|Positive WB detected in||HeLa cells, A431 cells, A549 cells, HEK-293 cells, HepG2 cells, mouse liver tissue, mouse ovary tissue|
|Western Blot (WB)||WB : 1:500-1:1000|
|Sample-dependent, check data in validation data gallery|
11431-2-AP targets SESN3 in WB, IHC,ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse, rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||SESN3 fusion protein Ag1961|
|Full Name||sestrin 3|
|Calculated molecular weight||492 aa, 57 kDa|
|Observed molecular weight||51-59 kDa|
|GenBank accession number||BC017296|
|Gene ID (NCBI)||143686|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
Sestrins, including sestrin-1 (PA26), sestrin-2 (Hi95), and sestrin-3, are 48 to 65 kDa cystein sulfinyl reductases and they modulate peroxide signaling and antioxidant defense. These proteins selectively reduce or repair hyperoxidized forms of typical 2-Cys peroxiredoxins within eukaryotes. Expression of these proteins is regulated by p53, a tumor suppressor protein. Sestrin 3 was identified as a forkhead box O (FoxO) target gene with antioxidant activity. Recently it was reported that sestrin 3 may play an important role in AKT induced increase in ROS and it might be a promising target in selectively killing cancer cells containing high levels of AKT activity.
Silencing rno-miR-155-5p in rat temporal lobe epilepsy model reduces pathophysiological features and cell apoptosis by activating Sestrin-3.
Biochim Biophys Acta
Exercise improves glucose uptake in murine myotubes through the AMPKα2-mediated induction of Sestrins.
Cell Physiol Biochem
Sestrin-Mediated Inhibition of Stress-Induced Intervertebral Disc Degradation Through the Enhancement of Autophagy.
Regulatory Effects of Sestrin 3 (SESN3) in BCR-ABL Expressing Cells.
Suppression of Sestrins in aging and osteoarthritic cartilage: dysfunction of an important stress defense mechanism.
Selective eradication of cancer displaying hyperactive Akt by exploiting the metabolic consequences of Akt activation.