Validation Data Gallery
|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.
FoxOs inhibit mTORC1 and activate Akt by inducing the expression of Sestrin3 and Rictor.
Proc Natl Acad Sci U S A
FOXO1 and FOXO3 transcription factors have unique functions in meniscus development and homeostasis during aging and osteoarthritis.
Selective eradication of cancer displaying hyperactive Akt by exploiting the metabolic consequences of Akt activation.
Suppression of Sestrins in aging and osteoarthritic cartilage: dysfunction of an important stress defense mechanism.
Regulatory Effects of Sestrin 3 (SESN3) in BCR-ABL Expressing Cells.
Inhibition of mTORC1 through ATF4-induced REDD1 and Sestrin2 expression by Metformin.