SESN2 Blocking Peptide for STJ502957 is synthetically produced from the 1-80 sequence and is suitable for use in western blot applications.
Applications
Immunodepletion/Immunocompetition
Note
STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Product Properties
Formulation
Liquid form at 2.5mg/ml concentration in PBS. Up to 5% DMSO can be added. Orders with >1mg can be supplied in lyophilized powder form, or in buffer of choice.
Storage Instruction
Store at-20°C for long term storage. Avoid freeze-thaw cycles.
Synthetic peptide taken within amino acid region 1-80 on SESN2 protein.
Immunogen Region
1-80
Specificity
This blocking peptide is recommended for use in combination with SESN2 antibody, STJ502957
Additional Info
Tissue Specificity
Widely expressed.
Post Translational Modifications
Phosphorylated by ULK1 at multiple sites. Ubiquitinated at Lys-175 by RNF167 via 'Lys-63'-linked polyubiquitination in response to leucine deprivation: ubiquitination promotes SESN2-interaction with the GATOR2 complex, leading to inhibit the TORC1 signaling pathway. Deubiquitinated at Lys-175 by STAMBPL1, promoting the TORC1 signaling pathway. Ubiquitinated by RNF186.ubiquitination mediates proteasomal degradation.
Function
Functions as an intracellular leucine sensor that negatively regulates the mTORC1 signaling pathway through the GATOR complex. In absence of leucine, binds the GATOR subcomplex GATOR2 and prevents mTORC1 signaling. Binding of leucine to SESN2 disrupts its interaction with GATOR2 thereby activating the TORC1 signaling pathway. This stress-inducible metabolic regulator also plays a role in protection against oxidative and genotoxic stresses. May negatively regulate protein translation in response to endoplasmic reticulum stress, via mTORC1. May positively regulate the transcription by NFE2L2 of genes involved in the response to oxidative stress by facilitating the SQSTM1-mediated autophagic degradation of KEAP1. May also mediate TP53 inhibition of TORC1 signaling upon genotoxic stress. Moreover, may prevent the accumulation of reactive oxygen species (ROS) through the alkylhydroperoxide reductase activity born by the N-terminal domain of the protein. Was originally reported to contribute to oxidative stress resistance by reducing PRDX1. However, this could not be confirmed.
