Seroatlas · Human Serome Atlas

AKAP9

A-kinase anchor protein 9

Also known as: AKAP350, AKAP450, AKAP9_HUMAN, CG-NAP, HYPERION, KIAA0803, LQT11, MU-RMS-40.16A, PPP1R45, PRKA9, YOTIAO

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

Protein identityUniProt · HPA

UniProt accession: Q99996
Gene: AKAP9
Ensembl: ENSG00000127914
Chromosome: 7
Canonical length: 3907 aa
Protein class: Cancer-related genes, Disease related genes, Human disease related genes, Plasma proteins, Predicted intracellular proteins
Subcellular location: Golgi apparatus,Vesicles,Centrosome

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. Alternate splicing of this gene results in at least two isoforms that localize to the centrosome and the Golgi apparatus, and interact with numerous signaling proteins from multiple signal transduction pathways. These signaling proteins include type II protein kinase A, serine/threonine kinase protein kinase N, protein phosphatase 1, protein phosphatase 2a, protein kinase C-epsilon and phosphodiesterase 4D3. [provided by RefSeq, Aug 2008]

Canonical amino-acid sequenceUniProt

3907 residues, UniProt reviewed canonical sequence.

>Q99996|AKAP9
     1  MEDEERQKKL EAGKAKLAQF RQRKAQSDGQ SPSKKQKKKR KTSSSKHDVS AHHDLNIDQS
    61  QCNEMYINSS QRVESTVIPE STIMRTLHSG EITSHEQGFS VELESEISTT ADDCSSEVNG
   121  CSFVMRTGKP TNLLREEEFG VDDSYSEQGA QDSPTHLEMM ESELAGKQHE IEELNRELEE
   181  MRVTYGTEGL QQLQEFEAAI KQRDGIITQL TANLQQARRE KDETMREFLE LTEQSQKLQI
   241  QFQQLQASET LRNSTHSSTA ADLLQAKQQI LTHQQQLEEQ DHLLEDYQKK KEDFTMQISF
   301  LQEKIKVYEM EQDKKVENSN KEEIQEKETI IEELNTKIIE EEKKTLELKD KLTTADKLLG
   361  ELQEQIVQKN QEIKNMKLEL TNSKQKERQS SEEIKQLMGT VEELQKRNHK DSQFETDIVQ
   421  RMEQETQRKL EQLRAELDEM YGQQIVQMKQ ELIRQHMAQM EEMKTRHKGE MENALRSYSN
   481  ITVNEDQIKL MNVAINELNI KLQDTNSQKE KLKEELGLIL EEKCALQRQL EDLVEELSFS
   541  REQIQRARQT IAEQESKLNE AHKSLSTVED LKAEIVSASE SRKELELKHE AEVTNYKIKL
   601  EMLEKEKNAV LDRMAESQEA ELERLRTQLL FSHEEELSKL KEDLEIEHRI NIEKLKDNLG
   661  IHYKQQIDGL QNEMSQKIET MQFEKDNLIT KQNQLILEIS KLKDLQQSLV NSKSEEMTLQ
   721  INELQKEIEI LRQEEKEKGT LEQEVQELQL KTELLEKQMK EKENDLQEKF AQLEAENSIL
   781  KDEKKTLEDM LKIHTPVSQE ERLIFLDSIK SKSKDSVWEK EIEILIEENE DLKQQCIQLN
   841  EEIEKQRNTF SFAEKNFEVN YQELQEEYAC LLKVKDDLED SKNKQELEYK SKLKALNEEL
   901  HLQRINPTTV KMKSSVFDED KTFVAETLEM GEVVEKDTTE LMEKLEVTKR EKLELSQRLS
   961  DLSEQLKQKH GEISFLNEEV KSLKQEKEQV SLRCRELEII INHNRAENVQ SCDTQVSSLL
  1021  DGVVTMTSRG AEGSVSKVNK SFGEESKIMV EDKVSFENMT VGEESKQEQL ILDHLPSVTK
  1081  ESSLRATQPS ENDKLQKELN VLKSEQNDLR LQMEAQRICL SLVYSTHVDQ VREYMENEKD
  1141  KALCSLKEEL IFAQEEKIKE LQKIHQLELQ TMKTQETGDE GKPLHLLIGK LQKAVSEECS
  1201  YFLQTLCSVL GEYYTPALKC EVNAEDKENS GDYISENEDP ELQDYRYEVQ DFQENMHTLL
  1261  NKVTEEYNKL LVLQTRLSKI WGQQTDGMKL EFGEENLPKE ETEFLSIHSQ MTNLEDIDVN
  1321  HKSKLSSLQD LEKTKLEEQV QELESLISSL QQQLKETEQN YEAEIHCLQK RLQAVSESTV
  1381  PPSLPVDSVV ITESDAQRTM YPGSCVKKNI DGTIEFSGEF GVKEETNIVK LLEKQYQEQL
  1441  EEEVAKVIVS MSIAFAQQTE LSRISGGKEN TASSKQAHAV CQQEQHYFNE MKLSQDQIGF
  1501  QTFETVDVKF KEEFKPLSKE LGEHGKEILL SNSDPHDIPE SKDCVLTISE EMFSKDKTFI
  1561  VRQSIHDEIS VSSMDASRQL MLNEEQLEDM RQELVRQYQE HQQATELLRQ AHMRQMERQR
  1621  EDQEQLQEEI KRLNRQLAQR SSIDNENLVS ERERVLLEEL EALKQLSLAG REKLCCELRN
  1681  SSTQTQNGNE NQGEVEEQTF KEKELDRKPE DVPPEILSNE RYALQKANNR LLKILLEVVK
  1741  TTAAVEETIG RHVLGILDRS SKSQSSASLI WRSEAEASVK SCVHEEHTRV TDESIPSYSG
  1801  SDMPRNDINM WSKVTEEGTE LSQRLVRSGF AGTEIDPENE ELMLNISSRL QAAVEKLLEA
  1861  ISETSSQLEH AKVTQTELMR ESFRQKQEAT ESLKCQEELR ERLHEESRAR EQLAVELSKA
  1921  EGVIDGYADE KTLFERQIQE KTDIIDRLEQ ELLCASNRLQ ELEAEQQQIQ EERELLSRQK
  1981  EAMKAEAGPV EQQLLQETEK LMKEKLEVQC QAEKVRDDLQ KQVKALEIDV EEQVSRFIEL
  2041  EQEKNTELMD LRQQNQALEK QLEKMRKFLD EQAIDREHER DVFQQEIQKL EQQLKVVPRF
  2101  QPISEHQTRE VEQLANHLKE KTDKCSELLL SKEQLQRDIQ ERNEEIEKLE FRVRELEQAL
  2161  LVSADTFQKV EDRKHFGAVE AKPELSLEVQ LQAERDAIDR KEKEITNLEE QLEQFREELE
  2221  NKNEEVQQLH MQLEIQKKES TTRLQELEQE NKLFKDDMEK LGLAIKESDA MSTQDQHVLF
  2281  GKFAQIIQEK EVEIDQLNEQ VTKLQQQLKI TTDNKVIEEK NELIRDLETQ IECLMSDQEC
  2341  VKRNREEEIE QLNEVIEKLQ QELANIGQKT SMNAHSLSEE ADSLKHQLDV VIAEKLALEQ
  2401  QVETANEEMT FMKNVLKETN FKMNQLTQEL FSLKRERESV EKIQSIPENS VNVAIDHLSK
  2461  DKPELEVVLT EDALKSLENQ TYFKSFEENG KGSIINLETR LLQLESTVSA KDLELTQCYK
  2521  QIKDMQEQGQ FETEMLQKKI VNLQKIVEEK VAAALVSQIQ LEAVQEYAKF CQDNQTISSE
  2581  PERTNIQNLN QLREDELGSD ISALTLRISE LESQVVEMHT SLILEKEQVE IAEKNVLEKE
  2641  KKLLELQKLL EGNEKKQREK EKKRSPQDVE VLKTTTELFH SNEESGFFNE LEALRAESVA
  2701  TKAELASYKE KAEKLQEELL VKETNMTSLQ KDLSQVRDHL AEAKEKLSIL EKEDETEVQE
  2761  SKKACMFEPL PIKLSKSIAS QTDGTLKISS SNQTPQILVK NAGIQINLQS ECSSEEVTEI
  2821  ISQFTEKIEK MQELHAAEIL DMESRHISET ETLKREHYVA VQLLKEECGT LKAVIQCLRS
  2881  KEGSSIPELA HSDAYQTREI CSSDSGSDWG QGIYLTHSQG FDIASEGRGE ESESATDSFP
  2941  KKIKGLLRAV HNEGMQVLSL TESPYSDGED HSIQQVSEPW LEERKAYINT ISSLKDLITK
  3001  MQLQREAEVY DSSQSHESFS DWRGELLLAL QQVFLEERSV LLAAFRTELT ALGTTDAVGL
  3061  LNCLEQRIQE QGVEYQAAME CLQKADRRSL LSEIQALHAQ MNGRKITLKR EQESEKPSQE
  3121  LLEYNIQQKQ SQMLEMQVEL SSMKDRATEL QEQLSSEKMV VAELKSELAQ TKLELETTLK
  3181  AQHKHLKELE AFRLEVKDKT DEVHLLNDTL ASEQKKSREL QWALEKEKAK LGRSEERDKE
  3241  ELEDLKFSLE SQKQRNLQLN LLLEQQKQLL NESQQKIESQ RMLYDAQLSE EQGRNLELQV
  3301  LLESEKVRIR EMSSTLDRER ELHAQLQSSD GTGQSRPPLP SEDLLKELQK QLEEKHSRIV
  3361  ELLNETEKYK LDSLQTRQQM EKDRQVHRKT LQTEQEANTE GQKKMHELQS KVEDLQRQLE
  3421  EKRQQVYKLD LEGQRLQGIM QEFQKQELER EEKRESRRIL YQNLNEPTTW SLTSDRTRNW
  3481  VLQQKIEGET KESNYAKLIE MNGGGTGCNH ELEMIRQKLQ CVASKLQVLP QKASERLQFE
  3541  TADDEDFIWV QENIDEIILQ LQKLTGQQGE EPSLVSPSTS CGSLTERLLR QNAELTGHIS
  3601  QLTEEKNDLR NMVMKLEEQI RWYRQTGAGR DNSSRFSLNG GANIEAIIAS EKEVWNREKL
  3661  TLQKSLKRAE AEVYKLKAEL RNDSLLQTLS PDSEHVTLKR IYGKYLRAES FRKALIYQKK
  3721  YLLLLLGGFQ ECEDATLALL ARMGGQPAFT DLEVITNRPK GFTRFRSAVR VSIAISRMKF
  3781  LVRRWHRVTG SVSININRDG FGLNQGAEKT DSFYHSSGGL ELYGEPRHTT YRSRSDLDYI
  3841  RSPLPFQNRY PGTPADFNPG SLACSQLQNY DPDRALTDYI TRLEALQRRL GTIQSGSTTQ
  3901  FHAGMRR

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against AKAP9 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: 29 nTPM

Expression across tissuesHPA

Tissue

retina: 29 nTPM
liver: 26 nTPM
pancreas: 20 nTPM
pituitary gland: 18 nTPM
small intestine: 18 nTPM
cerebellum: 16 nTPM

Single-cell type

cone photoreceptor cells: 1,923 nCPM
rod photoreceptor cells: 1,210 nCPM
respiratory ciliated cells: 1,088 nCPM
myonuclei: 892 nCPM
corticotrophs: 869 nCPM
somatotrophs: 821 nCPM

Immune cell

plasmacytoid DC: 3.2 nTPM
memory B-cell: 1.9 nTPM
naive B-cell: 1.6 nTPM
gdT-cell: 1.3 nTPM
naive CD4 T-cell: 1.2 nTPM
NK-cell: 1.2 nTPM

Brain region

choroid plexus: 31 nTPM
cerebellum: 30 nTPM
hypothalamus: 23 nTPM
midbrain: 18 nTPM
white matter: 18 nTPM
cerebral cortex: 18 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about AKAP9.

Disease | AllUniProt

Conditions AKAP9 is implicated in, by any mechanism.

Long QT syndrome 11 (LQT11) MIM:611820

Disease | GeneticClinVar

3 pathogenic / likely-pathogenic of 3,707 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

Long QT syndrome
Long QT syndrome 11

Disease | ImmuneIEDB

Conditions an epitope on AKAP9 was assayed in.

skin melanoma T cell

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): 0.4
gnomAD pLI: 0
gnomAD missense Z: -0.13
DepMap mean gene effect: -0.08
DepMap dependency class: none

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 6% 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 AKAP9 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 AKAP9 as an antibody target. Whether an autoantibody or antibody against AKAP9 could matter depends on whether native AKAP9 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

AKAP9 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 AKAP9 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

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