MGA
MAX gene-associated protein
Also known as: FLJ12634, KIAA0518, MAD5, MGAP_HUMAN, MXD5
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q8IWI9
- Gene
- MGA
- Ensembl
- ENSG00000174197
- Chromosome
- 15
- Canonical length
- 3065 aa
- Protein class
- Cancer-related genes, Predicted intracellular proteins, Transcription factors
- Subcellular location
- Nucleoplasm,Cytosol
OverviewNCBI Gene
Predicted to enable DNA-binding transcription activator activity, RNA polymerase II-specific and RNA polymerase II cis-regulatory region sequence-specific DNA binding activity. Predicted to be involved in cell fate specification and positive regulation of transcription by RNA polymerase II. Predicted to act upstream of or within cellular response to leukemia inhibitory factor. Part of MLL1 complex. [provided by Alliance of Genome Resources, Jul 2025]
Canonical amino-acid sequenceUniProt
3065 residues, UniProt reviewed canonical sequence.
>Q8IWI9|MGA
1 MEEKQQIILA NQDGGTVAGA APTFFVILKQ PGNGKTDQGI LVTNQDACAL ASSVSSPVKS
61 KGKICLPADC TVGGITVTLD NNSMWNEFYH RSTEMILTKQ GRRMFPYCRY WITGLDSNLK
121 YILVMDISPV DNHRYKWNGR WWEPSGKAEP HVLGRVFIHP ESPSTGHYWM HQPVSFYKLK
181 LTNNTLDQEG HIILHSMHRY LPRLHLVPAE KAVEVIQLNG PGVHTFTFPQ TEFFAVTAYQ
241 NIQITQLKID YNPFAKGFRD DGLNNKPQRD GKQKNSSDQE GNNISSSSGH RVRLTEGQGS
301 EIQPGDLDPL SRGHETSGKG LEKTSLNIKR DFLGFMDTDS ALSEVPQLKQ EISECLIASS
361 FEDDSRVASP LDQNGSFNVV IKEEPLDDYD YELGECPEGV TVKQEETDEE TDVYSNSDDD
421 PILEKQLKRH NKVDNPEADH LSSKWLPSSP SGVAKAKMFK LDTGKMPVVY LEPCAVTRST
481 VKISELPDNM LSTSRKDKSS MLAELEYLPT YIENSNETAF CLGKESENGL RKHSPDLRVV
541 QKYPLLKEPQ WKYPDISDSI STERILDDSK DSVGDSLSGK EDLGRKRTTM LKIATAAKVV
601 NANQNASPNV PGKRGRPRKL KLCKAGRPPK NTGKSLISTK NTPVSPGSTF PDVKPDLEDV
661 DGVLFVSFES KEALDIHAVD GTTEESSSLQ ASTTNDSGYR ARISQLEKEL IEDLKTLRHK
721 QVIHPGLQEV GLKLNSVDPT MSIDLKYLGV QLPLAPATSF PFWNLTGTNP ASPDAGFPFV
781 SRTGKTNDFT KIKGWRGKFH SASASRNEGG NSESSLKNRS AFCSDKLDEY LENEGKLMET
841 SMGFSSNAPT SPVVYQLPTK STSYVRTLDS VLKKQSTISP STSYSLKPHS VPPVSRKAKS
901 QNRQATFSGR TKSSYKSILP YPVSPKQKYS HVILGDKVTK NSSGIISENQ ANNFVVPTLD
961 ENIFPKQISL RQAQQQQQQQ QGSRPPGLSK SQVKLMDLED CALWEGKPRT YITEERADVS
1021 LTTLLTAQAS LKTKPIHTII RKRAPPCNND FCRLGCVCSS LALEKRQPAH CRRPDCMFGC
1081 TCLKRKVVLV KGGSKTKHFQ RKAAHRDPVF YDTLGEEARE EEEGIREEEE QLKEKKKRKK
1141 LEYTICETEP EQPVRHYPLW VKVEGEVDPE PVYIPTPSVI EPMKPLLLPQ PEVLSPTVKG
1201 KLLTGIKSPR SYTPKPNPVI REEDKDPVYL YFESMMTCAR VRVYERKKED QRQPSSSSSP
1261 SPSFQQQTSC HSSPENHNNA KEPDSEQQPL KQLTCDLEDD SDKLQEKSWK SSCNEGESSS
1321 TSYMHQRSPG GPTKLIEIIS DCNWEEDRNK ILSILSQHIN SNMPQSLKVG SFIIELASQR
1381 KSRGEKNPPV YSSRVKISMP SCQDQDDMAE KSGSETPDGP LSPGKMEDIS PVQTDALDSV
1441 RERLHGGKGL PFYAGLSPAG KLVAYKRKPS SSTSGLIQVA SNAKVAASRK PRTLLPSTSN
1501 SKMASSSGTA TNRPGKNLKA FVPAKRPIAA RPSPGGVFTQ FVMSKVGALQ QKIPGVSTPQ
1561 TLAGTQKFSI RPSPVMVVTP VVSSEPVQVC SPVTAAVTTT TPQVFLENTT AVTPMTAISD
1621 VETKETTYSS GATTTGVVEV SETNTSTSVT STQSTATVNL TKTTGITTPV ASVAFPKSLV
1681 ASPSTITLPV ASTASTSLVV VTAAASSSMV TTPTSSLGSV PIILSGINGS PPVSQRPENA
1741 AQIPVATPQV SPNTVKRAGP RLLLIPVQQG SPTLRPVSNT QLQGHRMVLQ PVRSPSGMNL
1801 FRHPNGQIVQ LLPLHQLRGS NTQPNLQPVM FRNPGSVMGI RLPAPSKPSE TPPSSTSSSA
1861 FSVMNPVIQA VGSSSAVNVI TQAPSLLSSG ASFVSQAGTL TLRISPPEPQ SFASKTGSET
1921 KITYSSGGQP VGTASLIPLQ SGSFALLQLP GQKPVPSSIL QHVASLQMKR ESQNPDQKDE
1981 TNSIKREQET KKVLQSEGEA VDPEANVIKQ NSGAATSEET LNDSLEDRGD HLDEECLPEE
2041 GCATVKPSEH SCITGSHTDQ DYKDVNEEYG ARNRKSSKEK VAVLEVRTIS EKASNKTVQN
2101 LSKVQHQKLG DVKVEQQKGF DNPEENSSEF PVTFKEESKF ELSGSKVMEQ QSNLQPEAKE
2161 KECGDSLEKD RERWRKHLKG PLTRKCVGAS QECKKEADEQ LIKETKTCQE NSDVFQQEQG
2221 ISDLLGKSGI TEDARVLKTE CDSWSRISNP SAFSIVPRRA AKSSRGNGHF QGHLLLPGEQ
2281 IQPKQEKKGG RSSADFTVLD LEEDDEDDNE KTDDSIDEIV DVVSDYQSEE VDDVEKNNCV
2341 EYIEDDEEHV DIETVEELSE EINVAHLKTT AAHTQSFKQP SCTHISADEK AAERSRKAPP
2401 IPLKLKPDYW SDKLQKEAEA FAYYRRTHTA NERRRRGEMR DLFEKLKITL GLLHSSKVSK
2461 SLILTRAFSE IQGLTDQADK LIGQKNLLTR KRNILIRKVS SLSGKTEEVV LKKLEYIYAK
2521 QQALEAQKRK KKMGSDEFDI SPRISKQQEG SSASSVDLGQ MFINNRRGKP LILSRKKDQA
2581 TENTSPLNTP HTSANLVMTP QGQLLTLKGP LFSGPVVAVS PDLLESDLKP QVAGSAVALP
2641 ENDDLFMMPR IVNVTSLATE GGLVDMGGSK YPHEVPDSKP SDHLKDTVRN EDNSLEDKGR
2701 ISSRGNRDGR VTLGPTQVFL ANKDSGYPQI VDVSNMQKAQ EFLPKKISGD MRGIQYKWKE
2761 SESRGERVKS KDSSFHKLKM KDLKDSSIEM ELRKVTSAIE EAALDSSELL TNMEDEDDTD
2821 ETLTSLLNEI AFLNQQLNDD SVGLAELPSS MDTEFPGDAR RAFISKVPPG SRATFQVEHL
2881 GTGLKELPDV QGESDSISPL LLHLEDDDFS ENEKQLAEPA SEPDVLKIVI DSEIKDSLLS
2941 NKKAIDGGKN TSGLPAEPES VSSPPTLHMK TGLENSNSTD TLWRPMPKLA PLGLKVANPS
3001 SDADGQSLKV MPCLAPIAAK VGSVGHKMNL TGNDQEGRES KVMPTLAPVV AKLGNSGASP
3061 SSAGKLocalizationUniProt · AlphaFold · HPA
Whether an antibody against MGA can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Intracellular
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0
- Highest tissue expression
- 7.7 nTPM
Expression across tissuesHPA
Tissue
- thymus: 7.7 nTPM
- testis: 6.5 nTPM
- ovary: 6.3 nTPM
- thyroid gland: 5.5 nTPM
- cervix: 5.3 nTPM
- bone marrow: 5.1 nTPM
Single-cell type
- myonuclei: 206 nCPM
- somatotrophs: 198 nCPM
- thyrotrophs: 183 nCPM
- lactotrophs: 174 nCPM
- sertoli cells: 153 nCPM
- gonadotrophs: 146 nCPM
Immune cell
- NK-cell: 6.4 nTPM
- non-classical monocyte: 3.2 nTPM
- plasmacytoid DC: 3.1 nTPM
- basophil: 3 nTPM
- naive B-cell: 2.8 nTPM
- memory B-cell: 2.3 nTPM
Brain region
- cerebellum: 69 nTPM
- white matter: 39 nTPM
- hypothalamus: 38 nTPM
- basal ganglia: 37 nTPM
- cerebral cortex: 36 nTPM
- pons: 33 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about MGA.
Disease | AllUniProt
Conditions MGA is implicated in, by any mechanism.
- Premature ovarian failure 26 (POF26) MIM:621065
Disease | GeneticClinVar
4 pathogenic / likely-pathogenic of 97 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Premature ovarian failure 26
- Multiple myeloma
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 0.09
- gnomAD pLI
- 1
- gnomAD missense Z
- 1.1
- DepMap mean gene effect
- -0.21
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 3% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- cell fate specification
- positive regulation of DNA-templated transcription
- regulation of transcription by RNA polymerase II
Molecular functions
- DNA-binding transcription factor activity, RNA polymerase II-specific
- protein dimerization activity
- RNA polymerase II cis-regulatory region sequence-specific DNA binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
- T-box transcription factor
- p53-like transcription factor, DNA-binding domain superfamily
- Myc-type, basic helix-loop-helix (bHLH) domain
- Transcription factor, T-box, conserved site
- Helix-loop-helix DNA-binding domain superfamily
- T-box superfamily
- T-box transcription factor, DNA-binding domain
- Helix-loop-helix DNA-binding domain
- T-box
- MGA, conserved domain
- MAX gene-associated protein, basic Helix-Loop-Helix-zipper domain
- MGA, conserved domain
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of MGA in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads MGA as an antibody target. Whether an autoantibody or antibody against MGA could matter depends on whether native MGA is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
MGA is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.
Annotation status
The present source text does not explicitly label MGA as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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