Seroatlas · Human Serome Atlas

AKAP13

A-kinase anchor protein 13

Also known as: AKAP-Lbc, AKP13_HUMAN, ARHGEF13, BRX, c-lbc, HA-3, Ht31, LBC, PROTO-LB

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

Protein identityUniProt · HPA

UniProt accession: Q12802
Gene: AKAP13
Ensembl: ENSG00000170776
Chromosome: 15
Canonical length: 2813 aa
Protein class: Plasma proteins, Predicted intracellular proteins
Subcellular location: Cytosol

OverviewNCBI Gene

The A-kinase anchor proteins (AKAPs) are a group of structurally diverse proteins which have the common function of binding to the regulatory subunit of protein kinase A (PKA) and confining the holoenzyme to discrete locations within the cell. This gene encodes a member of the AKAP family. Alternative splicing of this gene results in multiple transcript variants encoding different isoforms containing c-terminal dbl oncogene homology (DH) and pleckstrin homology (PH) domains. The DH domain is associated with guanine nucleotide exchange activation for the Rho/Rac family of small GTP binding proteins, resulting in the conversion of the inactive GTPase to the active form capable of transducing signals. The PH domain has multiple functions. Therefore, these isoforms function as scaffolding proteins to coordinate a Rho signaling pathway, function as protein kinase A-anchoring proteins and, in addition, enhance ligand-dependent activity of estrogen receptors alpha and beta. [provided by RefSeq, Jul 2012]

Canonical amino-acid sequenceUniProt

2813 residues, UniProt reviewed canonical sequence.

>Q12802|AKAP13
     1  MKLNPQQAPL YGDCVVTVLL AEEDKAEDDV VFYLVFLGST LRHCTSTRKV SSDTLETIAP
    61  GHDCCETVKV QLCASKEGLP VFVVAEEDFH FVQDEAYDAA QFLATSAGNQ QALNFTRFLD
   121  QSGPPSGDVN SLDKKLVLAF RHLKLPTEWN VLGTDQSLHD AGPRETLMHF AVRLGLLRLT
   181  WFLLQKPGGR GALSIHNQEG ATPVSLALER GYHKLHQLLT EENAGEPDSW SSLSYEIPYG
   241  DCSVRHHREL DIYTLTSESD SHHEHPFPGD GCTGPIFKLM NIQQQLMKTN LKQMDSLMPL
   301  MMTAQDPSSA PETDGQFLPC APEPTDPQRL SSSEETESTQ CCPGSPVAQT ESPCDLSSIV
   361  EEENTDRSCR KKNKGVERKG EEVEPAPIVD SGTVSDQDSC LQSLPDCGVK GTEGLSSCGN
   421  RNEETGTKSS GMPTDQESLS SGDAVLQRDL VMEPGTAQYS SGGELGGIST TNVSTPDTAG
   481  EMEHGLMNPD ATVWKNVLQG GESTKERFEN SNIGTAGASD VHVTSKPVDK ISVPNCAPAA
   541  SSLDGNKPAE SSLAFSNEET STEKTAETET SRSREESADA PVDQNSVVIP AAAKDKISDG
   601  LEPYTLLAAG IGEAMSPSDL ALLGLEEDVM PHQNSETNSS HAQSQKGKSS PICSTTGDDK
   661  LCADSACQQN TVTSSGDLVA KLCDNIVSES ESTTARQPSS QDPPDASHCE DPQAHTVTSD
   721  PVRDTQERAD FCPFKVVDNK GQRKDVKLDK PLTNMLEVVS HPHPVVPKME KELVPDQAVI
   781  SDSTFSLANS PGSESVTKDD ALSFVPSQKE KGTATPELHT ATDYRDGPDG NSNEPDTRPL
   841  EDRAVGLSTS STAAELQHGM GNTSLTGLGG EHEGPAPPAI PEALNIKGNT DSSLQSVGKA
   901  TLALDSVLTE EGKLLVVSES SAAQEQDKDK AVTCSSIKEN ALSSGTLQEE QRTPPPGQDT
   961  QQFHEKSISA DCAKDKALQL SNSPGASSAF LKAETEHNKE VAPQVSLLTQ GGAAQSLVPP
  1021  GASLATESRQ EALGAEHNSS ALLPCLLPDG SDGSDALNCS QPSPLDVGVK NTQSQGKTSA
  1081  CEVSGDVTVD VTGVNALQGM AEPRRENISH NTQDILIPNV LLSQEKNAVL GLPVALQDKA
  1141  VTDPQGVGTP EMIPLDWEKG KLEGADHSCT MGDAEEAQID DEAHPVLLQP VAKELPTDME
  1201  LSAHDDGAPA GVREVMRAPP SGRERSTPSL PCMVSAQDAP LPKGADLIEE AASRIVDAVI
  1261  EQVKAAGALL TEGEACHMSL SSPELGPLTK GLESAFTEKV STFPPGESLP MGSTPEEATG
  1321  SLAGCFAGRE EPEKIILPVQ GPEPAAEMPD VKAEDEVDFR ASSISEEVAV GSIAATLKMK
  1381  QGPMTQAINR ENWCTIEPCP DAASLLASKQ SPECENFLDV GLGRECTSKQ GVLKRESGSD
  1441  SDLFHSPSDD MDSIIFPKPE EEHLACDITG SSSSTDDTAS LDRHSSHGSD VSLSQILKPN
  1501  RSRDRQSLDG FYSHGMGAEG RESESEPADP GDVEEEEMDS ITEVPANCSV LRSSMRSLSP
  1561  FRRHSWGPGK NAASDAEMNH RSSMRVLGDV VRRPPIHRRS FSLEGLTGGA GVGNKPSSSL
  1621  EVSSANAEEL RHPFSGEERV DSLVSLSEED LESDQREHRM FDQQICHRSK QQGFNYCTSA
  1681  ISSPLTKSIS LMTISHPGLD NSRPFHSTFH NTSANLTESI TEENYNFLPH SPSKKDSEWK
  1741  SGTKVSRTFS YIKNKMSSSK KSKEKEKEKD KIKEKEKDSK DKEKDKKTVN GHTFSSIPVV
  1801  GPISCSQCMK PFTNKDAYTC ANCSAFVHKG CRESLASCAK VKMKQPKGSL QAHDTSSLPT
  1861  VIMRNKPSQP KERPRSAVLL VDETATTPIF ANRRSQQSVS LSKSVSIQNI TGVGNDENMS
  1921  NTWKFLSHST DSLNKISKVN ESTESLTDEG VGTDMNEGQL LGDFEIESKQ LEAESWSRII
  1981  DSKFLKQQKK DVVKRQEVIY ELMQTEFHHV RTLKIMSGVY SQGMMADLLF EQQMVEKLFP
  2041  CLDELISIHS QFFQRILERK KESLVDKSEK NFLIKRIGDV LVNQFSGENA ERLKKTYGKF
  2101  CGQHNQSVNY FKDLYAKDKR FQAFVKKKMS SSVVRRLGIP ECILLVTQRI TKYPVLFQRI
  2161  LQCTKDNEVE QEDLAQSLSL VKDVIGAVDS KVASYEKKVR LNEIYTKTDS KSIMRMKSGQ
  2221  MFAKEDLKRK KLVRDGSVFL KNAAGRLKEV QAVLLTDILV FLQEKDQKYI FASLDQKSTV
  2281  ISLKKLIVRE VAHEEKGLFL ISMGMTDPEM VEVHASSKEE RNSWIQIIQD TINTLNRDED
  2341  EGIPSENEEE KKMLDTRARE LKEQLHQKDQ KILLLLEEKE MIFRDMAECS TPLPEDCSPT
  2401  HSPRVLFRSN TEEALKGGPL MKSAINEVEI LQGLVSGNLG GTLGPTVSSP IEQDVVGPVS
  2461  LPRRAETFGG FDSHQMNASK GGEKEEGDDG QDLRRTESDS GLKKGGNANL VFMLKRNSEQ
  2521  VVQSVVHLYE LLSALQGVVL QQDSYIEDQK LVLSERALTR SLSRPSSLIE QEKQRSLEKQ
  2581  RQDLANLQKQ QAQYLEEKRR REREWEARER ELREREALLA QREEEVQQGQ QDLEKEREEL
  2641  QQKKGTYQYD LERLRAAQKQ LEREQEQLRR EAERLSQRQT ERDLCQVSHP HTKLMRIPSF
  2701  FPSPEEPPSP SAPSIAKSGS LDSELSVSPK RNSISRTHKD KGPFHILSST SQTNKGPEGQ
  2761  SQAPASTSAS TRLFGLTKPK EKKEKKKKNK TSRSQPGDGP ASEVSAEGEE IFC

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against AKAP13 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: 82 nTPM

Expression across tissuesHPA

Tissue

skeletal muscle: 82 nTPM
endometrium: 76 nTPM
heart muscle: 61 nTPM
tongue: 56 nTPM
bone marrow: 53 nTPM
pancreas: 53 nTPM

Single-cell type

endometrial glandular cells: 3,019 nCPM
cardiomyocytes: 2,980 nCPM
mast cells: 2,691 nCPM
alveolar cells type 2: 2,273 nCPM
neutrophils: 2,178 nCPM
transitional alveolar cells: 1,843 nCPM

Immune cell

basophil: 287 nTPM
eosinophil: 182 nTPM
gdT-cell: 123 nTPM
NK-cell: 109 nTPM
neutrophil: 105 nTPM
plasmacytoid DC: 101 nTPM

Brain region

choroid plexus: 222 nTPM
midbrain: 84 nTPM
medulla oblongata: 83 nTPM
hypothalamus: 82 nTPM
white matter: 80 nTPM
thalamus: 78 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): 0.29
gnomAD pLI: 0.93
gnomAD missense Z: -1.64
DepMap mean gene effect: -0.03
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

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

InteractionsUniProt · HPA

Protein binding partners of AKAP13 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 AKAP13 as an antibody target. Whether an autoantibody or antibody against AKAP13 could matter depends on whether native AKAP13 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

AKAP13 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 AKAP13 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

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