Michaela Kneissel

Summary

Affiliation: Novartis Institutes for BioMedical Research

Publications

  1. ncbi request reprint Bone tissue and its mineralization in aged estrogen-depleted rats after long-term intermittent treatment with parathyroid hormone (PTH) analog SDZ PTS 893 or human PTH(1-34)
    M Kneissel
    Bone Metabolism Unit, Therapeutic Area of Arthritis and Bone Metabolism, Novartis Pharma AG, Basel, Switzerland
    Bone 28:237-50. 2001
  2. ncbi request reprint Retinoid-induced bone thinning is caused by subperiosteal osteoclast activity in adult rodents
    Michaela Kneissel
    Bone Metabolism, Novartis Institutes for BioMedical Research Basel, WK 125 10 15, CH 4002 Basel, Switzerland
    Bone 36:202-14. 2005
  3. doi request reprint Mef2c deletion in osteocytes results in increased bone mass
    Ina Kramer
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, Novartis Pharma, Basel, Switzerland
    J Bone Miner Res 27:360-73. 2012
  4. pmc Parathyroid hormone (PTH)-induced bone gain is blunted in SOST overexpressing and deficient mice
    Ina Kramer
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, CH 4002 Basel, Switzerland
    J Bone Miner Res 25:178-89. 2010
  5. doi request reprint Does osteocytic SOST suppression mediate PTH bone anabolism?
    Ina Kramer
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, CH 4002 Basel, Switzerland
    Trends Endocrinol Metab 21:237-44. 2010
  6. doi request reprint Ubiquitous overexpression of Hey1 transcription factor leads to osteopenia and chondrocyte hypertrophy in bone
    Rishard Salie
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, Basel, Switzerland
    Bone 46:680-94. 2010
  7. ncbi request reprint Everolimus suppresses cancellous bone loss, bone resorption, and cathepsin K expression by osteoclasts
    Michaela Kneissel
    Arthritis and Bone Metabolism Disease Area, Novartis Institutes for BioMedical Research Basel, Basel, Switzerland
    Bone 35:1144-56. 2004
  8. pmc Osteocyte Wnt/beta-catenin signaling is required for normal bone homeostasis
    Ina Kramer
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, Novartis Pharma AG, CH 4002 Basel, Switzerland
    Mol Cell Biol 30:3071-85. 2010
  9. doi request reprint ATF936, a novel oral calcilytic, increases bone mineral density in rats and transiently releases parathyroid hormone in humans
    Markus R John
    Novartis Pharma AG, Basel, Switzerland
    Bone 49:233-41. 2011
  10. doi request reprint Reversing LRP5-dependent osteoporosis and SOST deficiency-induced sclerosing bone disorders by altering WNT signaling activity
    Ming Kang Chang
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, Basel, Switzerland
    J Bone Miner Res 29:29-42. 2014

Collaborators

Detail Information

Publications23

  1. ncbi request reprint Bone tissue and its mineralization in aged estrogen-depleted rats after long-term intermittent treatment with parathyroid hormone (PTH) analog SDZ PTS 893 or human PTH(1-34)
    M Kneissel
    Bone Metabolism Unit, Therapeutic Area of Arthritis and Bone Metabolism, Novartis Pharma AG, Basel, Switzerland
    Bone 28:237-50. 2001
    ..As a result, a substantial amount of new bone, maintained at elevated turnover and adequate mineralization levels, formed predominantly at compartments exposed to bone marrow...
  2. ncbi request reprint Retinoid-induced bone thinning is caused by subperiosteal osteoclast activity in adult rodents
    Michaela Kneissel
    Bone Metabolism, Novartis Institutes for BioMedical Research Basel, WK 125 10 15, CH 4002 Basel, Switzerland
    Bone 36:202-14. 2005
    ..Our findings might explain why high intake of retinol is associated with increased hip fracture risk in the elderly and suggest a therapy to prevent such potential negative effects...
  3. doi request reprint Mef2c deletion in osteocytes results in increased bone mass
    Ina Kramer
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, Novartis Pharma, Basel, Switzerland
    J Bone Miner Res 27:360-73. 2012
    ..Yet, the increased bone mass phenotype of Mef2c mutants is not directly related to the reduced Sost expression. We identified a novel function for Mef2c in control of adult bone mass by regulation of osteoclastic bone resorption...
  4. pmc Parathyroid hormone (PTH)-induced bone gain is blunted in SOST overexpressing and deficient mice
    Ina Kramer
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, CH 4002 Basel, Switzerland
    J Bone Miner Res 25:178-89. 2010
    ..These data suggest that suppression of the bone formation inhibitor Sost by intermittent PTH treatment contributes to PTH bone anabolism...
  5. doi request reprint Does osteocytic SOST suppression mediate PTH bone anabolism?
    Ina Kramer
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, CH 4002 Basel, Switzerland
    Trends Endocrinol Metab 21:237-44. 2010
    ....
  6. doi request reprint Ubiquitous overexpression of Hey1 transcription factor leads to osteopenia and chondrocyte hypertrophy in bone
    Rishard Salie
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, Basel, Switzerland
    Bone 46:680-94. 2010
    ..Due to the complex role of Hey1 in bone, inhibition of Hey1 does not appear to be a straightforward therapeutic strategy to increase the bone mass...
  7. ncbi request reprint Everolimus suppresses cancellous bone loss, bone resorption, and cathepsin K expression by osteoclasts
    Michaela Kneissel
    Arthritis and Bone Metabolism Disease Area, Novartis Institutes for BioMedical Research Basel, Basel, Switzerland
    Bone 35:1144-56. 2004
    ..In conclusion, everolimus directly inhibits bone resorption by osteoclasts and thus could at least be neutral or protective for bone in vivo, which would favor its use in disease indications associated with bone loss...
  8. pmc Osteocyte Wnt/beta-catenin signaling is required for normal bone homeostasis
    Ina Kramer
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, Novartis Pharma AG, CH 4002 Basel, Switzerland
    Mol Cell Biol 30:3071-85. 2010
    ..Together, these results reveal a crucial novel function for osteocyte beta-catenin signaling in controlling bone homeostasis...
  9. doi request reprint ATF936, a novel oral calcilytic, increases bone mineral density in rats and transiently releases parathyroid hormone in humans
    Markus R John
    Novartis Pharma AG, Basel, Switzerland
    Bone 49:233-41. 2011
    ..In conclusion, ATF936 might hold potential as an oral bone-forming osteoporosis therapy...
  10. doi request reprint Reversing LRP5-dependent osteoporosis and SOST deficiency-induced sclerosing bone disorders by altering WNT signaling activity
    Ming Kang Chang
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, Basel, Switzerland
    J Bone Miner Res 29:29-42. 2014
    ....
  11. doi request reprint Isolation of mouse osteocytes using cell fractionation for gene expression analysis
    Christine Halleux
    Musculoskeletal Disease Department, Novartis Institutes for BioMedical Research, Basel, Switzerland
    Methods Mol Biol 816:55-66. 2012
    ..The osteocyte-enriched cell fraction isolated by this method can further be purified by FACS and selectively expresses osteocytic marker genes, such as Dmp1 and Sost...
  12. pmc Control of the SOST bone enhancer by PTH using MEF2 transcription factors
    Olivier Leupin
    Bone and Cartilage Unit, Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, Basel, Switzerland
    J Bone Miner Res 22:1957-67. 2007
    ..Expression of the osteocyte-derived bone formation inhibitor sclerostin in adult bone requires a distant enhancer. We show that MEF2 transcription factors control this enhancer and mediate inhibition of sclerostin expression by PTH...
  13. pmc Bone overgrowth-associated mutations in the LRP4 gene impair sclerostin facilitator function
    Olivier Leupin
    Musculoskeletal Disease Area, Novartis Institutes for BioMedical Research, Novartis Pharma AG, Basel, Switzerland
    J Biol Chem 286:19489-500. 2011
    ..Together these data indicate that the interaction of sclerostin with LRP4 is required to mediate the inhibitory function of sclerostin on bone formation, thus identifying a novel role for LRP4 in bone...
  14. doi request reprint Penta-substituted benzimidazoles as potent antagonists of the calcium-sensing receptor (CaSR-antagonists)
    Marc Gerspacher
    Novartis Institutes for BioMedical Research, Novartis Pharma AG, Basel, Switzerland
    Bioorg Med Chem Lett 20:5161-4. 2010
    ..In addition, synthesis and structure-activity relationship data are provided...
  15. ncbi request reprint SOST is a target gene for PTH in bone
    Hansjoerg Keller
    Bone and Cartilage Unit, Novartis Institutes for BioMedical Research Basel, Switzerland
    Bone 37:148-58. 2005
    ..In summary, we have shown that PTH directly inhibits SOST transcription in vivo and in vitro, suggesting that SOST regulation may play a role in mediating PTH action in bone...
  16. doi request reprint AXT914 a novel, orally-active parathyroid hormone-releasing drug in two early studies of healthy volunteers and postmenopausal women
    Markus R John
    Novartis Pharma AG, Basel, Switzerland, Novartis Corporation, East Hanover, NJ, USA
    Bone 64:204-10. 2014
    ..PTH, did not translate into a bone anabolic response and was associated with a persistent dose-related increase in serum calcium concentrations...
  17. doi request reprint Studying gene expression in bone by in situ hybridization
    Ina Kramer
    Musculoskeletal Disease Department, Novartis Institutes for BioMedical Research, Basel, Switzerland
    Methods Mol Biol 816:305-20. 2012
    ..Here, we described a method for carrying out nonradioactive in situ hybridization to detect mRNA transcripts in cryostat sections of mouse bone using the CryoJane(®) Tape-Transfer System and digoxigenin (DIG)-labeled riboprobes...
  18. pmc High bone resorption in adult aging transgenic mice overexpressing cbfa1/runx2 in cells of the osteoblastic lineage
    Valerie Geoffroy
    Friedrich Miescher Institute for Biomedical Research, Zweigniederlassung Novartis Forschungsstiftung, Basel, Switzerland
    Mol Cell Biol 22:6222-33. 2002
    ....
  19. doi request reprint 1-Alkyl-4-phenyl-6-alkoxy-1H-quinazolin-2-ones: a novel series of potent calcium-sensing receptor antagonists
    Leo Widler
    Novartis Institutes for BioMedical Research, CH 4002 Basel, Switzerland
    J Med Chem 53:2250-63. 2010
    ..The required profile was achieved by using microemulsions. Excellent PK/PD correlation was found in rats and dogs. High levels of PTH were reached in plasma within minutes which reverted to baseline in about 1-2 h in both species...
  20. ncbi request reprint Reduction of c-Src activity by substituted 5,7-diphenyl-pyrrolo[2,3-d]-pyrimidines induces osteoclast apoptosis in vivo and in vitro. Involvement of ERK1/2 pathway
    Irene Recchia
    Department of Experimental Medicine, University of L Aquila, 67100 L Aquila, Italy
    Bone 34:65-79. 2004
    ....
  21. pmc Genomic deletion of a long-range bone enhancer misregulates sclerostin in Van Buchem disease
    Gabriela G Loots
    Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA
    Genome Res 15:928-35. 2005
    ..5 (E14.5) mouse embryo, and discovered a novel function for sclerostin during limb development. Our approach represents a framework for characterizing distant regulatory elements associated with abnormal human phenotypes...
  22. pmc Mice lacking histone deacetylase 6 have hyperacetylated tubulin but are viable and develop normally
    Yu Zhang
    Friedrich Miescher Institute for Biomedical Research, Novartis Research Foundation, P O Box 2543, Maulbeerstrasse 66, 4058 Basel, Switzerland
    Mol Cell Biol 28:1688-701. 2008
    ..Collectively, these data demonstrate that mice survive well without HDAC6 and that tubulin hyperacetylation is not detrimental to normal mammalian development...
  23. ncbi request reprint Bone structure and metabolism in a rodent model of male senile osteoporosis
    Peter Pietschmann
    Center of Physiology and Pathophysiology, Medical University of Vienna, Währingergürtel 18 20, 1090 Vienna, Austria
    Exp Gerontol 42:1099-108. 2007
    ....