|Positive WB detected in||human skeletal muscle tissue, human testis tissue, mouse liver tissue|
|Western Blot (WB)||WB : 1:500-1:1000|
|Sample-dependent, check data in validation data gallery|
The immunogen of 21668-1-AP is SESN1 Fusion Protein expressed in E. coli.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse, rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||SESN1 fusion protein Ag16462|
|Full Name||sestrin 1|
|Calculated molecular weight||551 aa, 64 kDa|
|Observed molecular weight||66-68 kDa|
|GenBank accession number||BC112036|
|Gene ID (NCBI)||27244|
|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 1 is implicated in the inhibition of cell growth. It is approximately a 66kDa protein in humans (551 amino acids).
Am J Physiol Endocrinol Metab
Evidence for a Role for Sestrin1 in Mediating Leucine-Induced Activation of mTORC1 in Skeletal Muscle.
Biochim Biophys Acta
Exercise improves glucose uptake in murine myotubes through the AMPKα2-mediated induction of Sestrins.
Repressors of mTORC1 act to blunt the anabolic response to feeding in the soleus muscle of a cast-immobilized mouse hindlimb.
Biomed Res Int
Pentamethylquercetin Attenuates Cardiac Remodeling via Activation of the Sestrins/Keap1/Nrf2 Pathway in MSG-Induced Obese Mice.
Cell Physiol Biochem
Sestrin-Mediated Inhibition of Stress-Induced Intervertebral Disc Degradation Through the Enhancement of Autophagy.
Suppression of Sestrins in aging and osteoarthritic cartilage: dysfunction of an important stress defense mechanism.