scholarly journals NF-Y-dependent regulation of glutamate receptor 4 expression and cell survival in cells of the oligodendrocyte lineage

Glia ◽  
2018 ◽  
Vol 66 (9) ◽  
pp. 1896-1914 ◽  
Author(s):  
Ghazala Begum ◽  
Masahiro Otsu ◽  
Usman Ahmed ◽  
Zubair Ahmed ◽  
Adam Stevens ◽  
...  
Keyword(s):  
Cell Survival ◽  
Glutamate Receptor ◽  
In Cells

Survival-promoting functions of 14-3-3 proteins

2002 ◽  
Vol 30 (4) ◽  
pp. 360-365 ◽  
Author(s):  
S. C. Masters ◽  
R. R. Subramanian ◽  
A. Truong ◽  
H. Yang ◽  
K. Fujii ◽  
...  
Keyword(s):  
Cell Survival ◽  
Anticancer Agents ◽  
Cellular Proteins ◽  
Support Cell ◽  
Antagonist Peptides ◽  
Ligand Interactions ◽  
Cellular Machinery ◽  
In Cells

The 14-3-3 proteins are a family of phosphoserine/phosphothreonine-binding molecules that control the function of a wide array of cellular proteins. We suggest that one function of 14-3-3 is to support cell survival. 14-3-3 proteins promote survival in part by antagonizing the activity of associated proapoptotic proteins, including Bad and apoptosis signal-regulating kinase 1 (ASK1). Indeed, expression of 14-3-3 inhibitor peptides in cells is sufficient to induce apoptosis. Interestingly, these 14-3-3 antagonist peptides can sensitize cells for effective killing by anticancer agents such as cisplatin. Thus, 14-3-3 may be part of the cellular machinery that maintains cell survival, and targeting 14-3-3-ligand interactions may be a useful strategy to enhance the efficacy of conventional anticancer agents.

The effects of glutamate receptor antagonists on cerebellar granule cell survival and development

2008 ◽  
Vol 29 (1) ◽  
pp. 101-108 ◽  
Author(s):  
Linda Klimavičiusa ◽  
Dzhamilja Safiulina ◽  
Allen Kaasik ◽  
Vija Kluša ◽  
Alexander Zharkovsky
Keyword(s):  
Cell Survival ◽  
Glutamate Receptor ◽  
Granule Cell ◽  
Cerebellar Granule Cell ◽  
Receptor Antagonists ◽  
Cerebellar Granule ◽  
Glutamate Receptor Antagonists ◽  
Survival And Development

scholarly journals SLC38A10 Transporter Plays a Role in Cell Survival Under Oxidative Stress and Glutamate Toxicity

2021 ◽  
Vol 8 ◽  
Author(s):  
Rekha Tripathi ◽  
Tanya Aggarwal ◽  
Robert Fredriksson
Keyword(s):  
Oxidative Stress ◽  
Cell Survival ◽  
Glutamate Toxicity ◽  
In Cells

Graphical AbstractSLC38A10 role in cells survival under stress.

Effects of riluzole (RZ) and ionizing radiation (IR) in metabotropic glutamate receptor-1 (GRM1) positive human melanoma

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 9083-9083
Author(s):  
C. Green ◽  
D. Schiff ◽  
A. Khan ◽  
S. Goyal ◽  
J. Goydos ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Western Blot ◽  
Cell Survival ◽  
Glutamate Receptor ◽  
Blot Analysis ◽  
Caspase 3 ◽  
Metabotropic Glutamate Receptor ◽  
Human Melanoma ◽  
Metabotropic Glutamate

9083 Background: Melanoma has long been known to be relatively radio-resistant. GRM1 is a metabotropic glutamate receptor that has been detected in human melanoma cell lines and biopsies. Riluzole (RZ), a glutamate release inhibitor, has been shown to arrest GRM1 positive human melanoma cells in G2/M and sub-G1 phases of the cell cycle. The purpose of this study was to determine if RZ enhances the lethal effects of IR in human melanoma. Methods: ATP luminescence assays were performed. Clonogenic assays were performed and cell survival curves generated. Cell cycle analysis was performed utilizing flow cytometry. Western blot analysis was performed utilizing cleaved PARP and caspase-3 antibodies as markers of apoptosis. Results: Luminescence assays revealed 25uM Riluzole to be the necessary concentration for clonogenic assays. At 2Gy, there was a 48% reduction (p≤0.05) in cell survival in RZ-treated cells. At 4 Gy, there was a 19% reduction (p≤0.05) in cell survival in RZ-treated cells. No differences were seen at 6 and 8 Gy. Cell cycle analysis showed that the combination of IR and RZ was superior to IR alone in increasing the number of cells in sub-G1, which represents apoptotic death. Western blot analysis showed that the combination of IR and RZ showed yielded increased cleaved PARP and caspase-3 activity when compared to IR alone. Conclusions: Riluzole is a FDA approved drug that has long been used in ALS. It is relatively non-toxic and crosses the blood brain barrier. Our data shows that Riluzole in combination with radiation eliminates the radio-resistant shoulder of the C8161 survival curve. RZ and IR, as combination therapy are more lethal than IR or RZ alone in human melanoma, as demonstrated by flow cytometry and WB analysis. This data has promising implications for melanoma patients with brain metastases. No significant financial relationships to disclose.

c-RAF IS DOWNREGULATED RATHER THAN REQUIRED FOR CELL SURVIVAL IN CELLS OVEREXPRESSING BCL-2

1996 ◽  
Vol 24 (4) ◽  
pp. 598S-598S
Author(s):  
Markus Wartmann ◽  
Reynald A. Olivier ◽  
Isabelle Otter ◽  
Laurent Monney ◽  
Silvia Stabel ◽  
...  
Keyword(s):  
Cell Survival ◽  
In Cells

Cell survival and changes in gene expression in cells unable to synthesize glutathione

BioFactors ◽  
2003 ◽  
Vol 17 (1-4) ◽  
pp. 13-19 ◽  
Author(s):  
E. Rojas ◽  
Z.-Z. Shi ◽  
M. Valverde ◽  
R. S. Paules ◽  
G. M. Habib ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Survival ◽  
In Cells

scholarly journals Tor Directly Controls the Atg1 Kinase Complex To Regulate Autophagy

2009 ◽  
Vol 30 (4) ◽  
pp. 1049-1058 ◽  
Author(s):  
Yoshiaki Kamada ◽  
Ken-ichi Yoshino ◽  
Chika Kondo ◽  
Tomoko Kawamata ◽  
Noriko Oshiro ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cell Growth ◽  
Cell Survival ◽  
Nutrient Deprivation ◽  
Direct Control ◽  
Direct Target ◽  
In Cells ◽  
Nutrient Conditions

ABSTRACT Autophagy is a bulk proteolytic process that is indispensable for cell survival during starvation. Autophagy is induced by nutrient deprivation via inactivation of the rapamycin-sensitive Tor complex1 (TORC1), a protein kinase complex regulating cell growth in response to nutrient conditions. However, the mechanism by which TORC1 controls autophagy and the direct target of TORC1 activity remain unclear. Atg13 is an essential regulatory component of autophagy upstream of the Atg1 kinase complex, and here we show that yeast TORC1 directly phosphorylates Atg13 at multiple Ser residues. Additionally, expression of an unphosphorylatable Atg13 mutant bypasses the TORC1 pathway to induce autophagy through activation of Atg1 in cells growing under nutrient-rich conditions. Our findings suggest that the direct control of the Atg1 complex by TORC1 induces autophagy.

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