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Alterations in insulin signalling pathway induced by prolonged insulin treatment of 3T3-L1 adipocytes
TLDR
Insulin-induced glucose transport stimulation, which results from the translocation of glucose transporter 4 (GLUT 4)-containing vesicles, is completely blocked after prolonged insulin treatment of 3T3-L1 adipocytes, and an insulin-resistant state with a reduced ability of insulin to stimulate the PI3-kinase and the MAP-kinases is indicated. Expand
Insulin-like growth factor binding protein (IGFBP) signalling.
  • J. Ricort
  • Chemistry, Medicine
  • Growth hormone & IGF research : official journal…
  • 1 August 2004
TLDR
This review aims to provide an overview of the various intracellular signalling pathways via which IGFBPs are purported to mediate their IGF-independent action. Expand
Insulin‐like growth factor binding protein‐3 increases intracellular calcium concentrations in MCF‐7 breast carcinoma cells
TLDR
It is demonstrated that binding of IGFBP‐3 to a cell surface receptor in MCF‐7 breast carcinoma cells induces a rapid and transient increase in intracellular free calcium, and this increase was mediated via a pertussis toxin‐sensitive pathway, indicating that the IGF BP‐3 receptor may be specifically coupled to a Gi protein. Expand
Insulin-like growth factor (IGF) binding protein-3 inhibits type 1 IGF receptor activation independently of its IGF binding affinity.
TLDR
The results provide the first demonstration that IGFBP-3 can specifically modulate the IGF-I signaling pathway independently of its IGF- I-binding ability and reveal a regulatory mechanism specific to the type 1 IGF receptor, with no effect on insulin receptor activation. Expand
Different effects of insulin and platelet-derived growth factor on phosphatidylinositol 3-kinase at the subcellular level in 3T3-L1 adipocytes. A possible explanation for their specific effects on
TLDR
It is suggested that a crucial event in the stimulation of glucose uptake by insulin could be that insulin, but not PDGF, induces activation of PtdIns 3-kinase in the cytosol and in LDM, the compartment enriched in Glut-4-containing vesicles. Expand
Protein Kinase D1 Regulates Erα-positive Breast Cancer Cell Growth Response To 17β­estradiol And Contributes To Poor Prognosis In Patients
TLDR
The role of the serine/threonine-protein kinase D1 in ERα-positive breast cancers is highlighted and is defined as a novel attractive prognostic factor and a potential therapeutic target in breast cancer. Expand
Partial primary deficiency of insulin-like growth factor (IGF)-I activity associated with IGF1 mutation demonstrates its critical role in growth and brain development.
TLDR
It is shown that the integrity of IGF-I signaling is important for normal growth and brain development, and the characterization of this complex phenotype and identification of such molecular defects have therapeutic implications, particularly now that, in addition to GH, recombinant IGF-i is available for clinical use. Expand
Cross-talk between the Platelet-derived Growth Factor and the Insulin Signaling Pathways in 3T3-L1 Adipocytes*
TLDR
A cross-talk exists between the different pathways stimulated by PDGF and insulin in intact cells, which is suggested to be due to activation of PI 3-kinase pathway. Expand
Protein kinase D1 stimulates proliferation and enhances tumorigenesis of MCF-7 human breast cancer cells through a MEK/ERK-dependent signaling pathway.
TLDR
Protein kinase D1 overexpression increases the aggressiveness of MCF-7 breast cancer cells through enhancing their oncogenic properties and would define PKD1 as a potentially new promising anti-tumor therapeutic target. Expand
Insulin-Like Growth Factor (IGF) Binding Protein-3 Inhibits Type 1 IGF Receptor Activation Independently of Its IGF Binding Affinity** This work was supported by the Institut National de la Santé et
TLDR
The effects of IGFBP-3 on the initial steps in the IGF signaling pathway are investigated, finding that it modulates IGF-I binding to its receptor via a different mechanism possibly involving conformational alteration of the receptor. Expand
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