M Mercola

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi Gap junction-mediated transfer of left-right patterning signals in the early chick blastoderm is upstream of Shh asymmetry in the node
    M Levin
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Development 126:4703-14. 1999
  2. ncbi Left-right asymmetry determination in vertebrates
    M Mercola
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, Massachusetts 02115, USA
    Annu Rev Cell Dev Biol 17:779-805. 2001
  3. ncbi TGF-beta superfamily signaling and left-right asymmetry
    M Whitman
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA
    Sci STKE 2001:re1. 2001
  4. ncbi Evolutionary conservation of mechanisms upstream of asymmetric Nodal expression: reconciling chick and Xenopus
    M Levin
    Cell Biology Dept, Harvard Medical School, Boston, MA 02115, USA
    Dev Genet 23:185-93. 1998
  5. ncbi Zebrafish narrowminded suggests a genetic link between formation of neural crest and primary sensory neurons
    K B Artinger
    Cardiovascular Research Center, Massachusetts General Hospital Harvard Medical School, Charlestown, MA 02129, USA
    Development 126:3969-79. 1999
  6. ncbi Spina bifida occulta in homozygous Patch mouse embryos
    J Payne
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Dev Dyn 209:105-16. 1997
  7. ncbi Isolation and characterization of Xenopus Hey-1: a downstream mediator of Notch signaling
    M S Rones
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts, USA
    Dev Dyn 225:554-60. 2002
  8. ncbi Expression of mouse PDGF-A and PDGF alpha-receptor genes during pre- and post-implantation development: evidence for a developmental shift from an autocrine to a paracrine mode of action
    S L Palmieri
    Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, MA
    Mech Dev 39:181-91. 1992

Collaborators

Detail Information

Publications8

  1. ncbi Gap junction-mediated transfer of left-right patterning signals in the early chick blastoderm is upstream of Shh asymmetry in the node
    M Levin
    Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
    Development 126:4703-14. 1999
    ..We propose that left-right information is transferred unidirectionally throughout the epiblast by gap junction channels in order to pattern left-sided Shh expression at Hensen's node...
  2. ncbi Left-right asymmetry determination in vertebrates
    M Mercola
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, Massachusetts 02115, USA
    Annu Rev Cell Dev Biol 17:779-805. 2001
    ..Here we examine the molecular biology of the three principal steps in left-right determination: breaking bilateral symmetry, propagation and reinforcement of pattern, and the translation of pattern into asymmetric organ morphogenesis...
  3. ncbi TGF-beta superfamily signaling and left-right asymmetry
    M Whitman
    Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA
    Sci STKE 2001:re1. 2001
    ..Also discussed is the problem of how signal transduction mediated by the Smad proteins can pattern LR asymmetry without interfering with coincident dorsoventral patterning, which relies on the same Smad proteins...
  4. ncbi Evolutionary conservation of mechanisms upstream of asymmetric Nodal expression: reconciling chick and Xenopus
    M Levin
    Cell Biology Dept, Harvard Medical School, Boston, MA 02115, USA
    Dev Genet 23:185-93. 1998
    ..Thus our results are consistent with Shh being necessary for nodal induction in both species, and we provide an explanation for both sets of data in terms of a single conserved mechanism upstream of nodal expression...
  5. ncbi Zebrafish narrowminded suggests a genetic link between formation of neural crest and primary sensory neurons
    K B Artinger
    Cardiovascular Research Center, Massachusetts General Hospital Harvard Medical School, Charlestown, MA 02129, USA
    Development 126:3969-79. 1999
    ..We discuss the implications of these findings for the possibility that RB sensory neurons and neural crest cells share a common evolutionary origin...
  6. ncbi Spina bifida occulta in homozygous Patch mouse embryos
    J Payne
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Dev Dyn 209:105-16. 1997
    ..Furthermore, since the neural tube appears to close normally, we suggest that spina bifida in the Ph homozygote is caused primarily by a somitic mesoderm abnormality rather than a neural tube defect...
  7. ncbi Isolation and characterization of Xenopus Hey-1: a downstream mediator of Notch signaling
    M S Rones
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts, USA
    Dev Dyn 225:554-60. 2002
    ....
  8. ncbi Expression of mouse PDGF-A and PDGF alpha-receptor genes during pre- and post-implantation development: evidence for a developmental shift from an autocrine to a paracrine mode of action
    S L Palmieri
    Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, MA
    Mech Dev 39:181-91. 1992
    ..We propose that chronic autostimulation of PDGF alpha-receptors occurs in pre-implantation embryos, whereas, following implantation, early mesoderm development is dependent on stimulation by ectodermally produced PDGF-A...