PRKDC
DNA-dependent protein kinase catalytic subunit
Also known as: DNA-PKC, DNA-PKcs, DNAPK, DNAPKc, DNPK1, HYRC, HYRC1, p350, p460, PRKDC_HUMAN, XRCC7
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P78527
- Gene
- PRKDC
- Ensembl
- ENSG00000253729
- Chromosome
- 8
- Canonical length
- 4128 aa
- Protein class
- Cancer-related genes, Disease related genes, Enzymes, Human disease related genes, Plasma proteins, Potential drug targets, Predicted intracellular proteins
- Subcellular location
- Nucleoplasm
OverviewNCBI Gene
This gene encodes the catalytic subunit of the DNA-dependent protein kinase (DNA-PK). It functions with the Ku70/Ku80 heterodimer protein in DNA double strand break repair and recombination. The protein encoded is a member of the PI3/PI4-kinase family.[provided by RefSeq, Jul 2010]
Canonical amino-acid sequenceUniProt
4128 residues, UniProt reviewed canonical sequence.
>P78527|PRKDC
1 MAGSGAGVRC SLLRLQETLS AADRCGAALA GHQLIRGLGQ ECVLSSSPAV LALQTSLVFS
61 RDFGLLVFVR KSLNSIEFRE CREEILKFLC IFLEKMGQKI APYSVEIKNT CTSVYTKDRA
121 AKCKIPALDL LIKLLQTFRS SRLMDEFKIG ELFSKFYGEL ALKKKIPDTV LEKVYELLGL
181 LGEVHPSEMI NNAENLFRAF LGELKTQMTS AVREPKLPVL AGCLKGLSSL LCNFTKSMEE
241 DPQTSREIFN FVLKAIRPQI DLKRYAVPSA GLRLFALHAS QFSTCLLDNY VSLFEVLLKW
301 CAHTNVELKK AALSALESFL KQVSNMVAKN AEMHKNKLQY FMEQFYGIIR NVDSNNKELS
361 IAIRGYGLFA GPCKVINAKD VDFMYVELIQ RCKQMFLTQT DTGDDRVYQM PSFLQSVASV
421 LLYLDTVPEV YTPVLEHLVV MQIDSFPQYS PKMQLVCCRA IVKVFLALAA KGPVLRNCIS
481 TVVHQGLIRI CSKPVVLPKG PESESEDHRA SGEVRTGKWK VPTYKDYVDL FRHLLSSDQM
541 MDSILADEAF FSVNSSSESL NHLLYDEFVK SVLKIVEKLD LTLEIQTVGE QENGDEAPGV
601 WMIPTSDPAA NLHPAKPKDF SAFINLVEFC REILPEKQAE FFEPWVYSFS YELILQSTRL
661 PLISGFYKLL SITVRNAKKI KYFEGVSPKS LKHSPEDPEK YSCFALFVKF GKEVAVKMKQ
721 YKDELLASCL TFLLSLPHNI IELDVRAYVP ALQMAFKLGL SYTPLAEVGL NALEEWSIYI
781 DRHVMQPYYK DILPCLDGYL KTSALSDETK NNWEVSALSR AAQKGFNKVV LKHLKKTKNL
841 SSNEAISLEE IRIRVVQMLG SLGGQINKNL LTVTSSDEMM KSYVAWDREK RLSFAVPFRE
901 MKPVIFLDVF LPRVTELALT ASDRQTKVAA CELLHSMVMF MLGKATQMPE GGQGAPPMYQ
961 LYKRTFPVLL RLACDVDQVT RQLYEPLVMQ LIHWFTNNKK FESQDTVALL EAILDGIVDP
1021 VDSTLRDFCG RCIREFLKWS IKQITPQQQE KSPVNTKSLF KRLYSLALHP NAFKRLGASL
1081 AFNNIYREFR EEESLVEQFV FEALVIYMES LALAHADEKS LGTIQQCCDA IDHLCRIIEK
1141 KHVSLNKAKK RRLPRGFPPS ASLCLLDLVK WLLAHCGRPQ TECRHKSIEL FYKFVPLLPG
1201 NRSPNLWLKD VLKEEGVSFL INTFEGGGCG QPSGILAQPT LLYLRGPFSL QATLCWLDLL
1261 LAALECYNTF IGERTVGALQ VLGTEAQSSL LKAVAFFLES IAMHDIIAAE KCFGTGAAGN
1321 RTSPQEGERY NYSKCTVVVR IMEFTTTLLN TSPEGWKLLK KDLCNTHLMR VLVQTLCEPA
1381 SIGFNIGDVQ VMAHLPDVCV NLMKALKMSP YKDILETHLR EKITAQSIEE LCAVNLYGPD
1441 AQVDRSRLAA VVSACKQLHR AGLLHNILPS QSTDLHHSVG TELLSLVYKG IAPGDERQCL
1501 PSLDLSCKQL ASGLLELAFA FGGLCERLVS LLLNPAVLST ASLGSSQGSV IHFSHGEYFY
1561 SLFSETINTE LLKNLDLAVL ELMQSSVDNT KMVSAVLNGM LDQSFRERAN QKHQGLKLAT
1621 TILQHWKKCD SWWAKDSPLE TKMAVLALLA KILQIDSSVS FNTSHGSFPE VFTTYISLLA
1681 DTKLDLHLKG QAVTLLPFFT SLTGGSLEEL RRVLEQLIVA HFPMQSREFP PGTPRFNNYV
1741 DCMKKFLDAL ELSQSPMLLE LMTEVLCREQ QHVMEELFQS SFRRIARRGS CVTQVGLLES
1801 VYEMFRKDDP RLSFTRQSFV DRSLLTLLWH CSLDALREFF STIVVDAIDV LKSRFTKLNE
1861 STFDTQITKK MGYYKILDVM YSRLPKDDVH AKESKINQVF HGSCITEGNE LTKTLIKLCY
1921 DAFTENMAGE NQLLERRRLY HCAAYNCAIS VICCVFNELK FYQGFLFSEK PEKNLLIFEN
1981 LIDLKRRYNF PVEVEVPMER KKKYIEIRKE AREAANGDSD GPSYMSSLSY LADSTLSEEM
2041 SQFDFSTGVQ SYSYSSQDPR PATGRFRRRE QRDPTVHDDV LELEMDELNR HECMAPLTAL
2101 VKHMHRSLGP PQGEEDSVPR DLPSWMKFLH GKLGNPIVPL NIRLFLAKLV INTEEVFRPY
2161 AKHWLSPLLQ LAASENNGGE GIHYMVVEIV ATILSWTGLA TPTGVPKDEV LANRLLNFLM
2221 KHVFHPKRAV FRHNLEIIKT LVECWKDCLS IPYRLIFEKF SGKDPNSKDN SVGIQLLGIV
2281 MANDLPPYDP QCGIQSSEYF QALVNNMSFV RYKEVYAAAA EVLGLILRYV MERKNILEES
2341 LCELVAKQLK QHQNTMEDKF IVCLNKVTKS FPPLADRFMN AVFFLLPKFH GVLKTLCLEV
2401 VLCRVEGMTE LYFQLKSKDF VQVMRHRDDE RQKVCLDIIY KMMPKLKPVE LRELLNPVVE
2461 FVSHPSTTCR EQMYNILMWI HDNYRDPESE TDNDSQEIFK LAKDVLIQGL IDENPGLQLI
2521 IRNFWSHETR LPSNTLDRLL ALNSLYSPKI EVHFLSLATN FLLEMTSMSP DYPNPMFEHP
2581 LSECEFQEYT IDSDWRFRST VLTPMFVETQ ASQGTLQTRT QEGSLSARWP VAGQIRATQQ
2641 QHDFTLTQTA DGRSSFDWLT GSSTDPLVDH TSPSSDSLLF AHKRSERLQR APLKSVGPDF
2701 GKKRLGLPGD EVDNKVKGAA GRTDLLRLRR RFMRDQEKLS LMYARKGVAE QKREKEIKSE
2761 LKMKQDAQVV LYRSYRHGDL PDIQIKHSSL ITPLQAVAQR DPIIAKQLFS SLFSGILKEM
2821 DKFKTLSEKN NITQKLLQDF NRFLNTTFSF FPPFVSCIQD ISCQHAALLS LDPAAVSAGC
2881 LASLQQPVGI RLLEEALLRL LPAELPAKRV RGKARLPPDV LRWVELAKLY RSIGEYDVLR
2941 GIFTSEIGTK QITQSALLAE ARSDYSEAAK QYDEALNKQD WVDGEPTEAE KDFWELASLD
3001 CYNHLAEWKS LEYCSTASID SENPPDLNKI WSEPFYQETY LPYMIRSKLK LLLQGEADQS
3061 LLTFIDKAMH GELQKAILEL HYSQELSLLY LLQDDVDRAK YYIQNGIQSF MQNYSSIDVL
3121 LHQSRLTKLQ SVQALTEIQE FISFISKQGN LSSQVPLKRL LNTWTNRYPD AKMDPMNIWD
3181 DIITNRCFFL SKIEEKLTPL PEDNSMNVDQ DGDPSDRMEV QEQEEDISSL IRSCKFSMKM
3241 KMIDSARKQN NFSLAMKLLK ELHKESKTRD DWLVSWVQSY CRLSHCRSRS QGCSEQVLTV
3301 LKTVSLLDEN NVSSYLSKNI LAFRDQNILL GTTYRIIANA LSSEPACLAE IEEDKARRIL
3361 ELSGSSSEDS EKVIAGLYQR AFQHLSEAVQ AAEEEAQPPS WSCGPAAGVI DAYMTLADFC
3421 DQQLRKEEEN ASVIDSAELQ AYPALVVEKM LKALKLNSNE ARLKFPRLLQ IIERYPEETL
3481 SLMTKEISSV PCWQFISWIS HMVALLDKDQ AVAVQHSVEE ITDNYPQAIV YPFIISSESY
3541 SFKDTSTGHK NKEFVARIKS KLDQGGVIQD FINALDQLSN PELLFKDWSN DVRAELAKTP
3601 VNKKNIEKMY ERMYAALGDP KAPGLGAFRR KFIQTFGKEF DKHFGKGGSK LLRMKLSDFN
3661 DITNMLLLKM NKDSKPPGNL KECSPWMSDF KVEFLRNELE IPGQYDGRGK PLPEYHVRIA
3721 GFDERVTVMA SLRRPKRIII RGHDEREHPF LVKGGEDLRQ DQRVEQLFQV MNGILAQDSA
3781 CSQRALQLRT YSVVPMTSRL GLIEWLENTV TLKDLLLNTM SQEEKAAYLS DPRAPPCEYK
3841 DWLTKMSGKH DVGAYMLMYK GANRTETVTS FRKRESKVPA DLLKRAFVRM STSPEAFLAL
3901 RSHFASSHAL ICISHWILGI GDRHLNNFMV AMETGGVIGI DFGHAFGSAT QFLPVPELMP
3961 FRLTRQFINL MLPMKETGLM YSIMVHALRA FRSDPGLLTN TMDVFVKEPS FDWKNFEQKM
4021 LKKGGSWIQE INVAEKNWYP RQKICYAKRK LAGANPAVIT CDELLLGHEK APAFRDYVAV
4081 ARGSKDHNIR AQEPESGLSE ETQVKCLMDQ ATDPNILGRT WEGWEPWMLocalizationUniProt · AlphaFold · HPA
Whether an antibody against PRKDC 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
- thymus: 29 nTPM
- skeletal muscle: 25 nTPM
- esophagus: 23 nTPM
- retina: 23 nTPM
- endometrium: 20 nTPM
- ovary: 19 nTPM
Single-cell type
- neutrophils: 1,216 nCPM
- erythrocyte progenitors: 780 nCPM
- megakaryocyte progenitors: 512 nCPM
- monocyte progenitors: 415 nCPM
- megakaryocyte-erythroid progenitors: 364 nCPM
- thyrotrophs: 225 nCPM
Immune cell
- neutrophil: 14 nTPM
- naive B-cell: 10 nTPM
- plasmacytoid DC: 8.9 nTPM
- NK-cell: 8.8 nTPM
- non-classical monocyte: 7.8 nTPM
- memory B-cell: 7.6 nTPM
Brain region
- white matter: 51 nTPM
- cerebral cortex: 47 nTPM
- choroid plexus: 46 nTPM
- medulla oblongata: 45 nTPM
- basal ganglia: 45 nTPM
- spinal cord: 45 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about PRKDC.
Disease | AllUniProt
Conditions PRKDC is implicated in, by any mechanism.
- Immunodeficiency 26 with or without neurologic abnormalities (IMD26) MIM:615966
Disease | GeneticClinVar
3 pathogenic / likely-pathogenic of 5,088 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Severe combined immunodeficiency due to DNA-PKcs deficiency
- IMMUNODEFICIENCY 26 WITHOUT NEUROLOGIC ABNORMALITIES
Disease | ImmuneIEDB
Conditions an epitope on PRKDC was assayed in.
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)
- 0.05
- gnomAD pLI
- 1
- gnomAD missense Z
- 2.76
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 10% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- activation of innate immune response
- B cell lineage commitment
- brain development
- cellular response to insulin stimulus
- DNA damage response
- double-strand break repair
- double-strand break repair via alternative nonhomologous end joining
- double-strand break repair via nonhomologous end joining
- ectopic germ cell programmed cell death
- heart development
- immature B cell differentiation
- immunoglobulin V(D)J recombination
- innate immune response
- intrinsic apoptotic signaling pathway in response to DNA damage
- maturation of 5.8S rRNA
- mitotic G1 DNA damage checkpoint signaling
- negative regulation of apoptotic process
- negative regulation of cGAS/STING signaling pathway
- negative regulation of protein phosphorylation
- peptidyl-serine phosphorylation
- peptidyl-threonine phosphorylation
- positive regulation of apoptotic process
- positive regulation of double-strand break repair via nonhomologous end joining
- positive regulation of erythrocyte differentiation
- positive regulation of lymphocyte differentiation
- positive regulation of platelet formation
- positive regulation of transcription by RNA polymerase II
- positive regulation of translation
- pro-B cell differentiation
- protein destabilization
- protein modification process
- protein phosphorylation
- regulation of circadian rhythm
- regulation of epithelial cell proliferation
- regulation of hematopoietic stem cell differentiation
- regulation of smooth muscle cell proliferation
- response to gamma radiation
- rhythmic process
- small-subunit processome assembly
- somitogenesis
- T cell differentiation in thymus
- T cell lineage commitment
- T cell receptor V(D)J recombination
- telomere capping
- telomere maintenance
Molecular functions
- ATP binding
- DNA-dependent protein kinase activity
- double-stranded DNA binding
- enzyme binding
- histone H2AXS139 kinase activity
- protein domain specific binding
- protein kinase activity
- protein serine kinase activity
- protein serine/threonine kinase activity
- RNA binding
- RNA polymerase II-specific DNA-binding transcription factor binding
- U3 snoRNA binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Phosphatidylinositol 3-/4-kinase, catalytic domain
- PIK-related kinase, FAT
- FATC domain
- Protein kinase-like domain superfamily
- Armadillo-like helical
- PIK-related kinase, FAT domain
- Armadillo-type fold
- Phosphatidylinositol 3-/4-kinase, conserved site
- Phosphatidylinositol 3-/4-kinase, catalytic domain superfamily
- DNA Damage Response and Repair Kinase
- Phosphatidylinositol 3- and 4-kinase
- FAT domain
- FATC domain
- DNA-dependent protein kinase catalytic subunit, CC3
- DNA-dependent protein kinase catalytic subunit, catalytic domain
- DNA-dependent protein kinase catalytic subunit, CC5
- DNA-dependent protein kinase catalytic subunit, CC1/2
- DNA-PKcs, N-terminal
- DNA-dependent protein kinase catalytic subunit, CC3
- DNA-PKcs, CC5
- DNA-PKcs, N-terminal
- DNA-dependent protein kinase catalytic subunit, CC1/2
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of PRKDC 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 PRKDC as an antibody target. Whether an autoantibody or antibody against PRKDC could matter depends on whether native PRKDC is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
PRKDC 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 PRKDC as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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