scholarly journals Generation and characterization of polyclonal antibodies specific to N-terminal extension of p85 isoform of ribosomal protein S6 kinase 1 (p85 S6K1)

2015 ◽  
Vol 31 (4) ◽  
pp. 294-300 ◽  
Author(s):  
L. O. Savinska ◽  
O. M. Klipa ◽  
A. I. Khoruzenko ◽  
K. S. Shkarina ◽  
O. M. Garifulin ◽  
...  
Keyword(s):  
Ribosomal Protein ◽  
Polyclonal Antibodies ◽  
S6 Kinase ◽  
Ribosomal Protein S6 ◽  
Ribosomal Protein S6 Kinase

scholarly journals Generation and characterization of the MCF-7 cell line with a knockout of a p85-S6K1 isoform of the ribosomal protein S6 kinase 1

2019 ◽  
Vol 35 (4) ◽  
pp. 303-312
Author(s):  
V. V. Holiar ◽  
N. Ya. Gotsulyak ◽  
A. I. Khoruzhenko ◽  
I. V. Zaiets
Keyword(s):  
Ribosomal Protein ◽  
Cell Line ◽  
S6 Kinase ◽  
Ribosomal Protein S6 ◽  
Mcf 7 ◽  
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.

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