scholarly journals Role of phospholipase Cγ-induced activation of protein kinase Cϵ (PKCϵ) and PKCβI in epidermal growth factor-mediated protection of tight junctions from acetaldehyde in Caco-2 cell monolayers.

2012 ◽  
Vol 287 (9) ◽  
pp. 6959-6959
Author(s):  
Takuya Suzuki ◽  
Ankur Seth ◽  
Radhakrishna Rao
Keyword(s):  
Growth Factor ◽  
Protein Kinase ◽  
Epidermal Growth Factor ◽  
Tight Junctions ◽  
Cell Monolayers ◽  
Epidermal Growth

Role of epidermal growth factor-stimulated protein kinase in control of proliferation of A431 cells

1982 ◽  
Vol 19 (3) ◽  
pp. 249-257 ◽  
Author(s):  
Gordon N. Gill ◽  
Janice E. Buss ◽  
Cheri S. Lazar ◽  
Aliza Lifshitz ◽  
Jonathan A. Cooper
Keyword(s):  
Growth Factor ◽  
Protein Kinase ◽  
Epidermal Growth Factor ◽  
A431 Cells ◽  
Epidermal Growth

scholarly journals Role of the Different Mitogen-Activated Protein Kinase Subfamilies in the Stimulation of Dog and Human Thyroid Epithelial Cell Proliferation by Cyclic Adenosine 5′-Monophosphate and Growth Factors

Endocrinology ◽  
2003 ◽  
Vol 144 (4) ◽  
pp. 1341-1349 ◽  
Author(s):  
Fabrice Vandeput ◽  
Sandrine Perpete ◽  
Katia Coulonval ◽  
Françoise Lamy ◽  
Jacques E. Dumont
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Protein Kinase ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
P38 Mapk ◽  
Primary Cultures ◽  
Human Thyroid ◽  
Epidermal Growth

Abstract We have investigated the role of the different classes of MAPKs, i.e. ERKs, c-Jun N-terminal kinases (JNKs), and p38 MAPK in the proliferation of dog and human thyroid epithelial cells (thyrocytes) in primary cultures. In these cells, TSH, acting through cAMP, epidermal growth factor, hepatocyte growth factor (HGF), and phorbol 12-myristate 13-acetate induce DNA synthesis. With the exception of HGF, all of these factors require the presence of insulin for mitogenic effects to be expressed. We found that TSH and forskolin are without effect on the phosphorylation and activity of the different classes of MAPKs. In contrast, all the cAMP-independent growth factors, whereas without effect on the phosphorylation and activity of JNKs and p38 MAPK, stimulated the ERKs. This effect was strong and sustained in response to HGF, epidermal growth factor and 12-myristate 13-acetate but weak and transient in response to insulin. Moreover, whereas in stimulated cells DNA synthesis was inhibited by PD 098059, an inhibitor of MAPK kinase 1 and consequently of ERKs, it was not modified by SB 203580, an inhibitor of p38 MAPK. Taken together, these data 1) exclude a role of JNKs and p38 MAPK in the proliferation of dog and human thyrocytes; 2) suggest that the mitogenic action of the cAMP-independent agents requires a strong and sustained activation of both ERKs and phosphatidylinositol 3-kinase/protein kinase B as realized by HGF alone or by the other agents together with insulin; and 3) show that TSH and cAMP do not activate ERKs but that the weak activation of ERKs by insulin is nevertheless necessary for DNA synthesis to occur.

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