Thomas A Hawkins

Summary

Affiliation: University College London
Country: UK

Publications

  1. ncbi The small molecule Mek1/2 inhibitor U0126 disrupts the chordamesoderm to notochord transition in zebrafish
    Thomas A Hawkins
    Department of Anatomy and Developmental Biology, University College London, Gower Street, London, WC1E 6BT, UK
    BMC Dev Biol 8:42. 2008
  2. ncbi The ATPase-dependent chaperoning activity of Hsp90a regulates thick filament formation and integration during skeletal muscle myofibrillogenesis
    Thomas A Hawkins
    Department of Anatomy and Developmental Biology, UCL, London, UK
    Development 135:1147-56. 2008
  3. ncbi A genetic screen identifies genes essential for development of myelinated axons in zebrafish
    Hans Martin Pogoda
    Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Dev Biol 298:118-31. 2006

Collaborators

Detail Information

Publications3

  1. ncbi The small molecule Mek1/2 inhibitor U0126 disrupts the chordamesoderm to notochord transition in zebrafish
    Thomas A Hawkins
    Department of Anatomy and Developmental Biology, University College London, Gower Street, London, WC1E 6BT, UK
    BMC Dev Biol 8:42. 2008
    ....
  2. ncbi The ATPase-dependent chaperoning activity of Hsp90a regulates thick filament formation and integration during skeletal muscle myofibrillogenesis
    Thomas A Hawkins
    Department of Anatomy and Developmental Biology, UCL, London, UK
    Development 135:1147-56. 2008
    ..Our studies reveal a surprisingly specific developmental role for a single Hsp90 gene in a regulatory pathway controlling late steps in sarcomere assembly...
  3. ncbi A genetic screen identifies genes essential for development of myelinated axons in zebrafish
    Hans Martin Pogoda
    Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Dev Biol 298:118-31. 2006
    ..The analysis of these mutations will advance our understanding of myelination, and the mutants will serve as models of human diseases of myelin...