Seroatlas · Human Serome Atlas

MGAM

Maltase-glucoamylase

Also known as: MGA, MGA_HUMAN

Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession: O43451
Gene: MGAM
Ensembl: ENSG00000257335
Chromosome: 7
Canonical length: 2753 aa
Protein class: Enzymes, FDA approved drug targets, Metabolic proteins, Plasma proteins, Predicted membrane proteins

OverviewNCBI Gene

This gene encodes maltase-glucoamylase, which is a brush border membrane enzyme that plays a role in the final steps of digestion of starch. The protein has two catalytic sites identical to those of sucrase-isomaltase, but the proteins are only 59% homologous. Both are members of glycosyl hydrolase family 31, which has a variety of substrate specificities. [provided by RefSeq, Jul 2008]

Canonical amino-acid sequenceUniProt

2753 residues, UniProt reviewed canonical sequence.

>O43451|MGAM
     1  MARKKLKKFT TLEIVLSVLL LVLFIISIVL IVLLAKESLK STAPDPGTTG TPDPGTTGTP
    61  DPGTTGTTHA RTTGPPDPGT TGTTPVSAEC PVVNELERIN CIPDQPPTKA TCDQRGCCWN
   121  PQGAVSVPWC YYSKNHSYHV EGNLVNTNAG FTARLKNLPS SPVFGSNVDN VLLTAEYQTS
   181  NRFHFKLTDQ TNNRFEVPHE HVQSFSGNAA ASLTYQVEIS RQPFSIKVTR RSNNRVLFDS
   241  SIGPLLFADQ FLQLSTRLPS TNVYGLGEHV HQQYRHDMNW KTWPIFNRDT TPNGNGTNLY
   301  GAQTFFLCLE DASGLSFGVF LMNSNAMEVV LQPAPAITYR TIGGILDFYV FLGNTPEQVV
   361  QEYLELIGRP ALPSYWALGF HLSRYEYGTL DNMREVVERN RAAQLPYDVQ HADIDYMDER
   421  RDFTYDSVDF KGFPEFVNEL HNNGQKLVII VDPAISNNSS SSKPYGPYDR GSDMKIWVNS
   481  SDGVTPLIGE VWPGQTVFPD YTNPNCAVWW TKEFELFHNQ VEFDGIWIDM NEVSNFVDGS
   541  VSGCSTNNLN NPPFTPRILD GYLFCKTLCM DAVQHWGKQY DIHNLYGYSM AVATAEAAKT
   601  VFPNKRSFIL TRSTFAGSGK FAAHWLGDNT ATWDDLRWSI PGVLEFNLFG IPMVGPDICG
   661  FALDTPEELC RRWMQLGAFY PFSRNHNGQG YKDQDPASFG ADSLLLNSSR HYLNIRYTLL
   721  PYLYTLFFRA HSRGDTVARP LLHEFYEDNS TWDVHQQFLW GPGLLITPVL DEGAEKVMAY
   781  VPDAVWYDYE TGSQVRWRKQ KVEMELPGDK IGLHLRGGYI FPTQQPNTTT LASRKNPLGL
   841  IIALDENKEA KGELFWDNGE TKDTVANKVY LLCEFSVTQN RLEVNISQST YKDPNNLAFN
   901  EIKILGTEEP SNVTVKHNGV PSQTSPTVTY DSNLKVAIIT DIDLLLGEAY TVEWSIKIRD
   961  EEKIDCYPDE NGASAENCTA RGCIWEASNS SGVPFCYFVN DLYSVSDVQY NSHGATADIS
  1021  LKSSVYANAF PSTPVNPLRL DVTYHKNEML QFKIYDPNKN RYEVPVPLNI PSMPSSTPEG
  1081  QLYDVLIKKN PFGIEIRRKS TGTIIWDSQL LGFTFSDMFI RISTRLPSKY LYGFGETEHR
  1141  SYRRDLEWHT WGMFSRDQPP GYKKNSYGVH PYYMGLEEDG SAHGVLLLNS NAMDVTFQPL
  1201  PALTYRTTGG VLDFYVFLGP TPELVTQQYT ELIGRPVMVP YWSLGFQLCR YGYQNDSEIA
  1261  SLYDEMVAAQ IPYDVQYSDI DYMERQLDFT LSPKFAGFPA LINRMKADGM RVILILDPAI
  1321  SGNETQPYPA FTRGVEDDVF IKYPNDGDIV WGKVWPDFPD VVVNGSLDWD SQVELYRAYV
  1381  AFPDFFRNST AKWWKREIEE LYNNPQNPER SLKFDGMWID MNEPSSFVNG AVSPGCRDAS
  1441  LNHPPYMPHL ESRDRGLSSK TLCMESQQIL PDGSLVQHYN VHNLYGWSQT RPTYEAVQEV
  1501  TGQRGVVITR STFPSSGRWA GHWLGDNTAA WDQLKKSIIG MMEFSLFGIS YTGADICGFF
  1561  QDAEYEMCVR WMQLGAFYPF SRNHNTIGTR RQDPVSWDAA FVNISRNVLQ TRYTLLPYLY
  1621  TLMQKAHTEG VTVVRPLLHE FVSDQVTWDI DSQFLLGPAF LVSPVLERNA RNVTAYFPRA
  1681  RWYDYYTGVD INARGEWKTL PAPLDHINLH VRGGYILPWQ EPALNTHLSR KNPLGLIIAL
  1741  DENKEAKGEL FWDDGQTKDT VAKKVYLLCE FSVTQNHLEV TISQSTYKDP NNLAFNEIKI
  1801  LGMEEPSNVT VKHNGVPSQT SPTVTYDSNL KVAIITDINL FLGEAYTVEW SIKIRDEEKI
  1861  DCYPDENGDS AENCTARGCI WEASNSSGVP FCYFVNDLYS VSDVQYNSHG ATADISLKSS
  1921  VHANAFPSTP VNPLRLDVTY HKNEMLQFKI YDPNNNRYEV PVPLNIPSVP SSTPEGQLYD
  1981  VLIKKNPFGI EIRRKSTGTI IWDSQLLGFT FNDMFIRIST RLPSKYLYGF GETEHTSYRR
  2041  DLEWHTWGMF SRDQPPGYKK NSYGVHPYYM GLEEDGSAHG VLLLNSNAMD VTFQPLPALT
  2101  YRTTGGVLDF YVFLGPTPEL VTQQYTELIG RPVMVPYWSL GFQLCRYGYQ NDSEISSLYD
  2161  EMVAAQIPYD VQYSDIDYME RQLDFTLSPK FAGFPALINR MKADGMRVIL ILDPAISGNE
  2221  TQPYPAFTRG VEDDVFIKYP NDGDIVWGKV WPDFPDVVVN GSLDWDSQVE LYRAYVAFPD
  2281  FFRNSTAKWW KREIEELYNN PQNPERSLKF DGMWIDMNEP SSFVNGAVSP GCRDASLNHP
  2341  PYMPYLESRD RGLSSKTLCM ESQQILPDGS PVQHYNVHNL YGWSQTRPTY EAVQEVTGQR
  2401  GVVITRSTFP SSGRWAGHWL GDNTAAWDQL KKSIIGMMEF SLFGISYTGA DICGFFQDAE
  2461  YEMCVRWMQL GAFYPFSRNH NTIGTRRQDP VSWDVAFVNI SRTVLQTRYT LLPYLYTLMH
  2521  KAHTEGVTVV RPLLHEFVSD QVTWDIDSQF LLGPAFLVSP VLERNARNVT AYFPRARWYD
  2581  YYTGVDINAR GEWKTLPAPL DHINLHVRGG YILPWQEPAL NTHLSRQKFM GFKIALDDEG
  2641  TAGGWLFWDD GQSIDTYGKG LYYLASFSAS QNTMQSHIIF NNYITGTNPL KLGYIEIWGV
  2701  GSVPVTSVSI SVSGMVITPS FNNDPTTQVL SIDVTDRNIS LHNFTSLTWI STL

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against MGAM 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: Cell surface
Secreted: No
Transmembrane segments: 1
Mean surface accessibility (rSASA): 0
Highest tissue expression: 83 nTPM

Expression across tissuesHPA

Tissue

small intestine: 83 nTPM
duodenum: 56 nTPM
epididymis: 24 nTPM
kidney: 17 nTPM
bone marrow: 17 nTPM
spleen: 12 nTPM

Single-cell type

neutrophils: 491 nCPM
late spermatids: 308 nCPM
proximal tubule cells: 295 nCPM
enterocytes: 256 nCPM
early spermatids: 173 nCPM
neutrophil progenitors: 153 nCPM

Immune cell

neutrophil: 14 nTPM
eosinophil: 1.9 nTPM
classical monocyte: 0.1 nTPM
basophil: 0 nTPM
gdT-cell: 0 nTPM
intermediate monocyte: 0 nTPM

Brain region

cerebral cortex: 6 nTPM
thalamus: 2.3 nTPM
pons: 2.2 nTPM
medulla oblongata: 2 nTPM
midbrain: 1.9 nTPM
basal ganglia: 1.7 nTPM

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): 0.84
gnomAD pLI: 0
gnomAD missense Z: -0.76
DepMap mean gene effect: 0.01
DepMap dependency class: selective

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

dextrin catabolic process
maltose catabolic process
starch catabolic process

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads MGAM as an antibody target. Whether an autoantibody or antibody against MGAM could matter depends on whether native MGAM is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

MGAM is annotated at the cell surface, where native MGAM is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.

Annotation status

The present source text does not explicitly label MGAM as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Loading the interactive Seroatlas protein explorer...