Aromatase and the Regulation of Estrogen Biosynthesis-Some New Perspectives. , 2001, Endocrinology.

[19]  Nancy A. Jenkins,et al.  Recombineering: a powerful new tool for mouse functional genomics , 2001, Nature Reviews Genetics.

[20]  Patricia Ducy,et al.  Leptin Regulates Bone Formation via the Sympathetic Nervous System , 2002, Cell.

[21]  Myles Brown,et al.  Molecular Determinants for the Tissue Specificity of SERMs , 2002, Science.

[22]  J. Gustafsson,et al.  Elucidation of estrogen receptor function in bone with the use of mouse models , 2002, Trends in Endocrinology & Metabolism.

[23]  E. Wagner,et al.  Reaching a genetic and molecular understanding of skeletal development. , 2002, Developmental cell.

[24]  Kozo Nakamura,et al.  Suppressive function of androgen receptor in bone resorption , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[25]  R. Baron,et al.  A functional androgen receptor is not sufficient to allow estradiol to protect bone after gonadectomy in estradiol receptor-deficient mice. , 2003, The Journal of clinical investigation.

[26]  L. Hartmann,et al.  Selective estrogen-receptor modulators -- mechanisms of action and application to clinical practice. , 2003, The New England journal of medicine.

[27]  Kunihiro Matsumoto,et al.  Cytokines suppress adipogenesis and PPAR-γ function through the TAK1/TAB1/NIK cascade , 2003, Nature Cell Biology.

[28]  Takashi Nakamura,et al.  Chondromodulin I Is a Bone Remodeling Factor , 2003, Molecular and Cellular Biology.

[29]  Gideon A. Rodan,et al.  Control of osteoblast function and regulation of bone mass , 2003, Nature.

[30]  Kunihiro Matsumoto,et al.  Cytokines suppress adipogenesis and PPAR-gamma function through the TAK1/TAB1/NIK cascade. , 2003, Nature cell biology.

[31]  S. Teitelbaum,et al.  Genetic regulation of osteoclast development and function , 2003, Nature Reviews Genetics.

[32]  M. Parker,et al.  Nuclear Receptors A Rendezvous for Chromatin Remodeling Factors , 2003, Cell.

[33]  C. Tohyama,et al.  Modulation of oestrogen receptor signalling by association with the activated dioxin receptor , 2003, Nature.

[34]  T. Taniguchi,et al.  Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis , 2004, Nature.

[35]  P. Chambon,et al.  Brain masculinization requires androgen receptor function. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[36]  J. Tolar,et al.  Osteopetrosis. , 2004, The New England journal of medicine.

[37]  S. Khosla,et al.  Mechanisms of sex steroid effects on bone. , 2005, Biochemical and biophysical research communications.

[38]  K. Chien,et al.  Longevity and Lineages: Toward the Integrative Biology of Degenerative Diseases in Heart, Muscle, and Bone , 2005, Cell.

[39]  Clifford A. Meyer,et al.  Chromosome-Wide Mapping of Estrogen Receptor Binding Reveals Long-Range Regulation Requiring the Forkhead Protein FoxA1 , 2005, Cell.

[40]  David Greenblatt,et al.  Treatment of Postmenopausal Osteoporosis , 2005, Pharmacotherapy.

[41]  L. Raisz.  Pathogenesis of osteoporosis: concepts, conflicts, and prospects. , 2005, The Journal of clinical investigation.

[42]  T. Martin,et al.  Osteoclast-derived activity in the coupling of bone formation to resorption. , 2005, Trends in molecular medicine.

[43]  A. Zallone,et al.  FSH Directly Regulates Bone Mass , 2006, Cell.

[44]  A. Pitsillides,et al.  Osteocytes Use Estrogen Receptor α to Respond to Strain but Their ERα Content Is Regulated by Estrogen , 2006 .

[45]  G. Karsenty,et al.  Convergence between bone and energy homeostases: leptin regulation of bone mass. , 2006, Cell metabolism.

[46]  G. Mundy,et al.  Boning up on Ephrin Signaling , 2006, Cell.

[47]  S. Teitelbaum.  Osteoclasts; culprits in inflammatory osteolysis , 2005, Arthritis research & therapy.

[48]  P. Chambon,et al.  Premature ovarian failure in androgen receptor-deficient mice. , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[49]  A. Pitsillides,et al.  Osteocytes use estrogen receptor alpha to respond to strain but their ERalpha content is regulated by estrogen. , 2006, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[50]  Chao Yang Li,et al.  Mice Lacking Cathepsin K Maintain Bone Remodeling but Develop Bone Fragility Despite High Bone Mass , 2006, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[51]  S. Teitelbaum.  Osteoclasts: what do they do and how do they do it? , 2007, The American journal of pathology.

[52]  K. Umesono,et al.  Retracted: A cell cycle‐dependent co‐repressor mediates photoreceptor cell‐specific nuclear receptor function , 2007, The EMBO journal.