|Institutional Source||Beutler Lab|
|Gene Name||SECIS binding protein 2|
|Synonyms||SBP2, 2210413N07Rik, 2810012K13Rik|
|Essential gene?||Probably non essential (E-score: 0.103)|
|Stock #||R8021 (G1)|
|Chromosomal Location||51651697-51684044 bp(+) (GRCm38)|
|Type of Mutation||makesense|
|DNA Base Change (assembly)||T to A at 51665628 bp (GRCm38)|
|Amino Acid Change||Stop codon to Arginine at position 415 (*415R)|
|Ref Sequence||ENSEMBL: ENSMUSP00000105671 (fasta)|
|Gene Model||predicted gene model for transcript(s): [ENSMUST00000040117] [ENSMUST00000110044]|
AA Change: *415R
AA Change: *415R
|Coding Region Coverage||
|Validation Efficiency||97% (74/76)|
FUNCTION: The incorporation of selenocysteine into a protein requires the concerted action of an mRNA element called a sec insertion sequence (SECIS), a selenocysteine-specific translation elongation factor and a SECIS binding protein. With these elements in place, a UGA codon can be decoded as selenocysteine. The gene described in this record encodes a nuclear protein that functions as a SECIS binding protein. Mutations in a similar gene in human have been associated with a reduction in activity of a specific thyroxine deiodinase, a selenocysteine-containing enzyme, and abnormal thyroid hormone metabolism. Alternate splicing results in multiple transcript variants. [provided by RefSeq, May 2015]
PHENOTYPE: Mice homozygous for a knock-out allele exhibit complete preweaning lethality while heterozygotes exhibit reduced serum selenium levels. [provided by MGI curators]
|Allele List at MGI|
|Other mutations in this stock||
|Other mutations in Secisbp2||
(F):5'- GAAAAGCGTGTTTATCCTGCTCC -3'
(R):5'- GCAGATCCATACAGTCATCATGG -3'
(F):5'- CTGCTCCAAAGGTATGCGTCAAG -3'
(R):5'- CATCATGGAAGCATGCCTTG -3'