|Application ||IHC-P, WB, E|
|Other Accession||NP_996809.1, NP_065184.2|
|Calculated MW||65813 Da|
|Antigen Region||417-445 aa|
|Other Names||Selenoprotein N, SelN, SEPN1, SELN|
|Target/Specificity||This SEPN1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 417-445 amino acids from the C-terminal region of human SEPN1.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||SEPN1 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Isoform 2: Plays an important role in cell protection against oxidative stress and in the regulation of redox-related calcium homeostasis. Regulates the calcium level of the ER by protecting the calcium pump ATP2A2 against the oxidoreductase ERO1A-mediated oxidative damage. Within the ER, ERO1A activity increases the concentration of H(2)O(2), which attacks the luminal thiols in ATP2A2 and thus leads to cysteinyl sulfenic acid formation (-SOH) and SEPN1 reduces the SOH back to free thiol (- SH), thus restoring ATP2A2 activity (PubMed:25452428). Acts as a modulator of ryanodine receptor (RyR) activity: protects RyR from oxidation due to increased oxidative stress, or directly controls the RyR redox state, regulating the RyR-mediated calcium mobilization required for normal muscle development and differentiation (PubMed:19557870, PubMed:18713863).|
|Cellular Location||Isoform 2: Endoplasmic reticulum membrane|
|Tissue Location||Isoform 1 and isoform 2 are expressed in skeletal muscle, brain, lung and placenta. Isoform 2 is also expressed in heart, diaphragm and stomach|
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Provided below are standard protocols that you may find useful for product applications.
This gene encodes a selenoprotein, which contains a selenocysteine (Sec) residue at its active site. The selenocysteine is encoded by the UGA codon that normally signals translation termination. The 3' UTR of selenoprotein genes have a common stem-loop structure, the sec insertion sequence (SECIS), that is necessary for the recognition of UGA as a Sec codon rather than as a stop signal. Mutations in this gene cause the classical phenotype of multiminicore disease and congenital muscular dystrophy with spinal rigidity and restrictive respiratory syndrome. Two alternatively spliced transcript variants encoding distinct isoforms have been found for this gene.
Arbogast, S., et al. Ann. Neurol. 65(6):677-686(2009)
Maiti, B., et al. Hum. Mutat. 30(3):411-416(2009)
Jurynec, M.J., et al. Proc. Natl. Acad. Sci. U.S.A. 105(34):12485-12490(2008)
Lin, L., et al. PLoS Genet. 4 (10), E1000225 (2008) :
Wu, C., et al. Proteomics 7(11):1775-1785(2007)
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