scholarly journals SH2B1 in  -Cells Regulates Glucose Metabolism by Promoting  -Cell Survival and Islet Expansion

Diabetes ◽  
2013 ◽  
Vol 63 (2) ◽  
pp. 585-595 ◽  
Author(s):  
Z. Chen ◽  
D. L. Morris ◽  
L. Jiang ◽  
Y. Liu ◽  
L. Rui
Keyword(s):  
Glucose Metabolism ◽  
Cell Survival ◽  
In Cells

Mitochondrial elongation-mediated glucose metabolism reprogramming is essential for tumour cell survival during energy stress

Oncogene ◽  
2017 ◽  
Vol 36 (34) ◽  
pp. 4901-4912 ◽  
Author(s):  
J Li ◽  
Q Huang ◽  
X Long ◽  
X Guo ◽  
X Sun ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Cell Survival ◽  
Tumour Cell ◽  
Energy Stress ◽  
Mitochondrial Elongation

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.

Roles for hypoxia inducible factor 1 and glucose metabolism in tumor cell survival following photodynamic therapy

2013 ◽  
Vol 65 ◽  
pp. S26-S27
Author(s):  
Mans Broekgaarden ◽  
Milan Kos ◽  
Ruud Weijer ◽  
Massis Krekorian ◽  
Thomas M. van Gulik ◽  
...  
Keyword(s):  
Photodynamic Therapy ◽  
Glucose Metabolism ◽  
Tumor Cell ◽  
Cell Survival ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1 ◽  
Tumor Cell Survival

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

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.

scholarly journals Liraglutide Treatment Ameliorates Neurotoxicity Induced by Stable Silencing of Pin1

2019 ◽  
Vol 20 (20) ◽  
pp. 5064 ◽  
Author(s):  
Marzia Bianchi ◽  
Valentina D’Oria ◽  
Maria Rita Braghini ◽  
Stefania Petrini ◽  
Melania Manco
Keyword(s):  
Glucose Metabolism ◽  
Cell Viability ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Protein Glycation ◽  
Oxygen Species ◽  
Impaired Glucose Metabolism ◽  
Altered Glucose ◽  
Peptidylprolyl Isomerase ◽  
In Cells

Post-translational modulation of peptidylprolyl isomerase Pin1 might link impaired glucose metabolism and neurodegeneration, being Pin1 effectors target for the glucagon-Like-Peptide1 analog liraglutide. We tested the hypotheses in Pin1 silenced cells (SH-SY5Y) treated with 2-deoxy-d-glucose (2DG) and methylglyoxal (MG), stressors causing altered glucose trafficking, glucotoxicity and protein glycation. Rescue by liraglutide was investigated. Pin1 silencing caused increased levels of reactive oxygen species, upregulated energy metabolism as suggested by raised levels of total ATP content and mRNA of SIRT1, PGC1α, NRF1; enhanced mitochondrial fission events as supported by raised protein expression of FIS1 and DRP1. 2DG and MG reduced significantly cell viability in all the cell lines. In Pin1 KD clones, 2DG exacerbated altered mitochondrial dynamics causing higher rate of fission events. Liraglutide influenced insulin signaling pathway (GSK3b/Akt); improved cell viability also in cells treated with 2DG; but it did not revert mitochondrial dysfunction in Pin1 KD model. In cells treated with MG, liraglutide enhanced cell viability, reduced ROS levels and cell death (AnnexinV/PI); and trended to reduce anti-apoptotic signals (BAX, BCL2, CASP3). Pin1 silencing mimics neuronal metabolic impairment of patients with impaired glucose metabolism and neurodegeneration. Liraglutide rescues to some extent cellular dysfunctions induced by Pin1 silencing.

Glutamine and glucose metabolism in rat splenocytes and mesenteric lymph node lymphocytes

1991 ◽  
Vol 260 (1) ◽  
pp. E141-E147 ◽  
Author(s):  
G. Y. Wu ◽  
C. J. Field ◽  
E. B. Marliss
Keyword(s):  
Lymph Node ◽  
Glucose Metabolism ◽  
Mesenteric Lymph Node ◽  
Lymphoid Organs ◽  
Glutamine Metabolism ◽  
Metabolite Formation ◽  
Physiological Concentration ◽  
Mesenteric Lymph ◽  
The Individual ◽  
In Cells

The metabolism of glutamine (2 mM) and glucose (5 mM) was studied in splenocytes and mesenteric lymph node lymphocytes of Wistar-Furth rats to assess their relative importance as energy substrates. The major products from glutamine were ammonia, glutamate, aspartate, and CO2, whereas those from glucose were lactate, pyruvate, and CO2 in cells from both lymphoid organs. The individual rates of glutamine and glucose metabolism were decreased in the presence of both substrates, compared with the rates when present separately. The rates of glucose and some (but not all) aspects of glutamine metabolism were higher (P less than 0.01) in splenocytes than in mesenteric lymphocytes. In cells from both lymphoid organs, glutamine and glucose could potentially contribute almost equal amounts of ATP in the presence of both substrates. Glutamine and glucose individually were able to provide sufficient amounts of ATP to maintain its concentrations in the cells throughout a 2-h incubation period at the same levels as with both substrates present. We also found that splenocyte concentration (3.3-100 x 10(6) cells/ml) in the incubations is an important determinant of rates of metabolite formation from glutamine when expressed per 10(6) cells. We conclude that glucose is not the only quantitatively significant energy substrate or even the major one for lymphocytes, because glutamine at near-physiological concentration can be readily utilized by these cells.

scholarly journals Enhanced oxidative phosphorylation in NKT cells is essential for their survival and function

2019 ◽  
Vol 116 (15) ◽  
pp. 7439-7448 ◽  
Author(s):  
Ajay Kumar ◽  
Kalyani Pyaram ◽  
Emily L. Yarosz ◽  
Hanna Hong ◽  
Costas A. Lyssiotis ◽  
...  
Keyword(s):  
T Cells ◽  
Glucose Metabolism ◽  
Cell Survival ◽  
Glucose Uptake ◽  
Cell Fate ◽  
Cd4 T Cells ◽  
Cell Function ◽  
Nkt Cells ◽  
Nkt Cell ◽  
And Function

Cellular metabolism and signaling pathways are key regulators to determine conventional T cell fate and function, but little is understood about the role of cell metabolism for natural killer T (NKT) cell survival, proliferation, and function. We found that NKT cells operate distinct metabolic programming from CD4 T cells. NKT cells are less efficient in glucose uptake than CD4 T cells with or without activation. Gene-expression data revealed that, in NKT cells, glucose is preferentially metabolized by the pentose phosphate pathway and mitochondria, as opposed to being converted into lactate. In fact, glucose is essential for the effector functions of NKT cells and a high lactate environment is detrimental for NKT cell survival and proliferation. Increased glucose uptake and IFN-γ expression in NKT cells is inversely correlated with bacterial loads in response to bacterial infection, further supporting the significance of glucose metabolism for NKT cell function. We also found that promyelocytic leukemia zinc finger seemed to play a role in regulating NKT cells’ glucose metabolism. Overall, our study reveals that NKT cells use distinct arms of glucose metabolism for their survival and function.

Sign in / Sign up

Export Citation Format

Share Document