L E Rameh

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi A new pathway for synthesis of phosphatidylinositol-4,5-bisphosphate
    L E Rameh
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 390:192-6. 1997
  2. ncbi Type I phosphatidylinositol-4-phosphate 5-kinases synthesize the novel lipids phosphatidylinositol 3,5-bisphosphate and phosphatidylinositol 5-phosphate
    K F Tolias
    Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA
    J Biol Chem 273:18040-6. 1998
  3. ncbi Downregulation of JE and KC genes by glucocorticoids does not prevent the G0----G1 transition in BALB/3T3 cells
    L E Rameh
    Instituto de Quimica, Universidade de Sao Paulo, Brazil
    Mol Cell Biol 12:4612-21. 1992

Detail Information

Publications3

  1. ncbi A new pathway for synthesis of phosphatidylinositol-4,5-bisphosphate
    L E Rameh
    Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 390:192-6. 1997
    ..Although PtdIns-5-P was previously thought not to exist in vivo, we find evidence for the presence of this lipid in mammalian fibroblasts, establishing a new pathway for PtdIns-4,5-P2 synthesis...
  2. ncbi Type I phosphatidylinositol-4-phosphate 5-kinases synthesize the novel lipids phosphatidylinositol 3,5-bisphosphate and phosphatidylinositol 5-phosphate
    K F Tolias
    Division of Signal Transduction, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA
    J Biol Chem 273:18040-6. 1998
    ..The ability of PIP5Ks to produce multiple signaling molecules indicates that they may participate in a variety of cellular processes...
  3. ncbi Downregulation of JE and KC genes by glucocorticoids does not prevent the G0----G1 transition in BALB/3T3 cells
    L E Rameh
    Instituto de Quimica, Universidade de Sao Paulo, Brazil
    Mol Cell Biol 12:4612-21. 1992
    ..These results suggest that (i) JE and KC are not necessary for the G0----G1----S transition and (ii) c-myc overexpression is likely to be the basis for the potentiating effect of glucocorticoids on serum growth factors...