B. Neel

Publications431
h-index113
Citations46,771
Highly Influential Citations1,965
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  • Publications
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New insights into tumor suppression: PTEN suppresses tumor formation by restraining the phosphoinositide 3-kinase/AKT pathway.
  • L. Cantley, B. Neel
  • Biology
    Proceedings of the National Academy of Sciences…
  • 13 April 1999
TLDR
A series of publications over the past year now suggest a mechanism by which PTEN loss of function results in tumors, and PTEN appears to negatively control the phosphoinositide 3-kinase signaling pathway for regulation of cell growth and survival by dephosphorylating the 3 position ofosphoinositides.
STAT3 signalling is required for leptin regulation of energy balance but not reproduction
TLDR
It is shown that, like db/db mice, leprS1138 homozygotes (s/s) are hyperphagic and obese, however, whereas db/ db mice are infertile, short and diabetic, s/s mice are fertile, long and less hyperglycaemic.
The 'Shp'ing news: SH2 domain-containing tyrosine phosphatases in cell signaling.
SH2 domains recognize specific phosphopeptide sequences
Solubilization and purification of enzymatically active glutathione S-transferase (pGEX) fusion proteins.
TLDR
This work has adapted a protocol, previously used to solubilize actin, for the purification of otherwise insoluble GST fusion proteins, and demonstrates that saturation of glutathione agarose is dependent on fusion protein molecular weight.
Mathematical models of protein kinase signal transduction.
PTP1B regulates leptin signal transduction in vivo.
Neuronal PTP1B regulates body weight, adiposity and leptin action
TLDR
Mice lacking the tyrosine phosphatase PTP1B are protected from diet-induced obesity and are hypersensitive to leptin, despite paradoxically elevated leptin levels, and show improved glucose homeostasis, suggesting PTP 1B regulates body mass and adiposity primarily through actions in the brain.
The "Gab" in signal transduction.
Germline gain-of-function mutations in SOS1 cause Noonan syndrome
TLDR
SOS1 mutants are identified as a major cause of Noonan syndrome, representing the first example of activating GEF mutations associated with human disease and providing new insights into RAS-GEF regulation.
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