scholarly journals EphrinA5 acts as a tumor suppressor in glioma by negative regulation of epidermal growth factor receptor

Oncogene ◽  
2009 ◽  
Vol 28 (15) ◽  
pp. 1759-1768 ◽  
Author(s):  
J-J Li ◽  
D-P Liu ◽  
G-T Liu ◽  
D Xie
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Tumor Suppressor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Negative Regulation ◽  
Epidermal Growth

scholarly journals Novel tumor suppressor microRNA at frequently deleted chromosomal region 8p21 regulates Epidermal Growth Factor Receptor in prostate cancer

Oncotarget ◽  
2016 ◽  
Vol 7 (43) ◽  
pp. 70388-70403 ◽  
Author(s):  
Nathan Bucay ◽  
Kirandeep Sekhon ◽  
Shahana Majid ◽  
Soichiro Yamamura ◽  
Varahram Shahryari ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Tumor Suppressor ◽  
Epidermal Growth Factor ◽  
Chromosomal Region ◽  
Growth Factor Receptor ◽  
Epidermal Growth

scholarly journals Positive and negative tissue-specific signaling by a nematode epidermal growth factor receptor.

1997 ◽  
Vol 8 (5) ◽  
pp. 779-793 ◽  
Author(s):  
G M Lesa ◽  
P W Sternberg
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Binding Sites ◽  
Growth Factor Receptor ◽  
Cell Types ◽  
Negative Regulation ◽  
Tissue Specific ◽  
Epidermal Growth

The major determinants of receptor tissue tyrosine kinase (RTK) signaling specificity have been proposed to be Src homology 2 (SH2) binding sites, phosphotyrosine-containing oligopeptides in the cytoplasmic domain of the receptor. The Caenorhabditis elegans epidermal growth factor receptor homologue LET-23 has multiple functions during development and has eight potential SH2-binding sites in a region carboxyl terminal to its kinase domain. By analyzing transgenic nematodes for three distinct LET-23 functions, we show that six of eight potential sites function in vivo and that they are required for most, but not all, of LET-23 activity. A single site is necessary and sufficient to promote wild-type fertility. Three other sites activate the RAS pathway and are involved only in viability and vulval differentiation. A fifth site is promiscuous and can mediate all three LET-23 functions. An additional site mediates tissue-specific negative regulation. Putative SH2 binding sites are thus key effectors of both cell-specific and negative regulation in an intact organism. We suggest two distinct mechanisms for tissue-specific RTK-mediated signaling. A positive mechanism would promote RTK function through effectors present only in certain cell types. A negative mechanism would inhibit RTK function through tissue-specific negative regulators.

scholarly journals Epidermal Growth Factor Receptor Acts as a Negative Regulator for Bacterium Nontypeable Haemophilus influenzae-induced Toll-like Receptor 2 Expression via an Src-dependent p38 Mitogen-activated Protein Kinase Signaling Pathway

2005 ◽  
Vol 280 (43) ◽  
pp. 36185-36194 ◽  
Author(s):  
Fumi Mikami ◽  
He Gu ◽  
Hirofumi Jono ◽  
Ali Andalibi ◽  
Hirofumi Kai ◽  
...  
Keyword(s):  
Immune Response ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Host Defense ◽  
Growth Factor Receptor ◽  
Negative Regulation ◽  
Negative Regulator ◽  
Egfr Signaling ◽  
Epidermal Growth

Epidermal growth factor receptor (EGFR) has been shown to play important roles in regulating diverse biological processes, including cell growth, differentiation, apoptosis, adhesion, and migration. Its role in regulating human Toll-like receptors (TLRs), key host defense receptors that recognize invading bacterial pathogens, however, remains unknown. Here we show for the first time that EGFR acts as a negative regulator for TLR2 induction by the bacterium nontypeable Haemophilus influenzae (NTHi) in vitro and in vivo. The negative regulation of TLR2 induction by EGFR is mediated via an Src-MKK3/6-p38 α/β MAP kinase-dependent mechanism. Moreover, direct activation of EGFR signaling by the bacterium NTHi-derived EGF-like factor appears to be responsible for triggering the downstream Src-MKK3/6-p38 MAPK signaling, which in turn leads to the negative regulation of TLR2 induction. Finally, exogenous EGF increases NTHi invasion of host epithelial cells, thereby demonstrating the biological significance of TLR2 regulation by EGFR signaling. The evidence we provided in the present study may suggest a novel strategy utilized by bacteria to attenuate host defensive and immune response by negatively regulating the expression of host defense receptor TLR2. These studies may bring new insight for fully understanding the important role of EGFR signaling in regulating host defense and immune response by tightly controlling TLR2 induction during bacterial infections.

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