scholarly journals Regulation of TGF-βSignal Transduction

Scientifica ◽  
2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Bing Zhao ◽  
Ye-Guang Chen
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Map Kinases ◽  
Transforming Growth Factor ◽  
Signaling Proteins ◽  
Cell Plasticity ◽  
Cellular Processes ◽  
Smad Proteins ◽  
And Migration ◽  
Different Levels

Transforming growth factor-β(TGF-β) signaling regulates diverse cellular processes, including cell proliferation, differentiation, apoptosis, cell plasticity, and migration. TGF-βsignaling can be mediated by Smad proteins or other signaling proteins such as MAP kinases and Akt. TGF-βsignaling is tightly regulated at different levels along the pathways to ensure its proper physiological functions in different cells and tissues. Deregulation of TGF-βsignaling has been associated with various kinds of diseases, such as cancer and tissue fibrosis. This paper focuses on our recent work on regulation of TGF-βsignaling.

scholarly journals Cell-specificity of transforming growth factor-β response is dictated by receptor bioavailability

2006 ◽  
Vol 36 (3) ◽  
pp. 591-600 ◽  
Author(s):  
Magdalena I Suszko ◽  
Teresa K Woodruff
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Reproductive Function ◽  
Transforming Growth Factor Β ◽  
Family Control ◽  
Cellular Processes ◽  
Relative Contribution ◽  
A Cell ◽  
Mouse Pituitary ◽  
And Migration

Members of the transforming growth factor-β (TGFβ) family control diverse cellular responses including differentiation, proliferation, controlled cell death and migration. The response of a cell to an individual ligand is highly restricted yet the signaling pathways for TGFβ, activin and bone morphogenic proteins share a limited number of receptors and activate similar intracellular cytoplasmic co-regulators, Smads. A central question in the study of this family of ligands is how cells titrate and integrate each TGFβ-like signal in order to respond in a cell- and ligand-specific manner. This study uses the pituitary gonadotrope cell line, LβT2, as a model to delineate the relative contribution of TGFβ and activin ligands to follicle-stimulating hormone (FSH) biosynthesis. It was found that pituitary gonadotrope cells do not express the TGFβ type II (TβRII) receptor and are therefore not responsive to the TGFβ ligand. Transfection of the receptor restores TGFβ signaling capabilities and the TGFβ-mediated stimulation of FSHβ gene transcription in LβT2 cells. Consequently, we evaluated the presence of the TβRII in the adult mouse pituitary. TβRII does not co-localize with FSH-producing cells; however it is detected on the cell surface of prolactin- and growth hormone-positive cells. Taken together, these results suggest that the bioavailability of the TGFβ-specific receptor rather than TGFβ dictates pituitary gonadotrope selectivity to activin, which is necessary to maintain normal reproductive function. It is likely that the ligand-restricted mechanisms employed by the gonadotrope are present in other cells, which could explain the distinct control of many cellular processes by members of the TGFβ superfamily.

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