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SEPN1 Antibody (C-term) Blocking peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q9NZV5 |
|---|---|
| Clone Names | 100318233 |
| Gene ID | 57190 |
|---|---|
| Other Names | Selenoprotein N, SelN, SEPN1, SELN |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | SELENON {ECO:0000303|PubMed:27645994, ECO:0000312|HGNC:HGNC:15999} |
|---|---|
| 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.
Background
This gene encodes a selenoprotein, which contains aselenocysteine (Sec) residue at its active site. The selenocysteineis encoded by the UGA codon that normally signals translationtermination. The 3' UTR of selenoprotein genes have a commonstem-loop structure, the sec insertion sequence (SECIS), that isnecessary for the recognition of UGA as a Sec codon rather than asa stop signal. Mutations in this gene cause the classical phenotypeof multiminicore disease and congenital muscular dystrophy withspinal rigidity and restrictive respiratory syndrome. Twoalternatively spliced transcript variants encoding distinctisoforms have been found for this gene.
References
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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