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{{Infobox_gene}}
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'''Selenoprotein N''' is a [[protein]] that in humans is encoded by the ''SEPN1'' [[gene]].<ref name="pmid10608886">{{cite journal | vauthors = Lescure A, Gautheret D, Carbon P, Krol A | title = Novel selenoproteins identified in silico and in vivo by using a conserved RNA structural motif | journal = The Journal of Biological Chemistry | volume = 274 | issue = 53 | pages = 38147–54 | date = Dec 1999 | pmid = 10608886 | pmc =  | doi = 10.1074/jbc.274.53.38147 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: SEPN1 selenoprotein N, 1| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=57190| accessdate = }}</ref>
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| update_protein_box = yes
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<!-- The GNF_Protein_box is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
== Function ==
{{GNF_Protein_box
| image =
| image_source =
| PDB =
| Name = Selenoprotein N, 1
| HGNCid = 15999
| Symbol = SEPN1
| AltSymbols =; RSS; FLJ24021; MDRS1; RSMD1; SELN
| OMIM = 606210
| ECnumber = 
| Homologene = 10723
| MGIid = 
| Function = {{GNF_GO|id=GO:0003674 |text = molecular_function}} {{GNF_GO|id=GO:0005509 |text = calcium ion binding}} {{GNF_GO|id=GO:0008430 |text = selenium binding}}
| Component = {{GNF_GO|id=GO:0005576 |text = extracellular region}} {{GNF_GO|id=GO:0005783 |text = endoplasmic reticulum}}
| Process = {{GNF_GO|id=GO:0008150 |text = biological_process}}
| Orthologs = {{GNF_Ortholog_box
    | Hs_EntrezGene = 57190
    | Hs_Ensembl = 
    | Hs_RefseqProtein = NP_065184
    | Hs_RefseqmRNA = NM_020451
    | Hs_GenLoc_db = 
    | Hs_GenLoc_chr = 
    | Hs_GenLoc_start = 
    | Hs_GenLoc_end = 
    | Hs_Uniprot = 
    | Mm_EntrezGene = 
    | Mm_Ensembl = 
    | Mm_RefseqmRNA = 
    | Mm_RefseqProtein = 
    | Mm_GenLoc_db = 
    | Mm_GenLoc_chr = 
    | Mm_GenLoc_start = 
    | Mm_GenLoc_end = 
    | Mm_Uniprot = 
  }}
}}
'''Selenoprotein N, 1''', also known as '''SEPN1''', is a human [[gene]].<ref name="entrez">{{cite web | title = Entrez Gene: SEPN1 selenoprotein N, 1| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=57190| accessdate = }}</ref>


<!-- The PBB_Summary template is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
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.<ref name="entrez"/>
{{PBB_Summary
| section_title =
| summary_text = 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.<ref name="entrez">{{cite web | title = Entrez Gene: SEPN1 selenoprotein N, 1| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=57190| accessdate = }}</ref>
}}


==References==
==Model organisms==
{{reflist|2}}
{| class="wikitable sortable collapsible collapsed" border="1" cellpadding="2" style="float: right;" |
==Further reading==
|+ ''Sepn1'' knockout mouse phenotype
|-
! Characteristic!! Phenotype
 
|-
| [[Homozygote]] viability || bgcolor="#488ED3"|Normal
|-
| Fertility || bgcolor="#488ED3"|Normal
|-
| Body weight || bgcolor="#488ED3"|Normal
|-
| [[Open_Field_(animal_test)|Anxiety]] || bgcolor="#488ED3"|Normal
|-
| Neurological assessment || bgcolor="#488ED3"|Normal
|-
| Grip strength || bgcolor="#488ED3"|Normal
|-
| [[Hot_plate_test|Hot plate]] || bgcolor="#488ED3"|Normal
|-
| [[Dysmorphology]] || bgcolor="#488ED3"|Normal
|-
| [[Indirect calorimetry]] || bgcolor="#488ED3"|Normal
|-
| [[Glucose tolerance test]] || bgcolor="#488ED3"|Normal
|-
| [[Auditory brainstem response]] || bgcolor="#488ED3"|Normal
|-
| [[Dual-energy_X-ray_absorptiometry|DEXA]] || bgcolor="#488ED3"|Normal
|-
| [[Radiography]] || bgcolor="#C40000"|Abnormal<ref name="Radiography">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MAPJ/x-ray-imaging/ |title=Radiography data for Sepn1 |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| Body temperature || bgcolor="#488ED3"|Normal
|-
| Eye morphology || bgcolor="#488ED3"|Normal
|-
| [[Clinical chemistry]] || bgcolor="#488ED3"|Normal
|-
| [[Haematology]] || bgcolor="#488ED3"|Normal
|-
| [[Peripheral blood lymphocyte]]s || bgcolor="#488ED3"|Normal
|-
| [[Micronucleus test]] || bgcolor="#488ED3"|Normal
|-
| Heart weight || bgcolor="#488ED3"|Normal
|-
| Skin Histopathology || bgcolor="#488ED3"|Normal
|-
| Brain histopathology || bgcolor="#488ED3"|Normal
|-
| Eye Histopathology || bgcolor="#488ED3"|Normal
|-
| ''[[Salmonella]]'' infection || bgcolor="#488ED3"|Normal<ref name="''Salmonella'' infection">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MAPJ/salmonella-challenge/ |title=''Salmonella'' infection data for Sepn1 |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| ''[[Citrobacter]]'' infection || bgcolor="#488ED3"|Normal<ref name="''Citrobacter'' infection">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MAPJ/citrobacter-challenge/ |title=''Citrobacter'' infection data for Sepn1 |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| colspan=2; style="text-align: center;" | All tests and analysis from<ref name="mgp_reference">{{cite journal | doi = 10.1111/j.1755-3768.2010.4142.x | title = The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice | year = 2010 | author = Gerdin AK | journal = Acta Ophthalmologica | volume = 88 | pages =  925–7 }}</ref><ref>[http://www.sanger.ac.uk/mouseportal/ Mouse Resources Portal], Wellcome Trust Sanger Institute.</ref>
|}
[[Model organism]]s have been used in the study of SEPN1 function. A conditional [[knockout mouse]] line, called ''Sepn1<sup>tm1a(KOMP)Wtsi</sup>''<ref name="allele_ref">{{cite web |url=http://www.knockoutmouse.org/martsearch/search?query=Sepn1 |title=International Knockout Mouse Consortium}}</ref><ref name="mgi_allele_ref">{{cite web |url=http://www.informatics.jax.org/searchtool/Search.do?query=MGI:4363081 |title=Mouse Genome Informatics}}</ref> was generated as part of the [[International Knockout Mouse Consortium]] program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.<ref name="pmid21677750">{{cite journal | vauthors = Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A | title = A conditional knockout resource for the genome-wide study of mouse gene function | journal = Nature | volume = 474 | issue = 7351 | pages = 337–42 | date = Jun 2011 | pmid = 21677750 | pmc = 3572410 | doi = 10.1038/nature10163 }}</ref><ref name="mouse_library">{{cite journal | vauthors = Dolgin E | title = Mouse library set to be knockout | journal = Nature | volume = 474 | issue = 7351 | pages = 262–3 | date = Jun 2011 | pmid = 21677718 | doi = 10.1038/474262a }}</ref><ref name="mouse_for_all_reasons">{{cite journal | vauthors = Collins FS, Rossant J, Wurst W | title = A mouse for all reasons | journal = Cell | volume = 128 | issue = 1 | pages = 9–13 | date = Jan 2007 | pmid = 17218247 | doi = 10.1016/j.cell.2006.12.018 }}</ref>
 
Male and female animals underwent a standardized [[phenotypic screen]] to determine the effects of deletion.<ref name="mgp_reference" /><ref name="pmid21722353">{{cite journal | vauthors = van der Weyden L, White JK, Adams DJ, Logan DW | title = The mouse genetics toolkit: revealing function and mechanism | journal = Genome Biology | volume = 12 | issue = 6 | pages = 224 | year = 2011 | pmid = 21722353 | pmc = 3218837 | doi = 10.1186/gb-2011-12-6-224 }} </ref> Twenty five tests were carried out on homozygous [[mutant]] mice and one significant abnormality was observed: than animals displayed [[vertebral fusion]].<ref name="mgp_reference" />
 
== References ==
{{reflist}}
 
== Further reading ==
{{refbegin | 2}}
{{refbegin | 2}}
{{PBB_Further_reading
* {{cite journal | vauthors = Aho H, Schwemmer M, Tessman D, Murphy D, Mattei G, Engel W, Adham IM | title = Isolation, expression, and chromosomal localization of the human mitochondrial capsule selenoprotein gene (MCSP) | journal = Genomics | volume = 32 | issue = 2 | pages = 184–90 | date = Mar 1996 | pmid = 8833144 | doi = 10.1006/geno.1996.0104 }}
| citations =
* {{cite journal | vauthors = Moghadaszadeh B, Desguerre I, Topaloglu H, Muntoni F, Pavek S, Sewry C, Mayer M, Fardeau M, Tomé FM, Guicheney P | title = Identification of a new locus for a peculiar form of congenital muscular dystrophy with early rigidity of the spine, on chromosome 1p35-36 | journal = American Journal of Human Genetics | volume = 62 | issue = 6 | pages = 1439–45 | date = Jun 1998 | pmid = 9585610 | pmc = 1377161 | doi = 10.1086/301882 }}
*{{cite journal | author=Aho H, Schwemmer M, Tessman D, ''et al.'' |title=Isolation, expression, and chromosomal localization of the human mitochondrial capsule selenoprotein gene (MCSP). |journal=Genomics |volume=32 |issue= 2 |pages= 184-90 |year= 1997 |pmid= 8833144 |doi= }}
* {{cite journal | vauthors = Moghadaszadeh B, Petit N, Jaillard C, Brockington M, Quijano Roy S, Merlini L, Romero N, Estournet B, Desguerre I, Chaigne D, Muntoni F, Topaloglu H, Guicheney P | title = Mutations in SEPN1 cause congenital muscular dystrophy with spinal rigidity and restrictive respiratory syndrome | journal = Nature Genetics | volume = 29 | issue = 1 | pages = 17–8 | date = Sep 2001 | pmid = 11528383 | doi = 10.1038/ng713 }}
*{{cite journal | author=Moghadaszadeh B, Desguerre I, Topaloglu H, ''et al.'' |title=Identification of a new locus for a peculiar form of congenital muscular dystrophy with early rigidity of the spine, on chromosome 1p35-36. |journal=Am. J. Hum. Genet. |volume=62 |issue= 6 |pages= 1439-45 |year= 1998 |pmid= 9585610 |doi= }}
* {{cite journal | vauthors = Ferreiro A, Quijano-Roy S, Pichereau C, Moghadaszadeh B, Goemans N, Bönnemann C, Jungbluth H, Straub V, Villanova M, Leroy JP, Romero NB, Martin JJ, Muntoni F, Voit T, Estournet B, Richard P, Fardeau M, Guicheney P | title = Mutations of the selenoprotein N gene, which is implicated in rigid spine muscular dystrophy, cause the classical phenotype of multiminicore disease: reassessing the nosology of early-onset myopathies | journal = American Journal of Human Genetics | volume = 71 | issue = 4 | pages = 739–49 | date = Oct 2002 | pmid = 12192640 | pmc = 378532 | doi = 10.1086/342719 }}
*{{cite journal  | author=Lescure A, Gautheret D, Carbon P, Krol A |title=Novel selenoproteins identified in silico and in vivo by using a conserved RNA structural motif. |journal=J. Biol. Chem. |volume=274 |issue= 53 |pages= 38147-54 |year= 2000 |pmid= 10608886 |doi=  }}
* {{cite journal | vauthors = Petit N, Lescure A, Rederstorff M, Krol A, Moghadaszadeh B, Wewer UM, Guicheney P | title = Selenoprotein N: an endoplasmic reticulum glycoprotein with an early developmental expression pattern | journal = Human Molecular Genetics | volume = 12 | issue = 9 | pages = 1045–53 | date = May 2003 | pmid = 12700173 | doi = 10.1093/hmg/ddg115 }}
*{{cite journal | author=Moghadaszadeh B, Petit N, Jaillard C, ''et al.'' |title=Mutations in SEPN1 cause congenital muscular dystrophy with spinal rigidity and restrictive respiratory syndrome. |journal=Nat. Genet. |volume=29 |issue= 1 |pages= 17-8 |year= 2001 |pmid= 11528383 |doi= 10.1038/ng713 }}
* {{cite journal | vauthors = Ferreiro A, Ceuterick-de Groote C, Marks JJ, Goemans N, Schreiber G, Hanefeld F, Fardeau M, Martin JJ, Goebel HH, Richard P, Guicheney P, Bönnemann CG | title = Desmin-related myopathy with Mallory body-like inclusions is caused by mutations of the selenoprotein N gene | journal = Annals of Neurology | volume = 55 | issue = 5 | pages = 676–86 | date = May 2004 | pmid = 15122708 | doi = 10.1002/ana.20077 }}
*{{cite journal | author=Ferreiro A, Quijano-Roy S, Pichereau C, ''et al.'' |title=Mutations of the selenoprotein N gene, which is implicated in rigid spine muscular dystrophy, cause the classical phenotype of multiminicore disease: reassessing the nosology of early-onset myopathies. |journal=Am. J. Hum. Genet. |volume=71 |issue= 4 |pages= 739-49 |year= 2002 |pmid= 12192640 |doi=  }}
* {{cite journal | vauthors = Venance SL, Koopman WJ, Miskie BA, Hegele RA, Hahn AF | title = Rigid spine muscular dystrophy due to SEPN1 mutation presenting as cor pulmonale | journal = Neurology | volume = 64 | issue = 2 | pages = 395–6 | date = Jan 2005 | pmid = 15668457 | doi = 10.1212/01.WNL.0000149755.85666.DB }}
*{{cite journal  | author=Strausberg RL, Feingold EA, Grouse LH, ''et al.'' |title=Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue= 26 |pages= 16899-903 |year= 2003 |pmid= 12477932 |doi= 10.1073/pnas.242603899 }}
* {{cite journal | vauthors = Tajsharghi H, Darin N, Tulinius M, Oldfors A | title = Early onset myopathy with a novel mutation in the Selenoprotein N gene (SEPN1) | journal = Neuromuscular Disorders | volume = 15 | issue = 4 | pages = 299–302 | date = Apr 2005 | pmid = 15792869 | doi = 10.1016/j.nmd.2004.11.004 }}
*{{cite journal | author=Petit N, Lescure A, Rederstorff M, ''et al.'' |title=Selenoprotein N: an endoplasmic reticulum glycoprotein with an early developmental expression pattern. |journal=Hum. Mol. Genet. |volume=12 |issue= 9 |pages= 1045-53 |year= 2003 |pmid= 12700173 |doi= }}
* {{cite journal | vauthors = D'Amico A, Haliloglu G, Richard P, Talim B, Maugenre S, Ferreiro A, Guicheney P, Menditto I, Benedetti S, Bertini E, Bonne G, Topaloglu H | title = Two patients with 'Dropped head syndrome' due to mutations in LMNA or SEPN1 genes | journal = Neuromuscular Disorders | volume = 15 | issue = 8 | pages = 521–4 | date = Aug 2005 | pmid = 15961312 | doi = 10.1016/j.nmd.2005.03.006 }}
*{{cite journal | author=Ferreiro A, Ceuterick-de Groote C, Marks JJ, ''et al.'' |title=Desmin-related myopathy with Mallory body-like inclusions is caused by mutations of the selenoprotein N gene. |journal=Ann. Neurol. |volume=55 |issue= 5 |pages= 676-86 |year= 2004 |pmid= 15122708 |doi= 10.1002/ana.20077 }}
* {{cite journal | vauthors = Clarke NF, Kidson W, Quijano-Roy S, Estournet B, Ferreiro A, Guicheney P, Manson JI, Kornberg AJ, Shield LK, North KN | title = SEPN1: associated with congenital fiber-type disproportion and insulin resistance | journal = Annals of Neurology | volume = 59 | issue = 3 | pages = 546–52 | date = Mar 2006 | pmid = 16365872 | doi = 10.1002/ana.20761 }}
*{{cite journal | author=Gerhard DS, Wagner L, Feingold EA, ''et al.'' |title=The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121-7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504 }}
* {{cite journal | vauthors = Allamand V, Richard P, Lescure A, Ledeuil C, Desjardin D, Petit N, Gartioux C, Ferreiro A, Krol A, Pellegrini N, Urtizberea JA, Guicheney P | title = A single homozygous point mutation in a 3'untranslated region motif of selenoprotein N mRNA causes SEPN1-related myopathy | journal = EMBO Reports | volume = 7 | issue = 4 | pages = 450–4 | date = Apr 2006 | pmid = 16498447 | pmc = 1456920 | doi = 10.1038/sj.embor.7400648 }}
*{{cite journal  | author=Venance SL, Koopman WJ, Miskie BA, ''et al.'' |title=Rigid spine muscular dystrophy due to SEPN1 mutation presenting as cor pulmonale. |journal=Neurology |volume=64 |issue= 2 |pages= 395-6 |year= 2005 |pmid= 15668457 |doi= 10.1212/01.WNL.0000149755.85666.DB }}
* {{cite journal | vauthors = Okamoto Y, Takashima H, Higuchi I, Matsuyama W, Suehara M, Nishihira Y, Hashiguchi A, Hirano R, Ng AR, Nakagawa M, Izumo S, Osame M, Arimura K | title = Molecular mechanism of rigid spine with muscular dystrophy type 1 caused by novel mutations of selenoprotein N gene | journal = Neurogenetics | volume = 7 | issue = 3 | pages = 175–83 | date = Jul 2006 | pmid = 16779558 | doi = 10.1007/s10048-006-0046-0 }}
*{{cite journal | author=Tajsharghi H, Darin N, Tulinius M, Oldfors A |title=Early onset myopathy with a novel mutation in the Selenoprotein N gene (SEPN1). |journal=Neuromuscul. Disord. |volume=15 |issue= 4 |pages= 299-302 |year= 2005 |pmid= 15792869 |doi= 10.1016/j.nmd.2004.11.004 }}
*{{cite journal | author=D'Amico A, Haliloglu G, Richard P, ''et al.'' |title=Two patients with 'Dropped head syndrome' due to mutations in LMNA or SEPN1 genes. |journal=Neuromuscul. Disord. |volume=15 |issue= 8 |pages= 521-4 |year= 2005 |pmid= 15961312 |doi= 10.1016/j.nmd.2005.03.006 }}
*{{cite journal | author=Clarke NF, Kidson W, Quijano-Roy S, ''et al.'' |title=SEPN1: associated with congenital fiber-type disproportion and insulin resistance. |journal=Ann. Neurol. |volume=59 |issue= 3 |pages= 546-52 |year= 2006 |pmid= 16365872 |doi= 10.1002/ana.20761 }}
*{{cite journal | author=Allamand V, Richard P, Lescure A, ''et al.'' |title=A single homozygous point mutation in a 3'untranslated region motif of selenoprotein N mRNA causes SEPN1-related myopathy. |journal=EMBO Rep. |volume=7 |issue= 4 |pages= 450-4 |year= 2006 |pmid= 16498447 |doi= 10.1038/sj.embor.7400648 }}
*{{cite journal | author=Gregory SG, Barlow KF, McLay KE, ''et al.'' |title=The DNA sequence and biological annotation of human chromosome 1. |journal=Nature |volume=441 |issue= 7091 |pages= 315-21 |year= 2006 |pmid= 16710414 |doi= 10.1038/nature04727 }}
*{{cite journal  | author=Okamoto Y, Takashima H, Higuchi I, ''et al.'' |title=Molecular mechanism of rigid spine with muscular dystrophy type 1 caused by novel mutations of selenoprotein N gene. |journal=Neurogenetics |volume=7 |issue= 3 |pages= 175-83 |year= 2007 |pmid= 16779558 |doi= 10.1007/s10048-006-0046-0 }}
}}
{{refend}}
{{refend}}


{{protein-stub}}
== External links ==
{{WikiDoc Sources}}
* [https://www.ncbi.nlm.nih.gov/books/NBK1291/  GeneReviews/NCBI/NIH/UW entry on Congenital Muscular Dystrophy Overview]
*[https://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=gene&part=mmd  GeneReviews/NCBI/NIH/UW entry on Multiminicore Disease]
 
[[Category:Selenoproteins]]
[[Category:Genes mutated in mice]]

Latest revision as of 06:07, 11 September 2017

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez

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Ensembl

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UniProt

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RefSeq (mRNA)

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RefSeq (protein)

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Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

Selenoprotein N is a protein that in humans is encoded by the SEPN1 gene.[1][2]

Function

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.[2]

Model organisms

Model organisms have been used in the study of SEPN1 function. A conditional knockout mouse line, called Sepn1tm1a(KOMP)Wtsi[8][9] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.[10][11][12]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[6][13] Twenty five tests were carried out on homozygous mutant mice and one significant abnormality was observed: than animals displayed vertebral fusion.[6]

References

  1. ↑ Lescure A, Gautheret D, Carbon P, Krol A (Dec 1999). "Novel selenoproteins identified in silico and in vivo by using a conserved RNA structural motif". The Journal of Biological Chemistry. 274 (53): 38147–54. doi:10.1074/jbc.274.53.38147. PMID 10608886.
  2. ↑ 2.0 2.1 "Entrez Gene: SEPN1 selenoprotein N, 1".
  3. ↑ "Radiography data for Sepn1". Wellcome Trust Sanger Institute.
  4. ↑ "Salmonella infection data for Sepn1". Wellcome Trust Sanger Institute.
  5. ↑ "Citrobacter infection data for Sepn1". Wellcome Trust Sanger Institute.
  6. ↑ 6.0 6.1 6.2 Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica. 88: 925–7. doi:10.1111/j.1755-3768.2010.4142.x.
  7. ↑ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  8. ↑ "International Knockout Mouse Consortium".
  9. ↑ "Mouse Genome Informatics".
  10. ↑ Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (Jun 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
  11. ↑ Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  12. ↑ Collins FS, Rossant J, Wurst W (Jan 2007). "A mouse for all reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247.
  13. ↑ van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biology. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.

Further reading

External links

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