Seroatlas · Human Serome Atlas

DNAH9

Dynein axonemal heavy chain 9

Also known as: DNAH17L, Dnahc9, DNAL1, DYH9, DYH9_HUMAN, HL-20, HL20, KIAA0357

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

Protein identityUniProt · HPA

UniProt accession: Q9NYC9
Gene: DNAH9
Ensembl: ENSG00000007174
Chromosome: 17
Canonical length: 4486 aa
Protein class: Disease related genes, Human disease related genes, Plasma proteins, Predicted intracellular proteins
Subcellular location: Cytosol,Flagellar centriole,End piece

OverviewNCBI Gene

This gene encodes the heavy chain subunit of axonemal dynein, a large multi-subunit molecular motor. Axonemal dynein attaches to microtubules and hydrolyzes ATP to mediate the movement of cilia and flagella. The gene expresses at least two transcript variants; additional variants have been described, but their full length nature has not been determined. [provided by RefSeq, Jul 2008]

Canonical amino-acid sequenceUniProt

4486 residues, UniProt reviewed canonical sequence.

>Q9NYC9|DNAH9
     1  MRLAEERAAL AAENADGEPG ADRRLRLLGT YVAMSLRPAA GAWERCAGSA EAEQLLQAFL
    61  GRDAAEGPRP LLVVRPGPRG LAIRPGLEVG PESGLAGAKA LFFLRTGPEP PGPDSFRGAV
   121  VCGDLPAAPL EHLAALFSEV VLPVLANEKN RLNWPHMICE DVRRHAHSLQ CDLSVILEQV
   181  KGKTLLPLPA GSEKMEFADS KSETVLDSID KSVIYAIESA VIKWSYQVQV VLKRESSQPL
   241  LQGENPTPKV ELEFWKSRYE DLKYIYNQLR TITVRGMAKL LDKLQSSYFP AFKAMYRDVV
   301  AALAEAQDIH VHLIPLQRHL EALENAEFPE VKPQLRPLLH VVCLIWATCK SYRSPGRLTV
   361  LLQEICNLLI QQASNYLSPE DLLRSEVEES QRKLQVVSDT LSFFKQEFQD RRENLHTYFK
   421  ENQEVKEWDF QSSLVFVRLD GFLGQLHVVE GLLKTALDFH KLGKVEFSGV RGNALSQQVQ
   481  QMHEEFQEMY RLLSGSSSDC LYLQSTDFEN DVSEFNQKVE DLDRRLGTIF IQAFDDAPGL
   541  EHAFKLLDIA GNLLERPLVA RDTSDKYLVL IQMFNKDLDA VRMIYSQHVQ EEAELGFSPV
   601  HKNMPTVAGG LRWAQELRQR IQGPFSNFGR ITHPCMESAE GKRMQQKYED MLSLLEKYET
   661  RLYEDWCRTV SEKSQYNLSQ PLLKRDPETK EITINFNPQL ISVLKEMSYL EPREMKHMPE
   721  TAAAMFSSRD FYRQLVANLE LMANWYNKVM KTLLEVEFPL VEEELQNIDL RLRAAEETLN
   781  WKTEGICDYV TEITSSIHDL EQRIQKTKDN VEEIQNIMKT WVTPIFKTKD GKRESLLSLD
   841  DRHDRMEKYY NLIKESGLKI HALVQENLGL FSADPTSNIW KTYVNSIDNL LLNGFFLAIE
   901  CSLKYLLENT ECKAGLTPIF EAQLSLAIPE LVFYPSLESG VKGGFCDIVE GLITSIFRIP
   961  SLVPRLSPQN GSPHYQVDLD GIPDLANMRR TLMERVQRMM GLCCGYQSTF SQYSYLYVED
  1021  RKEVLGQFLL YGHILTPEEI EDHVEDGIPE NPPLLSQFKV QIDSYETLYE EVCRLEPIKV
  1081  FDGWMKIDIR PFKASLLNII KRWSLLFKQH LVDHVTHSLA NLDAFIKKSE SGLLKKVEKG
  1141  DFQGLVEIMG HLMAVKERQS NTDEMFEPLK QTIELLKTYE QELPETVFKQ LEELPEKWNN
  1201  IKKVAITVKQ QVAPLQANEV TLLRQRCTAF DAEQQQFWEQ FHKEAPFRFD SIHPHQMLDA
  1261  RHIEIQQMES TMASISESAS LFEVNVPDYK QLRQCRKEVC QLKELWDTIG MVTSSIHAWE
  1321  TTPWRNINVE AMELECKQFA RHIRNLDKEV RAWDAFTGLE STVWNTLSSL RAVAELQNPA
  1381  IRERHWRQLM QATGVSFTMD QDTTLAHLLQ LQLHHYEDEV RGIVDKAAKE MGMEKTLKEL
  1441  QTTWAGMEFQ YEPHPRTNVP LLCSDEDLIE VLEDNQVQLQ NLVMSKYVAF FLEEVSGWQK
  1501  KLSTVDAVIS IWFEVQRTWT HLESIFTGSE DIRAQLPQDS KRFEGIDIDF KELAYDAQKI
  1561  PNVVQTTNKP GLYEKLEDIQ GRLCLCEKAL AEYLDTKRLA FPRFYFLSSS DLLDILSNGT
  1621  APQQVQRHLS KLFDNMAKMR FQLDASGEPT KTSLGMYSKE EEYVAFSEPC DCSGQVEIWL
  1681  NHVLGHMKAT VRHEMTEGVT AYEEKPREQW LFDHPAQVAL TCTQIWWTTE VGMAFARLEE
  1741  GYESAMKDYY KKQVAQLKTL ITMLIGQLSK GDRQKIMTIC TIDVHARDVV AKMIAQKVDN
  1801  AQAFLWLSQL RHRWDDEVKH CFANICDAQF LYSYEYLGNT PRLVITPLTD RCYITLTQSL
  1861  HLTMSGAPAG PAGTGKTETT KDLGRALGIL VYVFNCSEQM DYKSCGNIYK GLAQTGAWGC
  1921  FDEFNRISVE VLSVVAVQVK SIQDAIRDKK QWFSFLGEEI SLNPSVGIFI TMNPGYAGRT
  1981  ELPENLKSLF RPCAMVVPDF ELICEIMLVA EGFIEAQSLA RKFITLYQLC KELLSKQDHY
  2041  DWGLRAIKSV LVVAGSLKRG DPDRPEDQVL MRSLRDFNIP KIVTDDMPIF MGLIGDLFPA
  2101  LDVPRRRDPN FEALVRKAIV DLKLQAEDNF VLKVVQLEEL LAVRHSVFVV GGAGTGKSQV
  2161  LRSLHKTYQI MKRRPVWTDL NPKAVTNDEL FGIINPATGE WKDGLFSSIM RELANITHDG
  2221  PKWILLDGDI DPMWIESLNT VMDDNKVLTL ASNERIPLNP TMKLLFEISH LRTATPATVS
  2281  RAGILYINPA DLGWNPPVSS WIEKREIQTE RANLTILFDK YLPTCLDTLR TRFKKIIPIP
  2341  EQSMVQMVCH LLECLLTTED IPADCPKEIY EHYFVFAAIW AFGGAMVQDQ LVDYRAEFSK
  2401  WWLTEFKTVK FPSQGTIFDY YIDPETKKFE PWSKLVPQFE FDPEMPLQAC LVHTSETIRV
  2461  CYFMERLMAR QRPVMLVGTA GTGKSVLVGA KLASLDPEAY LVKNVPFNYY TTSAMLQAVL
  2521  EKPLEKKAGR NYGPPGNKKL IYFIDDMNMP EVDAYGTVQP HTIIRQHLDY GHWYDRSKLS
  2581  LKEITNVQYV SCMNPTAGSF TINPRLQRHF SVFVLSFPGA DALSSIYSII LTQHLKLGNF
  2641  PASLQKSIPP LIDLALAFHQ KIATTFLPTG IKFHYIFNLR DFANIFQGIL FSSVECVKST
  2701  WDLIRLYLHE SNRVYRDKMV EEKDFDLFDK IQTEVLKKTF DDIEDPVEQT QSPNLYCHFA
  2761  NGIGEPKYMP VQSWELLTQT LVEALENHNE VNTVMDLVLF EDAMRHVCHI NRILESPRGN
  2821  ALLVGVGGSG KQSLTRLAAF ISSMDVFQIT LRKGYQIQDF KMDLASLCLK AGVKNLNTVF
  2881  LMTDAQVADE RFLVLINDLL ASGEIPDLYS DDEVENIISN VRNEVKSQGL VDNRENCWKF
  2941  FIDRIRRQLK VTLCFSPVGN KLRVRSRKFP AIVNCTAIHW FHEWPQQALE SVSLRFLQNT
  3001  EGIEPTVKQS ISKFMAFVHT SVNQTSQSYL SNEQRYNYTT PKSFLEFIRL YQSLLHRHRK
  3061  ELKCKTERLE NGLLKLHSTS AQVDDLKAKL AAQEVELKQK NEDADKLIQV VGVETDKVSR
  3121  EKAMADEEEQ KVAVIMLEVK QKQKDCEEDL AKAEPALTAA QAALNTLNKT NLTELKSFGS
  3181  PPLAVSNVSA AVMVLMAPRG RVPKDRSWKA AKVTMAKVDG FLDSLINFNK ENIHENCLKA
  3241  IRPYLQDPEF NPEFVATKSY AAAGLCSWVI NIVRFYEVFC DVEPKRQALN KATADLTAAQ
  3301  EKLAAIKAKI AHLNENLAKL TARFEKATAD KLKCQQEAEV TAVTISLANR LVGGLASENV
  3361  RWADAVQNFK QQERTLCGDI LLITAFISYL GFFTKKYRQS LLDRTWRPYL SQLKTPIPVT
  3421  PALDPLRMLM DDADVAAWQN EGLPADRMSV ENATILINCE RWPLMVDPQL QGIKWIKNKY
  3481  GEDLRVTQIG QKGYLQIIEQ ALEAGAVVLI ENLEESIDPV LGPLLGREVI KKGRFIKIGD
  3541  KECEYNPKFR LILHTKLANP HYQPELQAQA TLINFTVTRD GLEDQLLAAV VSMERPDLEQ
  3601  LKSDLTKQQN GFKITLKTLE DSLLSRLSSA SGNFLGETVL VENLEITKQT AAEVEKKVQE
  3661  AKVTEVKINE AREHYRPAAA RASLLYFIMN DLSKIHPMYQ FSLKAFSIVF QKAVERAAPD
  3721  ESLRERVANL IDSITFSVYQ YTIRGLFECD KLTYLAQLTF QILLMNREVN AVELDFLLRS
  3781  PVQTGTASPV EFLSHQAWGA VKVLSSMEEF SNLDRDIEGS AKSWKKFVES ECPEKEKLPQ
  3841  EWKNKTALQR LCMLRAMRPD RMTYALRDFV EEKLGSKYVV GRALDFATSF EESGPATPMF
  3901  FILSPGVDPL KDVESQGRKL GYTFNNQNFH NVSLGQGQEV VAEAALDLAA KKGHWVILQN
  3961  IHLVAKWLST LEKKLEEHSE NSHPEFRVFM SAEPAPSPEG HIIPQGILEN SIKITNEPPT
  4021  GMHANLHKAL DNFTQDTLEM CSRETEFKSI LFALCYFHAV VAERRKFGPQ GWNRSYPFNT
  4081  GDLTISVNVL YNFLEANAKV PYDDLRYLFG EIMYGGHITD DWDRRLCRTY LGEFIRPEML
  4141  EGELSLAPGF PLPGNMDYNG YHQYIDAELP PESPYLYGLH PNAEIGFLTQ TSEKLFRTVL
  4201  ELQPRDSQAR DGAGATREEK VKALLEEILE RVTDEFNIPE LMAKVEERTP YIVVAFQECG
  4261  RMNILTREIQ RSLRELELGL KGELTMTSHM ENLQNALYFD MVPESWARRA YPSTAGLAAW
  4321  FPDLLNRIKE LEAWTGDFTM PSTVWLTGFF NPQSFLTAIM QSTARKNEWP LDQMALQCDM
  4381  TKKNREEFRS PPREGAYIHG LFMEGACWDT QAGIITEAKL KDLTPPMPVM FIKAIPADKQ
  4441  DCRSVYSCPV YKTSQRGPTY VWTFNLKTKE NPSKWVLAGV ALLLQI

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against DNAH9 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: 33 nTPM

Expression across tissuesHPA

Tissue

fallopian tube: 33 nTPM
hippocampal formation: 14 nTPM
choroid plexus: 12 nTPM
hypothalamus: 11 nTPM
basal ganglia: 8.2 nTPM
amygdala: 7.8 nTPM

Single-cell type

ependymal cells: 3,139 nCPM
respiratory ciliated cells: 1,782 nCPM
fallopian tube ciliated cells: 904 nCPM
endometrial ciliated cells: 691 nCPM
epididymal efferent duct ciliated cells: 596 nCPM
choroid plexus epithelial cells: 346 nCPM

Immune cell

basophil: 0 nTPM
classical monocyte: 0 nTPM
eosinophil: 0 nTPM
gdT-cell: 0 nTPM
intermediate monocyte: 0 nTPM
MAIT T-cell: 0 nTPM

Brain region

midbrain: 55 nTPM
choroid plexus: 53 nTPM
medulla oblongata: 47 nTPM
spinal cord: 36 nTPM
pons: 25 nTPM
hippocampal formation: 20 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about DNAH9.

Disease | AllUniProt

Conditions DNAH9 is implicated in, by any mechanism.

Ciliary dyskinesia, primary, 40 (CILD40) MIM:618300

Disease | GeneticClinVar

164 pathogenic / likely-pathogenic of 2,567 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

Ciliary dyskinesia, primary, 40
DNAH9-related disorder
Fetal anomalies with a likely genetic cause
Congenital heart disease
Primary ciliary dyskinesia

Disease | ImmuneIEDB

Conditions an epitope on DNAH9 was assayed in.

human immunodeficiency virus infectious disease 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): 0.72
gnomAD pLI: 0
gnomAD missense Z: -0.04
DepMap mean gene effect: -0.06
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

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

InteractionsUniProt · HPA

Protein binding partners of DNAH9 in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.

ODAD1

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads DNAH9 as an antibody target. Whether an autoantibody or antibody against DNAH9 could matter depends on whether native DNAH9 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

DNAH9 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 DNAH9 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

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