Mikhail V Semenov

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi SOST is a ligand for LRP5/LRP6 and a Wnt signaling inhibitor
    Mikhail Semenov
    Division of Neuroscience, Children s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 280:26770-5. 2005
  2. ncbi LRP5 mutations linked to high bone mass diseases cause reduced LRP5 binding and inhibition by SOST
    Mikhail V Semenov
    Neurobiology Program, Children s Hospital Boston, 61 Binmney Street, Boston, MA 02115, USA
    J Biol Chem 281:38276-84. 2006
  3. pmc Dissecting molecular differences between Wnt coreceptors LRP5 and LRP6
    Bryan T MacDonald
    F M Kirby Neurobiology Center, Children s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 6:e23537. 2011
  4. pmc DKK1 antagonizes Wnt signaling without promotion of LRP6 internalization and degradation
    Mikhail V Semenov
    F M Kirby Neurobiology Center, Children s Hospital Boston and Department of Neurology, Harvard Medical School, 61 Binney Street, Boston, MA 02115, USA
    J Biol Chem 283:21427-32. 2008
  5. ncbi R-spondin1 is a high affinity ligand for LRP6 and induces LRP6 phosphorylation and beta-catenin signaling
    Qiou Wei
    Program of Neurobiology, Children s Hospital Boston, Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 282:15903-11. 2007
  6. ncbi SnapShot: Wnt/beta-catenin signaling
    Bryan T MacDonald
    The F M Kirb Neurobiology Center, Children s Hospital Boston, Harvard Medical School, Boston, MA 02115, USA
    Cell 131:1204. 2007

Collaborators

Detail Information

Publications6

  1. ncbi SOST is a ligand for LRP5/LRP6 and a Wnt signaling inhibitor
    Mikhail Semenov
    Division of Neuroscience, Children s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 280:26770-5. 2005
    ..Our findings suggest that SOST is an antagonist for Wnt signaling and that the loss of SOST function likely leads to the hyperactivation of Wnt signaling that underlies bone overgrowth seen in sclerosteosis patients...
  2. ncbi LRP5 mutations linked to high bone mass diseases cause reduced LRP5 binding and inhibition by SOST
    Mikhail V Semenov
    Neurobiology Program, Children s Hospital Boston, 61 Binmney Street, Boston, MA 02115, USA
    J Biol Chem 281:38276-84. 2006
    ....
  3. pmc Dissecting molecular differences between Wnt coreceptors LRP5 and LRP6
    Bryan T MacDonald
    F M Kirby Neurobiology Center, Children s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 6:e23537. 2011
    ..Our studies therefore uncover a new and important molecular tuning mechanism for differential regulation of LRP5 and LRP6 phosphorylation and signaling activity...
  4. pmc DKK1 antagonizes Wnt signaling without promotion of LRP6 internalization and degradation
    Mikhail V Semenov
    F M Kirby Neurobiology Center, Children s Hospital Boston and Department of Neurology, Harvard Medical School, 61 Binney Street, Boston, MA 02115, USA
    J Biol Chem 283:21427-32. 2008
    ..7 h) of LRP6. We conclude that DKK1 inhibition of LRP6 is independent of LRP6 internalization and degradation...
  5. ncbi R-spondin1 is a high affinity ligand for LRP6 and induces LRP6 phosphorylation and beta-catenin signaling
    Qiou Wei
    Program of Neurobiology, Children s Hospital Boston, Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 282:15903-11. 2007
    ..Our study reveals interesting similarity and distinction between Wnt and R-spondin signaling...
  6. ncbi SnapShot: Wnt/beta-catenin signaling
    Bryan T MacDonald
    The F M Kirb Neurobiology Center, Children s Hospital Boston, Harvard Medical School, Boston, MA 02115, USA
    Cell 131:1204. 2007