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MAGEL2 cDNA ORF clone, Homo sapiens(Human)

Gene Symbol MAGEL2
Entrez Gene ID 54551
Full Name MAGE family member L2
Synonyms NDNL1,PWLS,SHFYNG,nM15
General protein information
Preferred Names

MAGE family member L2

Names

MAGE-like protein 2
melanoma antigen family L2
necdin-like protein 1
protein nM15

Gene Type protein-coding
Organism Homo sapiens(Human)
Genome

15

15q11.2

Summary Prader-Willi syndrome (PWS) is caused by the loss of expression of imprinted genes in chromosome 15q11-q13 region. Affected individuals exhibit neonatal hypotonia, developmental delay, and childhood-onset obesity. Necdin (NDN), a gene involved in the terminal differentiation of neurons, localizes to this region of the genome and has been implicated as one of the genes responsible for the etiology of PWS. This gene is structurally similar to NDN, is also localized to the PWS chromosomal region, and is paternally imprinted, suggesting a possible role for it in PWS. [provided by RefSeq, Oct 2010].
Disorder MIM:

605283


mRNA and Protein(s)

mRNA Protein Name
NM_019066.4 NP_061939.3 MAGE-like protein 2



Canis lupus familiaris (dog) LOC100684492 XP_003434387.1
Rattus norvegicus (Norway rat) Magel2 XP_001054803.2
Homo sapiens (human) MAGEL2 NP_061939.3
Mus musculus (house mouse) Magel2 NP_038807.4
Macaca mulatta (rhesus monkey) MAGEL2 XP_001114423.2
Bos taurus (cattle) MAGEL2 XP_002696517.1


Related articles in PubMed

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.
Perry JR, Day F, Elks CE, Sulem P, Thompson DJ, Ferreira T, He C, Chasman DI, Esko T, Thorleifsson G, Albrecht E, Ang WQ, Corre T, Cousminer DL, Feenstra B, Franceschini N, Ganna A, Johnson AD, Kjellqvist S, Lunetta KL, McMahon G, Nolte IM, Paternoster L, Porcu E, Smith AV, Stolk L, Teumer A, Tšernikova N, Tikkanen E, Ulivi S, Wagner EK, Amin N, Bierut LJ, Byrne EM, Hottenga JJ, Koller DL, Mangino M, Pers TH, Yerges-Armstrong LM, Zhao JH, Andrulis IL, Anton-Culver H, Atsma F, Bandinelli S, Beckmann MW, Benitez J, Blomqvist C, Bojesen SE, Bolla MK, Bonanni B, Brauch H, Brenner H, Buring JE, Chang-Claude J, Chanock S, Chen J, Chenevix-Trench G, Collée JM, Couch FJ, Couper D, Coveillo AD, Cox A, Czene K, D'adamo AP, Smith GD, De Vivo I, Demerath EW, Dennis J, Devilee P, Dieffenbach AK, Dunning AM, Eiriksdottir G, Eriksson JG, Fasching PA, Ferrucci L, Flesch-Janys D, Flyger H, Foroud T, Franke L, Garcia ME, García-Closas M, Geller F, de Geus EE, Giles GG, Gudbjartsson DF, Gudnason V, Guénel P, Guo S, Hall P, Hamann U, Haring R, Hartman CA, Heath AC, Hofman A, Hooning MJ, Hopper JL, Hu FB, Hunter DJ, Karasik D, Kiel DP, Knight JA, Kosma VM, Kutalik Z, Lai S, Lambrechts D, Lindblom A, Mägi R, Magnusson PK, Mannermaa A, Martin NG, Masson G, McArdle PF, McArdle WL, Melbye M, Michailidou K, Mihailov E, Milani L, Milne RL, Nevanlinna H, Neven P, Nohr EA, Oldehinkel AJ, Oostra BA, Palotie A, Peacock M, Pedersen NL, Peterlongo P, Peto J, Pharoah PD, Postma DS, Pouta A, Pylkäs K, Radice P, Ring S, Rivadeneira F, Robino A, Rose LM, Rudolph A, Salomaa V, Sanna S, Schlessinger D, Schmidt MK, Southey MC, Sovio U, Stampfer MJ, Stöckl D, Storniolo AM, Timpson NJ, Tyrer J, Visser JA, Vollenweider P, Völzke H, Waeber G, Waldenberger M, Wallaschofski H, Wang Q, Willemsen G, Winqvist R, Wolffenbuttel BH, Wright MJ, , , , , , , Boomsma DI, Econs MJ, Khaw KT, Loos RJ, McCarthy MI, Montgomery GW, Rice JP, Streeten EA, Thorsteinsdottir U, van Duijn CM, Alizadeh BZ, Bergmann S, Boerwinkle E, Boyd HA, Crisponi L, Gasparini P, Gieger C, Harris TB, Ingelsson E, Järvelin MR, Kraft P, Lawlor D, Metspalu A, Pennell CE, Ridker PM, Snieder H, Sørensen TI, Spector TD, Strachan DP, Uitterlinden AG, Wareham NJ, Widen E, Zygmunt M, Murray A, Easton DF, Stefansson K, Murabito JM, Ong KK
Nature514(7520)92-97(2014 Oct)

Truncating mutations of MAGEL2 cause Prader-Willi phenotypes and autism.
Schaaf CP, Gonzalez-Garay ML, Xia F, Potocki L, Gripp KW, Zhang B, Peters BA, McElwain MA, Drmanac R, Beaudet AL, Caskey CT, Yang Y
Nature genetics45(11)1405-8(2013 Nov)

Regulation of WASH-dependent actin polymerization and protein trafficking by ubiquitination.
Hao YH, Doyle JM, Ramanathan S, Gomez TS, Jia D, Xu M, Chen ZJ, Billadeau DD, Rosen MK, Potts PR
Cell152(5)1051-64(2013 Feb)

Lack of association between MAGEL2 and schizophrenia and mood disorders in the Japanese population.
Fukuo Y, Kishi T, Okochi T, Kitajima T, Tsunoka T, Okumukura T, Kinoshita Y, Kawashima K, Yamanouchi Y, Umene-Nakano W, Naitoh H, Inada T, Yoshimura R, Nakamura J, Ozaki N, Iwata N
Neuromolecular medicine12(3)285-91(2010 Sep)

Expression and imprinting of MAGEL2 suggest a role in Prader-willi syndrome and the homologous murine imprinting phenotype.
Lee S, Kozlov S, Hernandez L, Chamberlain SJ, Brannan CI, Stewart CL, Wevrick R
Human molecular genetics9(12)1813-9(2000 Jul)

GeneRIFs: Gene References Into Functions What's a GeneRIF?

Truncating Mutations of MAGEL2, a Gene within the Prader-Willi Locus, Are Responsible for Severe Arthrogryposis.
Title: Truncating Mutations of MAGEL2, a Gene within the Prader-Willi Locus, Are Responsible for Severe Arthrogryposis.

A similar progressive loss of leptin sensitivity caused by loss of MAGEL2 in children with Prader-Willi syndrome could explain the delayed onset of increased appetite and weight gain in this complex disorder.
Title: Progressive postnatal decline in leptin sensitivity of arcuate hypothalamic neurons in the Magel2-null mouse model of Prader-Willi syndrome.

MAGEL2 is a new gene causing complex autism spectrum disorder and MAGEL2 loss of function can contribute to several aspects of the Prader-Willi syndrome phenotype.
Title: Truncating mutations of MAGEL2 cause Prader-Willi phenotypes and autism.

These findings provide a cellular and molecular function for MAGE-L2-TRIM27 in retrograde transport, including an unappreciated role of K63-linked ubiquitination and identification of an activating signal of the WASH regulatory complex.
Title: Regulation of WASH-dependent actin polymerization and protein trafficking by ubiquitination.

Results suggest that MAGEL2 may not play a role in the pathophysiology of schizophrenia and mood disorders in the Japanese population.
Title: Lack of association between MAGEL2 and schizophrenia and mood disorders in the Japanese population.

The following MAGEL2 gene cDNA ORF clone sequences were retrieved from the NCBI Reference Sequence Database (RefSeq). These sequences represent the protein coding region of the MAGEL2 cDNA ORF which is encoded by the open reading frame (ORF) sequence. ORF sequences can be delivered in our standard vector, pcDNA3.1+/C-(K)DYK or the vector of your choice as an expression/transfection-ready ORF clone. Not the clone you want? Click here to find your clone.

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***CloneID RefSeq Accession Definition **Vector *Turnaround time Price (USD) Select
OHu20638 NM_019066.4
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Homo sapiens MAGE family member L2 (MAGEL2), mRNA. pcDNA3.1+/C-(K)DYK or customized vector TBD $881.30
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** GenScript guarantees 100% sequence accuracy of all synthetic DNA constructs we deliver, but we do not guarantee protein expression in your experimental system. Protein expression is influenced by many factors that may vary between experiments or laboratories. In addition, please pay attention to the signal peptide, propeptide and transit peptide in target ORF, which may affect the choice of vector (N/C terminal tag vector).

***One clone ID might be correlated to multiple accession numbers, which share the same CDS sequence.


CloneID OHu20638
Clone ID Related Accession (Same CDS sequence) NM_019066.4
Accession Version NM_019066.4 Latest version! Documents for ORF clone product in dufault vector
Sequence Information ORF Nucleotide Sequence (Length: 3750bp)
Protein sequence
SNP
Vector pcDNA3.1+/C-(K)DYK or customized vector User Manual
Clone information Clone Map MSDS
Tag on pcDNA3.1+/C-(K)DYK C terminal DYKDDDDK tags
ORF Insert Method CloneEZ® Seamless cloning technology
Insert Structure linear
Update Date 2015-11-15
Organism Homo sapiens(Human)
Product MAGE-like protein 2
Comment REVIEWED REFSEQ: This record has been curated by NCBI staff. The reference sequence was derived from AC124309.7. This sequence is a reference standard in the RefSeqGene project. On Sep 12, 2009 this sequence version replaced NM_019066.3. Sequence Note: The RefSeq transcript and protein were derived from genomic sequence to make the sequence consistent with the reference genome assembly. The genomic coordinates used for the transcript record were based on alignments. ##RefSeq-Attributes-START## imprinted gene :: PMID: 10556298, 10915770 ##RefSeq-Attributes-END## COMPLETENESS: complete on the 3' end.

1
61
121
181
241
301
361
421
481
541
601
661
721
781
841
901
961
1021
1081
1141
1201
1261
1321
1381
1441
1501
1561
1621
1681
1741
1801
1861
1921
1981
2041
2101
2161
2221
2281
2341
2401
2461
2521
2581
2641
2701
2761
2821
2881
2941
3001
3061
3121
3181
3241
3301
3361
3421
3481
3541
3601
3661
3721
ATGTCGCAGC TAAGTAAGAA TCTGGGTGAC TCGAGTCCTC CGGCGGAGGC CCCGAAGCCG 
CCTGTCTATA GCCGCCCTAC GGTTCTGATG CGGGCCCCGC CCGCTTCCTC CCGGGCTCCG
CCAGTCCCTT GGGATCCACC TCCAATTGAC TTGCAGGCTT CATTGGCCGC TTGGCAGGCA
CCTCAGCCTG CCTGGGAGGC CCCACAGGGC CAGCTGCCCG CCCCGGTGGT TCCGATGACC
CAGCCTCCTG CCCTAGGGGG CCCGATAGTC CCGGCTCCCC CGCTGGGGGG CCCGATGGGT
AAGCCTCCGA CTCCCGGGGT CCTGATGGTG CATCCTCCAC CTCCGGGAGC CCCGATGGCC
CAGCCTCCGA CCCCGGGAGT CCTGATGGTG CATCCTTCAG CTCCCGGAGC TCCCATGGCC
CATCCTCCTC CTCCGGGGAC CCCAATGTCC CACCCTCCCC CTCCGGGGAC CCCAATGGCC
CATCCTCCTC CTCCGGGGAC CCCGATGGCC CATCCTCCTC CTCCGGGGAC CCCGATGGTG
CATCCTCCTC CTCCGGGGAC CCCGATGGCT CATCCTCCCC CTCCGGGGAC ACCGATGGCT
CATCCTCCCC CTCCGGGGAC ACCGATGGCT CATCCTCCAC CTCCGGGGAC ACCGATGGCT
CATCCTCCCC CTCCGGGTAC ACCGATGGCC CAGCCTCCAG CTCCGGGAGT CCTGATGGCC
CAGCCTCTGA CTCCGGGAGT CCTGATGGTC CAGCCTGCTG CTCCGGGAGC ACCGATGGTC
CAGCCGCCTC CAGCAGCCAT GATGACCCAG CCTCAGCCTT CAGGAGCACC GATGGCCAAG
CCTCCAGGTC CAGGAGTCCT GATGATTCAT CCTCCAGGTG CGAGAGCTCC GATGACCCAG
CCTCCAGCTT CAGGAGCACC GATGGCACAG CCGGCGGCCC CACCTGCACA GCCGATGGCC
CCACCTGCAC AGCCGATGGC TTCTTGGGCC CCGCAGGCTC AGCCTCTGAT CCTGCAAATC
CAGTCTCAAG TTATAAGGGC TCCTCCGCAG GTTCCCCAGG GCCCGCAGGC ACCCCCAGCG
CAGCTAGCCA CACCCCCGGG CTGGCAGGCG ACCTCGCCAG GATGGCAGGC CACGCAGCAA
GGCTGGCAGG CCACTCCCCT GACTTGGCAG ACCACGCAGG TCACCTGGCA GGCACCAGCC
GTTACCTGGC AGGTGCCGCC GCCCATGCGC CAGGGGCCCC CGCCCATCCG CCCTGGCCCA
CCACCCATCC GCCCTGGCCC ACCACCGGTG CGACAGGCCC CACCGCTGAT CCGCCAGGCC
CCACCGGTGA TCCGCCAGGC CCCACCCGTG ATCCGCCAGG CCCCACCCGT GATCCGCCAG
GCCCCCGCTG TGATCCGCCA GGCCCCACCT GTGATCCGCC AGGCCCCACC TGTGATCCGC
CAGGCTCCAC CTGTGATCCG CCAGGCCCCG CCGCTGATCC GCCAGGCGCC GCCGCCCATC
CGACCTGCCC CACAGGTCCT GGCCACCCAG CCACCGCTCT GGCAGGCCCT GCCACCCCCA
CCTCCACTGC GGCAGGCCCC GCAGGCTAGG CTGCCGGCCC CGCAGGTGCA GGCGGCGCCG
CAGGTGCCTA CGGCCCCACC TGCTACGCAG GTACCCGCGG CGCCGCCCGC TGGCCCGCAG
GTGCCCCAGC CTGTGCTGCC GGCCCCGCTG TCTGCCCCAC TGTCTGCCCC GCAGGCTGTG
CACTGCCCTT CCATCATCTG GCAGGCCCCC AAAGGTCAGC CCCCGGTGCC ACACGAGATT
CCAACGTCAA TGGAATTCCA GGAGGTGCAG CAGACACAGG CGCTGGCCTG GCAGGCCCAG
AAGGCCCCCA CTCACATCTG GCAGCCCCTG CCTGCCCAGG AGGCCCAGAG GCAGGCTCCC
CCCTTGGTCC AGCTGGAGCA GCCCTTTCAG GGAGCCCCGC CCTCCCAAAA AGCCGTGCAA
ATCCAGCTAC CCCCCCAGCA GGCCCAGGCA TCGGGTCCGC AAGCGGAGGT GCCCACACTG
CCGCTCCAGC CTTCCTGGCA GGCACCGCCT GCAGTCTTGC AGGCCCAGCC CGGACCCCCG
GTAGCAGCGG CAAATTTTCC CCTGGGCTCC GCTAAATCAT TGATGACTCC ATCAGGAGAA
TGCAGGGCCT CTTCTATAGA CCGCAGGGGC TCCTCTAAAG AGCGCAGGAC CTCCTCGAAG
GAGCGCAGGG CCCCTTCAAA AGACCGCATG ATCTTTGCTG CCACCTTCTG TGCTCCCAAG
GCAGTGTCAG CTGCGCGAGC ACACCTGCCA GCTGCCTGGA AAAACCTGCC TGCCACACCG
GAGACCTTTG CTCCCTCCTC AAGTGTCTTC CCAGCTACCT CCCAGTTTCA GCCTGCCTCT
CTGAATGCCT TTAAAGGCCC CTCTGCTGCC TCAGAGACCC CAAAGTCACT GCCATATGCT
CTGCAGGATC CCTTTGCCTG TGTAGAGGCC CTGCCTGCAG TTCCATGGGT CCCACAGCCC
AATATGAATG CCTCAAAGGC ATCGCAGGCA GTGCCCACCT TCCTGATGGC TACAGCAGCT
GCCCCCCAGG CAACTGCCAC CACTCAAGAG GCCTCCAAGA CCTCCGTCGA GCCGCCACGC
CGCTCCGGCA AGGCCACCCG GAAGAAGAAG CATCTGGAAG CCCAAGAGGA CAGCCGTGGC
CACACGCTAG CCTTTCATGA CTGGCAGGGC CCAAGGCCCT GGGAGAATCT AAATCTGAGT
GACTGGGAGG TCCAAAGCCC TATCCAGGTC TCGGGTGACT GGGAGCACCC AAACACCCCC
CGTGGCCTGA GTGGTTGGGA GGGCCCTAGC ACCTCCAGGA TCCTGAGTGG CTGGGAAGGG
CCCAGCGCAT CCTGGGCCCT GAGTGCCTGG GAGGGCCCGA GCACCTCCAG GGCCCTGGGT
CTCTCTGAAA GCCCAGGGAG CTCTCTGCCC GTAGTTGTGT CTGAGGTCGC AAGTGTCTCT
CCGGGATCCA GTGCCACCCA GGATAATTCC AAGGTGGAGG CACAGCCCTT GTCTCCCTTG
GATGAGAGGG CAAATGCGTT GGTGCAGTTC CTCTTAGTCA AGGACCAAGC CAAGGTGCCT
GTCCAGCGCT CGGAGATGGT GAAAGTCATC CTCCGAGAGT ATAAAGATGA GTGCTTAGAT
ATCATCAACC GTGCCAACAA TAAGCTGGAG TGTGCCTTTG GTTATCAATT GAAAGAAATT
GATACCAAAA ACCACGCCTA TATTATCATC AACAAGCTGG GCTACCATAC AGGGAATTTG
GTGGCATCCT ATTTAGACAG GCCCAAGTTT GGCCTTCTGA TGGTGGTCTT GAGCCTCATC
TTTATGAAAG GCAACTGTGT CAGGGAGGAT CTGATCTTTA ATTTTCTGTT CAAGTTAGGG
TTGGATGTCC GGGAGACAAA CGGTCTCTTT GGAAATACTA AGAAGCTCAT CACCGAAGTG
TTTGTCAGGC AGAAGTACCT AGAGTACAGG CGAATCCCTT ACACTGAGCC CGCAGAGTAT
GAGTTCCTCT GGGGCCCTCG AGCATTCCTG GAAACCAGCA AGATGCTTGT CCTGAGGTTT
TTGGCCAAGC TCCATAAGAA AGATCCACAG AGCTGGCCAT TCCATTACCT TGAAGCGCTC
GCAGAGTGTG AGTGGGAAGA CACAGATGAG GATGAACCTG ACACCGGTGA CAGTGCCCAC
GGCCCCACCA GCAGGCCCCC TCCCCGCTAA

The stop codons will be deleted if pcDNA3.1+/C-(K)DYK vector is selected.

RefSeq NP_061939.3
CDS105..3854
Misc Feature(1)27..29
Misc Feature(2)348..809
Misc Feature(3)<507..722
Misc Feature(4)3183..3689
Exon (1)1..4298
Translation

Target ORF information:

RefSeq Version NM_019066.4
Organism Homo sapiens(Human)
Definition Homo sapiens MAGE family member L2 (MAGEL2), mRNA.

Target ORF information:

Epitope DYKDDDDK
Bacterial selection AMPR
Mammalian selection NeoR
Vector pcDNA3.1+/C-(K)DYK
NM_019066.4

ORF Insert Sequence:

1
61
121
181
241
301
361
421
481
541
601
661
721
781
841
901
961
1021
1081
1141
1201
1261
1321
1381
1441
1501
1561
1621
1681
1741
1801
1861
1921
1981
2041
2101
2161
2221
2281
2341
2401
2461
2521
2581
2641
2701
2761
2821
2881
2941
3001
3061
3121
3181
3241
3301
3361
3421
3481
3541
3601
3661
3721
ATGTCGCAGC TAAGTAAGAA TCTGGGTGAC TCGAGTCCTC CGGCGGAGGC CCCGAAGCCG 
CCTGTCTATA GCCGCCCTAC GGTTCTGATG CGGGCCCCGC CCGCTTCCTC CCGGGCTCCG
CCAGTCCCTT GGGATCCACC TCCAATTGAC TTGCAGGCTT CATTGGCCGC TTGGCAGGCA
CCTCAGCCTG CCTGGGAGGC CCCACAGGGC CAGCTGCCCG CCCCGGTGGT TCCGATGACC
CAGCCTCCTG CCCTAGGGGG CCCGATAGTC CCGGCTCCCC CGCTGGGGGG CCCGATGGGT
AAGCCTCCGA CTCCCGGGGT CCTGATGGTG CATCCTCCAC CTCCGGGAGC CCCGATGGCC
CAGCCTCCGA CCCCGGGAGT CCTGATGGTG CATCCTTCAG CTCCCGGAGC TCCCATGGCC
CATCCTCCTC CTCCGGGGAC CCCAATGTCC CACCCTCCCC CTCCGGGGAC CCCAATGGCC
CATCCTCCTC CTCCGGGGAC CCCGATGGCC CATCCTCCTC CTCCGGGGAC CCCGATGGTG
CATCCTCCTC CTCCGGGGAC CCCGATGGCT CATCCTCCCC CTCCGGGGAC ACCGATGGCT
CATCCTCCCC CTCCGGGGAC ACCGATGGCT CATCCTCCAC CTCCGGGGAC ACCGATGGCT
CATCCTCCCC CTCCGGGTAC ACCGATGGCC CAGCCTCCAG CTCCGGGAGT CCTGATGGCC
CAGCCTCTGA CTCCGGGAGT CCTGATGGTC CAGCCTGCTG CTCCGGGAGC ACCGATGGTC
CAGCCGCCTC CAGCAGCCAT GATGACCCAG CCTCAGCCTT CAGGAGCACC GATGGCCAAG
CCTCCAGGTC CAGGAGTCCT GATGATTCAT CCTCCAGGTG CGAGAGCTCC GATGACCCAG
CCTCCAGCTT CAGGAGCACC GATGGCACAG CCGGCGGCCC CACCTGCACA GCCGATGGCC
CCACCTGCAC AGCCGATGGC TTCTTGGGCC CCGCAGGCTC AGCCTCTGAT CCTGCAAATC
CAGTCTCAAG TTATAAGGGC TCCTCCGCAG GTTCCCCAGG GCCCGCAGGC ACCCCCAGCG
CAGCTAGCCA CACCCCCGGG CTGGCAGGCG ACCTCGCCAG GATGGCAGGC CACGCAGCAA
GGCTGGCAGG CCACTCCCCT GACTTGGCAG ACCACGCAGG TCACCTGGCA GGCACCAGCC
GTTACCTGGC AGGTGCCGCC GCCCATGCGC CAGGGGCCCC CGCCCATCCG CCCTGGCCCA
CCACCCATCC GCCCTGGCCC ACCACCGGTG CGACAGGCCC CACCGCTGAT CCGCCAGGCC
CCACCGGTGA TCCGCCAGGC CCCACCCGTG ATCCGCCAGG CCCCACCCGT GATCCGCCAG
GCCCCCGCTG TGATCCGCCA GGCCCCACCT GTGATCCGCC AGGCCCCACC TGTGATCCGC
CAGGCTCCAC CTGTGATCCG CCAGGCCCCG CCGCTGATCC GCCAGGCGCC GCCGCCCATC
CGACCTGCCC CACAGGTCCT GGCCACCCAG CCACCGCTCT GGCAGGCCCT GCCACCCCCA
CCTCCACTGC GGCAGGCCCC GCAGGCTAGG CTGCCGGCCC CGCAGGTGCA GGCGGCGCCG
CAGGTGCCTA CGGCCCCACC TGCTACGCAG GTACCCGCGG CGCCGCCCGC TGGCCCGCAG
GTGCCCCAGC CTGTGCTGCC GGCCCCGCTG TCTGCCCCAC TGTCTGCCCC GCAGGCTGTG
CACTGCCCTT CCATCATCTG GCAGGCCCCC AAAGGTCAGC CCCCGGTGCC ACACGAGATT
CCAACGTCAA TGGAATTCCA GGAGGTGCAG CAGACACAGG CGCTGGCCTG GCAGGCCCAG
AAGGCCCCCA CTCACATCTG GCAGCCCCTG CCTGCCCAGG AGGCCCAGAG GCAGGCTCCC
CCCTTGGTCC AGCTGGAGCA GCCCTTTCAG GGAGCCCCGC CCTCCCAAAA AGCCGTGCAA
ATCCAGCTAC CCCCCCAGCA GGCCCAGGCA TCGGGTCCGC AAGCGGAGGT GCCCACACTG
CCGCTCCAGC CTTCCTGGCA GGCACCGCCT GCAGTCTTGC AGGCCCAGCC CGGACCCCCG
GTAGCAGCGG CAAATTTTCC CCTGGGCTCC GCTAAATCAT TGATGACTCC ATCAGGAGAA
TGCAGGGCCT CTTCTATAGA CCGCAGGGGC TCCTCTAAAG AGCGCAGGAC CTCCTCGAAG
GAGCGCAGGG CCCCTTCAAA AGACCGCATG ATCTTTGCTG CCACCTTCTG TGCTCCCAAG
GCAGTGTCAG CTGCGCGAGC ACACCTGCCA GCTGCCTGGA AAAACCTGCC TGCCACACCG
GAGACCTTTG CTCCCTCCTC AAGTGTCTTC CCAGCTACCT CCCAGTTTCA GCCTGCCTCT
CTGAATGCCT TTAAAGGCCC CTCTGCTGCC TCAGAGACCC CAAAGTCACT GCCATATGCT
CTGCAGGATC CCTTTGCCTG TGTAGAGGCC CTGCCTGCAG TTCCATGGGT CCCACAGCCC
AATATGAATG CCTCAAAGGC ATCGCAGGCA GTGCCCACCT TCCTGATGGC TACAGCAGCT
GCCCCCCAGG CAACTGCCAC CACTCAAGAG GCCTCCAAGA CCTCCGTCGA GCCGCCACGC
CGCTCCGGCA AGGCCACCCG GAAGAAGAAG CATCTGGAAG CCCAAGAGGA CAGCCGTGGC
CACACGCTAG CCTTTCATGA CTGGCAGGGC CCAAGGCCCT GGGAGAATCT AAATCTGAGT
GACTGGGAGG TCCAAAGCCC TATCCAGGTC TCGGGTGACT GGGAGCACCC AAACACCCCC
CGTGGCCTGA GTGGTTGGGA GGGCCCTAGC ACCTCCAGGA TCCTGAGTGG CTGGGAAGGG
CCCAGCGCAT CCTGGGCCCT GAGTGCCTGG GAGGGCCCGA GCACCTCCAG GGCCCTGGGT
CTCTCTGAAA GCCCAGGGAG CTCTCTGCCC GTAGTTGTGT CTGAGGTCGC AAGTGTCTCT
CCGGGATCCA GTGCCACCCA GGATAATTCC AAGGTGGAGG CACAGCCCTT GTCTCCCTTG
GATGAGAGGG CAAATGCGTT GGTGCAGTTC CTCTTAGTCA AGGACCAAGC CAAGGTGCCT
GTCCAGCGCT CGGAGATGGT GAAAGTCATC CTCCGAGAGT ATAAAGATGA GTGCTTAGAT
ATCATCAACC GTGCCAACAA TAAGCTGGAG TGTGCCTTTG GTTATCAATT GAAAGAAATT
GATACCAAAA ACCACGCCTA TATTATCATC AACAAGCTGG GCTACCATAC AGGGAATTTG
GTGGCATCCT ATTTAGACAG GCCCAAGTTT GGCCTTCTGA TGGTGGTCTT GAGCCTCATC
TTTATGAAAG GCAACTGTGT CAGGGAGGAT CTGATCTTTA ATTTTCTGTT CAAGTTAGGG
TTGGATGTCC GGGAGACAAA CGGTCTCTTT GGAAATACTA AGAAGCTCAT CACCGAAGTG
TTTGTCAGGC AGAAGTACCT AGAGTACAGG CGAATCCCTT ACACTGAGCC CGCAGAGTAT
GAGTTCCTCT GGGGCCCTCG AGCATTCCTG GAAACCAGCA AGATGCTTGT CCTGAGGTTT
TTGGCCAAGC TCCATAAGAA AGATCCACAG AGCTGGCCAT TCCATTACCT TGAAGCGCTC
GCAGAGTGTG AGTGGGAAGA CACAGATGAG GATGAACCTG ACACCGGTGA CAGTGCCCAC
GGCCCCACCA GCAGGCCCCC TCCCCGCTAA

The stop codons will be deleted if pcDNA3.1+/C-(K)DYK vector is selected.

book

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.
Nature514(7520)92-97(2014 Oct)
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Schaaf CP,Gonzalez-Garay ML,Xia F,Potocki L,Gripp KW,Zhang B,Peters BA,McElwain MA,Drmanac R,Beaudet AL,Caskey CT,Yang Y


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Regulation of WASH-dependent actin polymerization and protein trafficking by ubiquitination.
Cell152(5)1051-64(2013 Feb)
Hao YH,Doyle JM,Ramanathan S,Gomez TS,Jia D,Xu M,Chen ZJ,Billadeau DD,Rosen MK,Potts PR


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Lack of association between MAGEL2 and schizophrenia and mood disorders in the Japanese population.
Neuromolecular medicine12(3)285-91(2010 Sep)
Fukuo Y,Kishi T,Okochi T,Kitajima T,Tsunoka T,Okumukura T,Kinoshita Y,Kawashima K,Yamanouchi Y,Umene-Nakano W,Naitoh H,Inada T,Yoshimura R,Nakamura J,Ozaki N,Iwata N


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Expression and imprinting of MAGEL2 suggest a role in Prader-willi syndrome and the homologous murine imprinting phenotype.
Human molecular genetics9(12)1813-9(2000 Jul)
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