Robert Eferl

Summary

Affiliation: University of Vienna
Country: Austria

Publications

  1. ncbi request reprint AP-1: a double-edged sword in tumorigenesis
    Robert Eferl
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    Nat Rev Cancer 3:859-68. 2003
  2. ncbi request reprint Role of heterodimerization of c-Fos and Fra1 proteins in osteoclast differentiation
    Latifa Bakiri
    Research Institute of Molecular Pathology IMP, A 1030 Vienna, Austria
    Bone 40:867-75. 2007
  3. pmc c-Jun/AP-1 controls liver regeneration by repressing p53/p21 and p38 MAPK activity
    Ewa Stepniak
    Research Institute of Molecular Pathology IMP, A 1030 Vienna, Austria
    Genes Dev 20:2306-14. 2006
  4. pmc Development of pulmonary fibrosis through a pathway involving the transcription factor Fra-2/AP-1
    Robert Eferl
    Research Institute of Molecular Pathology, Doktor Bohr Gasse 7, A 1030 Vienna, Austria
    Proc Natl Acad Sci U S A 105:10525-30. 2008
  5. doi request reprint Osteoclast size is controlled by Fra-2 through LIF/LIF-receptor signalling and hypoxia
    Aline Bozec
    Research Institute of Molecular Pathology I M P, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    Nature 454:221-5. 2008
  6. ncbi request reprint Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins
    Rainer Zenz
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    Nature 437:369-75. 2005
  7. pmc Distinct functions of junD in cardiac hypertrophy and heart failure
    Romeo Ricci
    Institute of Molecular Pathology, A 1030 Vienna, Austria
    Genes Dev 19:208-13. 2005
  8. pmc Mice lacking JunB are osteopenic due to cell-autonomous osteoblast and osteoclast defects
    Lukas Kenner
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    J Cell Biol 164:613-23. 2004
  9. ncbi request reprint Rhabdomyosarcoma development in mice lacking Trp53 and Fos: tumor suppression by the Fos protooncogene
    Alexander Fleischmann
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    Cancer Cell 4:477-82. 2003
  10. pmc The Fos-related antigen Fra-1 is an activator of bone matrix formation
    Robert Eferl
    Research Institute of Molecular Pathology IMP, Vienna, Austria
    EMBO J 23:2789-99. 2004

Collaborators

Detail Information

Publications16

  1. ncbi request reprint AP-1: a double-edged sword in tumorigenesis
    Robert Eferl
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    Nat Rev Cancer 3:859-68. 2003
  2. ncbi request reprint Role of heterodimerization of c-Fos and Fra1 proteins in osteoclast differentiation
    Latifa Bakiri
    Research Institute of Molecular Pathology IMP, A 1030 Vienna, Austria
    Bone 40:867-75. 2007
    ..We propose that Fra1 together with a dimerization partner different from Jun proteins can rescue osteoclast differentiation in c-Fos-deficient precursors...
  3. pmc c-Jun/AP-1 controls liver regeneration by repressing p53/p21 and p38 MAPK activity
    Ewa Stepniak
    Research Institute of Molecular Pathology IMP, A 1030 Vienna, Austria
    Genes Dev 20:2306-14. 2006
    ..These data demonstrate that c-Jun/AP-1 regulates liver regeneration through a novel molecular pathway that involves p53, p21, and the stress kinase p38alpha...
  4. pmc Development of pulmonary fibrosis through a pathway involving the transcription factor Fra-2/AP-1
    Robert Eferl
    Research Institute of Molecular Pathology, Doktor Bohr Gasse 7, A 1030 Vienna, Austria
    Proc Natl Acad Sci U S A 105:10525-30. 2008
    ....
  5. doi request reprint Osteoclast size is controlled by Fra-2 through LIF/LIF-receptor signalling and hypoxia
    Aline Bozec
    Research Institute of Molecular Pathology I M P, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    Nature 454:221-5. 2008
    ..Thus placenta-induced hypoxia during embryogenesis leads to the formation of giant osteoclasts in young pups. These findings offer potential targets for the treatment of syndromes associated with increased osteoclastogenesis...
  6. ncbi request reprint Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins
    Rainer Zenz
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    Nature 437:369-75. 2005
    ..Thus, these data support the hypothesis that epidermal alterations are sufficient to initiate both skin lesions and arthritis in psoriasis...
  7. pmc Distinct functions of junD in cardiac hypertrophy and heart failure
    Romeo Ricci
    Institute of Molecular Pathology, A 1030 Vienna, Austria
    Genes Dev 19:208-13. 2005
    ..These data suggest that junD promotes both adaptive-protective and maladaptive hypertrophy in heart, depending on its expression levels...
  8. pmc Mice lacking JunB are osteopenic due to cell-autonomous osteoblast and osteoclast defects
    Lukas Kenner
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    J Cell Biol 164:613-23. 2004
    ..Thus, these data reveal a novel function of JunB as a positive regulator controlling primarily osteoblast as well as osteoclast activity...
  9. ncbi request reprint Rhabdomyosarcoma development in mice lacking Trp53 and Fos: tumor suppression by the Fos protooncogene
    Alexander Fleischmann
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, A 1030 Vienna, Austria
    Cancer Cell 4:477-82. 2003
    ..Moreover, Fos is able to repress Pax7 expression in rhabdomyosarcoma cell lines and primary myoblasts, suggesting a molecular link to genetic alterations involved in human rhabdomyosarcomas...
  10. pmc The Fos-related antigen Fra-1 is an activator of bone matrix formation
    Robert Eferl
    Research Institute of Molecular Pathology IMP, Vienna, Austria
    EMBO J 23:2789-99. 2004
    ..These results uncover a novel function of Fra-1 in regulating bone mass through bone matrix production by osteoblasts and chondrocytes...
  11. ncbi request reprint Fos/AP-1 proteins in bone and the immune system
    Erwin F Wagner
    Research Institute of Molecular Pathology IMP, Vienna, Austria
    Immunol Rev 208:126-40. 2005
    ..We also attempt to put potential therapeutic strategies for inflammatory bone diseases in perspective...
  12. pmc Activator protein 1 (Fos/Jun) functions in inflammatory bone and skin disease
    Rainer Zenz
    Ludwig Boltzmann Institute for Cancer Research, Währinger Strasse 13a, A 1090 Vienna, Austria
    Arthritis Res Ther 10:201. 2008
    ..These new data provide a better molecular understanding of disease pathways and should pave the road for the discovery of new targets for therapeutic applications...
  13. ncbi request reprint Liver tumor development. c-Jun antagonizes the proapoptotic activity of p53
    Robert Eferl
    Research Institute of Molecular Pathology IMP, Dr Bohrgasse 7, A 1030, Vienna, Austria
    Cell 112:181-92. 2003
    ..These data indicate that c-Jun prevents apoptosis by antagonizing p53 activity, illustrating a mechanism that might contribute to the early stages of human HCC development...
  14. ncbi request reprint The AP1 transcription factor Fra2 is required for efficient cartilage development
    Florian Karreth
    Research Institute of Molecular Pathology I M P Vienna, Austria
    Development 131:5717-25. 2004
    ..In addition, these mice suffer from a kyphosis-like phenotype, an abnormal bending of the spine. Hence, Fra2 is a novel transcription factor important for skeletogenesis by affecting chondrocyte differentiation...
  15. ncbi request reprint c-Jun regulates eyelid closure and skin tumor development through EGFR signaling
    Rainer Zenz
    Research Institute of Molecular Pathology IMP, A 1030, Vienna, Austria
    Dev Cell 4:879-89. 2003
    ..Thus, using three experimental systems, we show that EGFR and HB-EGF are regulated by c-Jun, which controls eyelid development, keratinocyte proliferation, and skin tumor formation...
  16. ncbi request reprint Induction of DNA synthesis in primary mouse hepatocytes is associated with nuclear pro-transforming growth factor alpha and erbb-1 and is independent of c-jun
    Elisabeth Schausberger
    Institut für Krebsforschung, University of Vienna, Borschkegasse 8a, Austria
    Carcinogenesis 24:835-41. 2003
    ....