SESN3 Antibody [FITC] Summary
| Immunogen |
Synthetic peptides corresponding to unique epitope on SESN3. The SESN3 peptide was selected from N-terminal, amino acids 1-50. This peptide was covalently modified post-synthetically to achieve desired antigenicity.
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| Clonality |
Polyclonal
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| Host |
Rabbit
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| Gene |
SESN3
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| Purity |
Immunogen affinity purified
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Applications/Dilutions
| Dilutions |
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| Application Notes |
The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
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| Theoretical MW |
57 kDa.
Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors. |
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| Positive Control |
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Packaging, Storage & Formulations
| Storage |
Store at -20C. Avoid freeze-thaw cycles.
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| Buffer |
Tris/Glycine buffer pH 7.5-7.9, stabilizing protein, and glycerol
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| Preservative |
0.02% Sodium Azide
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| Purity |
Immunogen affinity purified
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Alternate Names for SESN3 Antibody [FITC]
- SEST3MGC29667
- sestrin 3
- sestrin-3
Background
Sestrin 3(SESN3), located at human chromosome 11q21, belongs to the sestrin family of proteins. These proteins are cystein sulfinyl reductases and they modulate peroxide signaling and antioxidant defense (1). This family of proteins is only present in multicellular organisms ranging from nematodes to mammals. These proteins selectively reduce or repair hyperoxidized forms of typical 2-Cys peroxiredoxins within eukaryotes (2). Peroxiredoxins are the enzymes that metabolize peroxides. Expression of these proteins is regulated by p53, a tumor suppressor protein (3). Sestrin 3 was identified as a forkhead box O (FoxO) target gene with antioxidant activity (4). 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 (5). AKT is a protein kinase that is hyperactivated in cancer. This hyperactivity leads to an increase in intracellular ROS mainly by inhibiting the expression of ROS scavengers downstream of FoxO, such as sestrin 3 (4). This phenomenon was supported by the fact that AKT deficient cells contained high levels of sestrin 3 leading to low levels of ROS. Furthermore, downregulation of sestrin 3 restored ROS levels in these cells (5). Hyperactivation of AKT has been shown to promote uncontrolled cell growth and also protect cells from apoptosis (6). Inhibition of mRNAs from sestrin 3 as well as from sestrin 1 has also been shown to substantially increase intracellular ROS levels. This increase in ROS is linked to Ras-induced mutagenesis which is one of the most common events in cancer (7). Sestrin 3 is approximately a 38.5kDa protein (480 amino acids) in human and 59kDa protein (492 amino acids) in rat and mouse.