Recent advances in understanding the mechanism of action of bisphosphonates.

[1]  P. Hulley,et al.  Selective inhibition of Rab prenylation by a phosphonocarboxylate analogue of risedronate induces apoptosis, but not S‐phase arrest, in human myeloma cells , 2006, International journal of cancer.

[2]  C. Leu,et al.  Relative binding affinities of bisphosphonates for human bone and relationship to antiresorptive efficacy. , 2006, Bone.

[3]  G. H. Nancollas,et al.  Novel insights into actions of bisphosphonates on bone: differences in interactions with hydroxyapatite. , 2006, Bone.

[4]  M. Rogers,et al.  Inhibition of Protein Prenylation by Bisphosphonates Causes Sustained Activation of Rac, Cdc42, and Rho GTPases , 2006, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[5]  M. Rogers,et al.  Cytosolic Entry of Bisphosphonate Drugs Requires Acidification of Vesicles after Fluid-Phase Endocytosis , 2006, Molecular Pharmacology.

[6]  Wolfgang Jahnke,et al.  Structural Basis for the Exceptional in vivo Efficacy of Bisphosphonate Drugs , 2006, ChemMedChem.

[7]  B. Hendry,et al.  Prenylation is not necessary for endogenous Ras activation in non‐malignant cells , 2006, Journal of cellular biochemistry.

[8]  I. Hassinen,et al.  A new endogenous ATP analog (ApppI) inhibits the mitochondrial adenine nucleotide translocase (ANT) and is responsible for the apoptosis induced by nitrogen‐containing bisphosphonates , 2006, British journal of pharmacology.

[9]  M. Rogers,et al.  Alkylamines cause Vγ9Vδ2 T-cell activation and proliferation by inhibiting the mevalonate pathway , 2006 .

[10]  A. Schindeler,et al.  Osteoclasts but not osteoblasts are affected by a calcified surface treated with zoledronic acid in vitro. , 2005, Biochemical and biophysical research communications.

[11]  J. Koenigsknecht-Talboo,et al.  Mechanisms of Statin-mediated Inhibition of Small G-protein Function* , 2005, Journal of Biological Chemistry.

[12]  M. Rogers,et al.  Phosphonocarboxylate inhibitors of Rab geranylgeranyl transferase disrupt the prenylation and membrane localization of Rab proteins in osteoclasts in vitro and in vivo. , 2005, Bone.

[13]  M. Rogers,et al.  Molecular interactions of nitrogen-containing bisphosphonates within farnesyl diphosphate synthase , 2005 .

[14]  Petra Ross-Macdonald,et al.  Chemical genetics identifies Rab geranylgeranyl transferase as an apoptotic target of farnesyl transferase inhibitors. , 2005, Cancer cell.

[15]  A. Sewell,et al.  The bisphosphonate acute phase response: rapid and copious production of proinflammatory cytokines by peripheral blood gd T cells in response to aminobisphosphonates is inhibited by statins , 2005, Clinical and experimental immunology.

[16]  Jonathan R. Green.  Bisphosphonates: preclinical review. , 2004, The oncologist.

[17]  D. Hosfield,et al.  Structural Basis for Bisphosphonate-mediated Inhibition of Isoprenoid Biosynthesis* , 2004, Journal of Biological Chemistry.

[18]  D. Hosfield,et al.  Structural basis for bisphosphonate-mediated inhibition of isoprenoid biosynthesis , 2004 .

[19]  E. Oldfield,et al.  Quantitative Structure-Activity Relationships for γδ T Cell Activation by Bisphosphonates , 2004 .

[20]  M. Rogers,et al.  Statins Prevent Bisphosphonate‐Induced γ,δ‐T‐Cell Proliferation and Activation In Vitro , 2003 .

[21]  M. Rogers.  New insights into the molecular mechanisms of action of bisphosphonates. , 2003, Current pharmaceutical design.

[22]  C. Löwik,et al.  Differentiating the mechanisms of antiresorptive action of nitrogen containing bisphosphonates. , 2003, Bone.

[23]  N. Udagawa,et al.  Involvement of vacuolar H+ -ATPase in incorporation of risedronate into osteoclasts. , 2003, Bone.

[24]  J. Frith,et al.  Antagonistic Effects of Different Classes of Bisphosphonates in Osteoclasts and Macrophages In Vitro , 2003, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[25]  G. De Libero,et al.  Human T Cell Receptor γδ Cells Recognize Endogenous Mevalonate Metabolites in Tumor Cells , 2003, The Journal of experimental medicine.

[26]  A. Staal,et al.  The Ability of Statins to Inhibit Bone Resorption Is Directly Related to Their Inhibitory Effect on HMG‐CoA Reductase Activity , 2003, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.

[27]  R. Brandes,et al.  Withdrawal of 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Inhibitors Elicits Oxidative Stress and Induces Endothelial Dysfunction in Mice , 2002, Circulation research.

[28]  I. Hassinen,et al.  Further insight into mechanism of action of clodronate: inhibition of mitochondrial ADP/ATP translocase by a nonhydrolyzable, adenine-containing metabolite. , 2002, Molecular pharmacology.

[29]  E. Oldfield,et al.  Inhibition of geranylgeranyl diphosphate synthase by bisphosphonates and diphosphates: a potential route to new bone antiresorption and antiparasitic agents. , 2002, Journal of medicinal chemistry.

[30]  M. Horton,et al.  Identification of a Novel Phosphonocarboxylate Inhibitor of Rab Geranylgeranyl Transferase That Specifically Prevents Rab Prenylation in Osteoclasts and Macrophages* , 2001, The Journal of Biological Chemistry.

[31]  G. Rodan,et al.  Inhibition of bone resorption by alendronate and risedronate does not require osteoclast apoptosis. , 2001, Bone.

[32]  J. Mönkkönen,et al.  The molecular mechanism of action of the antiresorptive and antiinflammatory drug clodronate: evidence for the formation in vivo of a metabolite that inhibits bone resorption and causes osteoclast and macrophage apoptosis. , 2001, Arthritis and rheumatism.

[33]  C. Poulter,et al.  Structure-activity relationships for inhibition of farnesyl diphosphate synthase in vitro and inhibition of bone resorption in vivo by nitrogen-containing bisphosphonates. , 2001, The Journal of pharmacology and experimental therapeutics.

[34]  S. Sebti,et al.  RhoA Prenylation Is Required for Promotion of Cell Growth and Transformation and Cytoskeleton Organization but Not for Induction of Serum Response Element Transcription* , 2000, The Journal of Biological Chemistry.

[35]  P Delmas,et al.  Bisphosphonates inhibit breast and prostate carcinoma cell invasion, an early event in the formation of bone metastases. , 2000, Cancer research.

[36]  E. Pieterman,et al.  Farnesyl pyrophosphate synthase is the molecular target of nitrogen-containing bisphosphonates. , 1999, Biochemical and biophysical research communications.

[37]  E. Oldfield,et al.  Nitrogen-containing bisphosphonates as carbocation transition state analogs for isoprenoid biosynthesis. , 1999, Biochemical and biophysical research communications.

[38]  M. Wilhelm,et al.  Gamma/delta T-cell stimulation by pamidronate. , 1999, The New England journal of medicine.

[39]  G. Wesolowski,et al.  Alendronate mechanism of action: geranylgeraniol, an intermediate in the mevalonate pathway, prevents inhibition of osteoclast formation, bone resorption, and kinase activation in vitro. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[40]  J. Mönkkönen,et al.  Clodronate and Liposome‐Encapsulated Clodronate Are Metabolized to a Toxic ATP Analog, Adenosine 5′‐(β,γ‐Dichloromethylene) Triphosphate, by Mammalian Cells In Vitro , 1997 .

[41]  G. Rodan,et al.  Comparison of the distribution of 3H-alendronate and 3H-etidronate in rat and mouse bones. , 1996, Bone.

[42]  C. Der,et al.  Ras CAAX Peptidomimetic FTI-277 Selectively Blocks Oncogenic Ras Signaling by Inducing Cytoplasmic Accumulation of Inactive Ras-Raf Complexes (*) , 1995, The Journal of Biological Chemistry.

[43]  S. Adami,et al.  The acute-phase response after bisphosphonate administration , 1987, Calcified Tissue International.

[44]  M. Rogers,et al.  The Role of Prenylated Small GTP-Binding Proteins in the Regulation of Osteoclast Function , 2002, Calcified Tissue International.

[45]  G. Rodan,et al.  Alendronate is a specific, nanomolar inhibitor of farnesyl diphosphate synthase. , 2000, Archives of biochemistry and biophysics.