scholarly journals Evidence for glutathione involvement in platelet-derived growth-factor-mediated signal transduction

1997 ◽  
Vol 324 (3) ◽  
pp. 791-796 ◽  
Author(s):  
Stefania RIGACCI ◽  
Teresa IANTOMASI ◽  
Patrizia MARRACCINI ◽  
Andrea BERTI ◽  
Maria Teresa VINCENZINI ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Receptor Activation ◽  
Platelet Derived Growth Factor ◽  
Glutathione Depletion ◽  
Physiological Processes ◽  
Buthionine Sulphoximine ◽  
Precise Relationship

Recent studies show that glutathione, while being involved in the well-known physiological processes of amino acid transport and detoxification, can also play a part in cell proliferation events. Cell treatment with l-buthionine sulphoximine, which causes glutathione depletion, is accompanied by a decrease in cell proliferation. At present no precise relationship between this thiol and any critical intermediate of the mitogenic cascade has been proved. In this study, conducted on NIH/3T3 murine fibroblasts, we demonstrate a strict correlation between glutathione levels and platelet-derived growth-factor-receptor activation in response to stimulation and cell proliferation. The receptor autophosphorylation is severely impaired at low glutathione cellular levels. The interaction of glutathione with this growth-factor receptor in vivo, while being rather specific, is complex and may involve both cytosolic and extracellular receptor domains.

Engineered High-Affinity Affibody Molecules Targeting Platelet-Derived Growth Factor Receptor β In Vivo

2011 ◽  
Vol 407 (2) ◽  
pp. 298-315 ◽  
Author(s):  
M. Lindborg ◽  
E. Cortez ◽  
I. Höidén-Guthenberg ◽  
E. Gunneriusson ◽  
E. von Hage ◽  
...  
Keyword(s):  
Growth Factor ◽  
Growth Factor Receptor ◽  
Platelet Derived Growth Factor ◽  
Affibody Molecules ◽  
High Affinity

scholarly journals LINC00037 Inhibits Proliferation of Renal Cell Carcinoma Cells in an Epidermal Growth Factor Receptor-Dependent Way

2018 ◽  
Vol 45 (2) ◽  
pp. 523-536 ◽  
Author(s):  
Xiaohui Gong ◽  
Xianjin Du ◽  
Yong Xu ◽  
Wenze Zheng
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Epidermal Growth

Background/Aims: LINC00037 has previously been reported to be up-regulated in clear cell renal cell carcinoma (ccRCC), however, the underlying mechanism remained unknown. In this study, we designed to investigate the functional role of LINC00037 in ccRCC Methods: LINC00037 knockdown and re-expressing 786-O and A498 cells were established. CCK8 assay and EdU assay were performed to evaluate the proliferation rates of ccRCC cells. Flow cytometry assay was performed to detect the cell apoptosis and cell cycle. Subcutaneous injection xenotransplantation mouse model was used to observe the role of LINC00037 in tumor growth in vivo. Mass spectrometry (MS) was performed to find the interacting partner of LINC00037 and RNA immunoprecipitation (RIP) was carried out to validate their interaction. Results: We found that knockdown of LINC00037 resulted in inhibited cell proliferation with activated apoptosis and cell cycle arrest in vitro. Over-expression of LINC00037 in LINC00037 knockdown cells restored and enhanced cell proliferation. In vivo mouse model indicated reduced tumor progression by LINC00037 depletion and promoted tumor progression by LINC00037 overexpression. LINC00037 could bind to epidermal growth factor receptor (EGFR) and increase the protein level of EGFR. Conclusion: LINC00037 could inhibit proliferation of ccRCC in an epidermal growth factor receptor-dependent way.

scholarly journals Cbl-mediated Negative Regulation of Platelet-derived Growth Factor Receptor-dependent Cell Proliferation

1999 ◽  
Vol 274 (23) ◽  
pp. 16619-16628 ◽  
Author(s):  
Sachiko Miyake ◽  
Karen P. Mullane-Robinson ◽  
Nancy L. Lill ◽  
Patrice Douillard ◽  
Hamid Band
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Negative Regulation ◽  
Platelet Derived Growth Factor ◽  
Dependent Cell
Sign in / Sign up

Export Citation Format

Share Document