Adenosine triphosphate induces proliferation of human neural stem cells: Role of calcium and p70 ribosomal protein S6 kinase

2003 ◽  
Vol 72 (3) ◽  
pp. 352-362 ◽  
Author(s):  
Jae K. Ryu ◽  
Hyun B. Choi ◽  
Kozo Hatori ◽  
Rochelle L. Heisel ◽  
Steven L. Pelech ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Ribosomal Protein ◽  
Adenosine Triphosphate ◽  
S6 Kinase ◽  
Human Neural Stem Cells ◽  
Ribosomal Protein S6 ◽  
Ribosomal Protein S6 Kinase

scholarly journals The Prognostic Role of Ribosomal Protein S6 Kinase 1 Pathway in Patients With Solid Tumors: A Meta-Analysis

2019 ◽  
Vol 9 ◽  
Author(s):  
Shuo Zhang ◽  
Binwu Hu ◽  
Xiao Lv ◽  
Songfeng Chen ◽  
Weijian Liu ◽  
...  
Keyword(s):  
Ribosomal Protein ◽  
Solid Tumors ◽  
Meta Analysis ◽  
Prognostic Role ◽  
S6 Kinase ◽  
Ribosomal Protein S6 ◽  
Ribosomal Protein S6 Kinase

The adipose tissue triglyceride lipase ATGL/PNPLA2 is downregulated by insulin and TNF-α in 3T3-L1 adipocytes and is a target for transactivation by PPARγ

2006 ◽  
Vol 291 (1) ◽  
pp. E115-E127 ◽  
Author(s):  
Ji Young Kim ◽  
Kristin Tillison ◽  
Jun-Ho Lee ◽  
David A. Rearick ◽  
Cynthia M. Smas
Keyword(s):  
Adipose Tissue ◽  
Ribosomal Protein ◽  
Luciferase Reporter ◽  
Dependent Manner ◽  
S6 Kinase ◽  
Triglyceride Lipase ◽  
Ribosomal Protein S6 ◽  
Tnf Α ◽  
Adipose Tissue Triglyceride ◽  
Ribosomal Protein S6 Kinase

The minimal adipose phenotype of hormone-sensitive lipase (HSL)-null mice suggested that other hormonally responsive lipase(s) were present in adipocytes. Recent studies have characterized a new adipose tissue triglyceride lipase, ATGL/PNPLA2/destnutrin/iPLA2ζ/TTS2.2 (ATGL). We had previously cloned a novel adipose-enriched transcript by differential screening and recently determined its identity with murine ATGL. We report here on the regulation of ATGL by TNF-α and insulin in 3T3-L1 adipocytes and identify ATGL as a target for transcriptional activation by the key adipogenic transcription factor PPARγ. Insulin at 100 nM resulted in a marked decrease in ATGL transcript that was effectively blocked by inhibitors for PI 3-kinase and p70 ribosomal protein S6 kinase. TNF-α treatment decreased ATGL transcript in a time-dependent manner that paralleled TNF-α downregulation of PPARγ with a maximal decrease noted by 6 h. TNF-α effects on ATGL were attenuated by pretreatment with PD-98059, LY-294002, or rapamycin, suggesting involvement of the p44/42 MAP kinase, PI 3-kinase, and p70 ribosomal protein S6 kinase signals. To study transcriptional regulation of ATGL, we cloned 2,979 bp of the murine ATGL 5′-flanking region. Compared with promoterless pGL2-Basic, the −2979/+21 ATGL luciferase construct demonstrated 120- and 40-fold increases in activity in white and brown adipocytes, respectively. Luciferase reporter activities for a series of eight ATGL promoter deletions revealed that the −928/+21, −1738/+21, −1979/+21, and −2979/+21 constructs were transactivated by PPARγ. Our findings identify the novel lipase ATGL to be a target gene for TNF-α and insulin action in adipocytes and reveal that it is subject to transcriptional control by PPARγ-mediated signals.

P50. Role of glioma produced CM1 in the brain tumor tropism of human neural stem cells

2010 ◽  
Vol 80 ◽  
pp. S33-S34
Author(s):  
J. Jeon ◽  
S. Cho ◽  
K. Cho ◽  
Y. Lee ◽  
M. Lee
Keyword(s):  
Stem Cells ◽  
Brain Tumor ◽  
Neural Stem Cells ◽  
Human Neural Stem Cells ◽  
Tumor Tropism ◽  
The Brain
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