scholarly journals Downregulation of EGF Receptor Signaling in Pancreatic Islets Causes Diabetes Due to Impaired Postnatal  -Cell Growth

Diabetes ◽  
2006 ◽  
Vol 55 (12) ◽  
pp. 3299-3308 ◽  
Author(s):  
P. J. Miettinen ◽  
J. Ustinov ◽  
P. Ormio ◽  
R. Gao ◽  
J. Palgi ◽  
...  
Keyword(s):  
Cell Growth ◽  
Pancreatic Islets ◽  
Egf Receptor ◽  
Receptor Signaling

scholarly journals Versican G3 Promotes Mouse Mammary Tumor Cell Growth, Migration, and Metastasis by Influencing EGF Receptor Signaling

PLoS ONE ◽  
2010 ◽  
Vol 5 (11) ◽  
pp. e13828 ◽  
Author(s):  
William Weidong Du ◽  
Burton B. Yang ◽  
Tatiana A. Shatseva ◽  
Bing L. Yang ◽  
Zhaoqun Deng ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Mammary Tumor ◽  
Egf Receptor ◽  
Tumor Cell Growth ◽  
Receptor Signaling ◽  
Mammary Tumor Cell ◽  
Mouse Mammary Tumor ◽  
Mouse Mammary Tumor Cell

EGF-Receptor Signaling in Endocytosis Deficient Cells

2001 ◽  
Author(s):  
Brian Ceresa ◽  
Sandra L. Schmid
Keyword(s):  
Egf Receptor ◽  
Receptor Signaling

scholarly journals Targeted Expression of the Class II Phosphoinositide 3-Kinase in Drosophila melanogaster Reveals Lipid Kinase-Dependent Effects on Patterning and Interactions with Receptor Signaling Pathways

2004 ◽  
Vol 24 (2) ◽  
pp. 796-808 ◽  
Author(s):  
Lindsay K. MacDougall ◽  
Mary Elizabeth Gagou ◽  
Sally J. Leevers ◽  
Ernst Hafen ◽  
Michael D. Waterfield
Keyword(s):  
Drosophila Melanogaster ◽  
Signaling Pathways ◽  
Egf Receptor ◽  
Adaptor Protein ◽  
Class Ii ◽  
Notch Receptor ◽  
Mitogen Activated Protein Kinase ◽  
Class I ◽  
Wing Venation ◽  
Receptor Signaling

ABSTRACT Phosphoinositide 3-kinases (PI3Ks) can be divided into three distinct classes (I, II, and III) on the basis of their domain structures and the lipid signals that they generate. Functions have been assigned to the class I and class III enzymes but have not been established for the class II PI3Ks. We have obtained the first evidence for a biological function for a class II PI3K by expressing this enzyme during Drosophila melanogaster development and by using deficiencies that remove the endogenous gene. Wild-type and catalytically inactive PI3K_68D transgenes have opposite effects on the number of sensory bristles and on wing venation phenotypes induced by modified epidermal growth factor (EGF) receptor signaling. These results indicate that the endogenous PI3K_68D may act antagonistically to the EGF receptor-stimulated Ras-mitogen-activated protein kinase pathway and downstream of, or parallel to, the Notch receptor. A class II polyproline motif in PI3K_68D can bind the Drk adaptor protein in vitro, primarily via the N-terminal SH3 domain of Drk. Drk may thus be important for the localization of PI3K_68D, allowing it to modify signaling pathways downstream of cell surface receptors. The phenotypes obtained are markedly distinct from those generated by expression of the Drosophila class I PI3K, which affects growth but not pattern formation.

scholarly journals Phosphorylation of neurofibromin by PKC is a possible molecular switch in EGF receptor signaling in neural cells

Oncogene ◽  
2005 ◽  
Vol 25 (5) ◽  
pp. 735-745 ◽  
Author(s):  
D Mangoura ◽  
Y Sun ◽  
C Li ◽  
D Singh ◽  
D H Gutmann ◽  
...  
Keyword(s):  
Egf Receptor ◽  
Molecular Switch ◽  
Neural Cells ◽  
Receptor Signaling
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