Suppressor mechanism of serum thymic factor on tumor necrosis factor-α-induced apoptosis in the mouse pancreatic β-cell line

2003 ◽  
Vol 311 (2) ◽  
pp. 501-505 ◽  
Author(s):  
Junko Yasuda ◽  
Wakako Nishioka ◽  
Akikazu Sakudo ◽  
Sachiko Yama ◽  
Ruka Setoguchi ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Suppressor Mechanism ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Thymic Factor ◽  
Necrosis Factor

Baicalin prevents tumor necrosis factor-α−induced apoptosis and dysfunction of pancreatic β-cell line Min6 via upregulation of miR-205

2018 ◽  
Vol 119 (10) ◽  
pp. 8547-8554 ◽  
Author(s):  
Wenjun You ◽  
Kun Wang ◽  
Changhong Yu ◽  
Lijuan Song
Keyword(s):  
Tumor Necrosis Factor ◽  
Cell Line ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Cytokines Tumor Necrosis Factor-α and Interferon-γ Induce Pancreatic β-Cell Apoptosis through STAT1-mediated Bim Protein Activation

2011 ◽  
Vol 286 (45) ◽  
pp. 39632-39643 ◽  
Author(s):  
Jenny Barthson ◽  
Carla M. Germano ◽  
Fabrice Moore ◽  
Adriano Maida ◽  
Daniel J. Drucker ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Cell Apoptosis ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interferon Γ ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Protein Activation ◽  
Factor Α ◽  
Necrosis Factor

Endogenous tumor necrosis factor-α production by a pancreatic β-cell line: Inhibitory effects of hydrocortisone and nicotinamide

Life Sciences ◽  
1996 ◽  
Vol 59 (17) ◽  
pp. 1423-1429 ◽  
Author(s):  
Kentaro Yamada ◽  
Naoko Takane-Gyotoku ◽  
Chizuko Inada ◽  
Kyohei Nonaka
Keyword(s):  
Tumor Necrosis Factor ◽  
Cell Line ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Pancreatic Β Cell ◽  
Inhibitory Effects ◽  
Β Cell ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Role of NF-κB signaling pathway in increased tumor necrosis factor-α-induced apoptosis of lymphocytes in aged humans

2005 ◽  
Vol 12 (2) ◽  
pp. 177-183 ◽  
Author(s):  
S Gupta ◽  
R Bi ◽  
C Kim ◽  
S Chiplunkar ◽  
L Yel ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Signaling Pathway ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Estradiol Abrogates Apoptosis in Breast Cancer Cells through Inactivation of BAD: Ras-dependent Nongenomic Pathways Requiring Signaling through ERK and Akt

2004 ◽  
Vol 15 (7) ◽  
pp. 3266-3284 ◽  
Author(s):  
Romaine Ingrid Fernando ◽  
Jay Wimalasena
Keyword(s):  
Breast Cancer ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Dominant Negative ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

Estrogens such as 17-β estradiol (E2) play a critical role in sporadic breast cancer progression and decrease apoptosis in breast cancer cells. Our studies using estrogen receptor-positive MCF7 cells show that E2 abrogates apoptosis possibly through phosphorylation/inactivation of the proapoptotic protein BAD, which was rapidly phosphorylated at S112 and S136. Inhibition of BAD protein expression with specific antisense oligonucleotides reduced the effectiveness of tumor necrosis factor-α, H2O2, and serum starvation in causing apoptosis. Furthermore, the ability of E2 to prevent tumor necrosis factor-α-induced apoptosis was blocked by overexpression of the BAD S112A/S136A mutant but not the wild-type BAD. BAD S112A/S136A, which lacks phosphorylation sites for p90RSK1 and Akt, was not phosphorylated in response to E2 in vitro. E2 treatment rapidly activated phosphatidylinositol 3-kinase (PI-3K)/Akt and p90RSK1 to an extent similar to insulin-like growth factor-1 treatment. In agreement with p90RSK1 activation, E2 also rapidly activated extracellular signal-regulated kinase, and this activity was down-regulated by chemical and biological inhibition of PI-3K suggestive of cross talk between signaling pathways responding to E2. Dominant negative Ras blocked E2-induced BAD phosphorylation and the Raf-activator RasV12T35S induced BAD phosphorylation as well as enhanced E2-induced phosphorylation at S112. Chemical inhibition of PI-3K and mitogen-activated protein kinase kinase 1 inhibited E2-induced BAD phosphorylation at S112 and S136 and expression of dominant negative Ras-induced apoptosis in proliferating cells. Together, these data demonstrate a new nongenomic mechanism by which E2 prevents apoptosis.

scholarly journals Oncogenic Ras Sensitizes Normal Human Cells to Tumor Necrosis Factor-α-Related Apoptosis-Inducing Ligand-Induced Apoptosis

2004 ◽  
Vol 64 (11) ◽  
pp. 3922-3927 ◽  
Author(s):  
Alexandre Nesterov ◽  
Malti Nikrad ◽  
Thomas Johnson ◽  
Andrew S. Kraft
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Human Cells ◽  
Oncogenic Ras ◽  
Normal Human ◽  
Normal Human Cells ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

A selective estrogen receptor modulator inhibits tumor necrosis factor-α-induced apoptosis through the ERK1/2 signaling pathway in human chondrocytes

2012 ◽  
Vol 421 (3) ◽  
pp. 418-424 ◽  
Author(s):  
Yosuke Hattori ◽  
Toshihisa Kojima ◽  
Daizo Kato ◽  
Hiroyuki Matsubara ◽  
Masaharu Takigawa ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Tumor Necrosis Factor ◽  
Signaling Pathway ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Human Chondrocytes ◽  
Receptor Modulator ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Necrosis Factor
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