Aliases for MSRB1 Gene
External Ids for MSRB1 Gene
Previous HGNC Symbols for MSRB1 Gene
Previous GeneCards Identifiers for MSRB1 Gene
The protein encoded by this gene belongs to the methionine-R-sulfoxide reductase B (MsrB) family. Members of this family function as repair enzymes that protect proteins from oxidative stress by catalyzing the reduction of methionine-R-sulfoxides to methionines. This protein is highly expressed in liver and kidney, and is localized to the nucleus and cytosol. It is the only member of the MsrB family that is a selenoprotein, containing a selenocysteine (Sec) residue at its active site. It also has the highest methionine-R-sulfoxide reductase activity compared to other members containing cysteine in place of Sec. Sec is encoded by the UGA codon, which normally signals translation termination. The 3' UTRs of selenoprotein mRNAs contain a conserved stem-loop structure, designated the Sec insertion sequence (SECIS) element, that is necessary for the recognition of UGA as a Sec codon, rather than as a stop signal. A pseudogene of this locus has been identified on chromosome 19. [provided by RefSeq, Aug 2017]
GeneCards Summary for MSRB1 Gene
MSRB1 (Methionine Sulfoxide Reductase B1) is a Protein Coding gene. Diseases associated with MSRB1 include Deafness, Autosomal Recessive 74 and Staphyloenterotoxemia. Among its related pathways are Selenium Metabolism and Selenoproteins and Folate Metabolism. Gene Ontology (GO) annotations related to this gene include actin binding and methionine-R-sulfoxide reductase activity. An important paralog of this gene is MSRB2.
UniProtKB/Swiss-Prot Summary for MSRB1 Gene
Methionine-sulfoxide reductase that specifically reduces methionine (R)-sulfoxide back to methionine. While in many cases, methionine oxidation is the result of random oxidation following oxidative stress, methionine oxidation is also a post-translational modification that takes place on specific residue. Acts as a regulator of actin assembly by reducing methionine (R)-sulfoxide mediated by MICALs (MICAL1, MICAL2 or MICAL3) on actin, thereby promoting filament repolymerization. Plays a role in innate immunity by reducing oxidized actin, leading to actin repolymerization in macrophages.