CENPE
Centromere-associated protein E
Also known as: CENPE_HUMAN, KIF10, PPP1R61
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q02224
- Gene
- CENPE
- Ensembl
- ENSG00000138778
- Chromosome
- 4
- Canonical length
- 2701 aa
- Protein class
- Disease related genes, Human disease related genes, Plasma proteins, Predicted intracellular proteins
- Subcellular location
- Microtubules,Cytokinetic bridge,Mitotic spindle
OverviewNCBI Gene
Centrosome-associated protein E (CENPE) is a kinesin-like motor protein that accumulates in the G2 phase of the cell cycle. Unlike other centrosome-associated proteins, it is not present during interphase and first appears at the centromere region of chromosomes during prometaphase. This protein is required for stable spindle microtubule capture at kinetochores which is a necessary step in chromosome alignment during prometaphase. This protein also couples chromosome position to microtubule depolymerizing activity. Alternative splicing results in multiple transcript variants encoding distinct protein isoforms. [provided by RefSeq, Nov 2014]
Canonical amino-acid sequenceUniProt
2701 residues, UniProt reviewed canonical sequence.
>Q02224|CENPE
1 MAEEGAVAVC VRVRPLNSRE ESLGETAQVY WKTDNNVIYQ VDGSKSFNFD RVFHGNETTK
61 NVYEEIAAPI IDSAIQGYNG TIFAYGQTAS GKTYTMMGSE DHLGVIPRAI HDIFQKIKKF
121 PDREFLLRVS YMEIYNETIT DLLCGTQKMK PLIIREDVNR NVYVADLTEE VVYTSEMALK
181 WITKGEKSRH YGETKMNQRS SRSHTIFRMI LESREKGEPS NCEGSVKVSH LNLVDLAGSE
241 RAAQTGAAGV RLKEGCNINR SLFILGQVIK KLSDGQVGGF INYRDSKLTR ILQNSLGGNA
301 KTRIICTITP VSFDETLTAL QFASTAKYMK NTPYVNEVST DEALLKRYRK EIMDLKKQLE
361 EVSLETRAQA MEKDQLAQLL EEKDLLQKVQ NEKIENLTRM LVTSSSLTLQ QELKAKRKRR
421 VTWCLGKINK MKNSNYADQF NIPTNITTKT HKLSINLLRE IDESVCSESD VFSNTLDTLS
481 EIEWNPATKL LNQENIESEL NSLRADYDNL VLDYEQLRTE KEEMELKLKE KNDLDEFEAL
541 ERKTKKDQEM QLIHEISNLK NLVKHAEVYN QDLENELSSK VELLREKEDQ IKKLQEYIDS
601 QKLENIKMDL SYSLESIEDP KQMKQTLFDA ETVALDAKRE SAFLRSENLE LKEKMKELAT
661 TYKQMENDIQ LYQSQLEAKK KMQVDLEKEL QSAFNEITKL TSLIDGKVPK DLLCNLELEG
721 KITDLQKELN KEVEENEALR EEVILLSELK SLPSEVERLR KEIQDKSEEL HIITSEKDKL
781 FSEVVHKESR VQGLLEEIGK TKDDLATTQS NYKSTDQEFQ NFKTLHMDFE QKYKMVLEEN
841 ERMNQEIVNL SKEAQKFDSS LGALKTELSY KTQELQEKTR EVQERLNEME QLKEQLENRD
901 STLQTVEREK TLITEKLQQT LEEVKTLTQE KDDLKQLQES LQIERDQLKS DIHDTVNMNI
961 DTQEQLRNAL ESLKQHQETI NTLKSKISEE VSRNLHMEEN TGETKDEFQQ KMVGIDKKQD
1021 LEAKNTQTLT ADVKDNEIIE QQRKIFSLIQ EKNELQQMLE SVIAEKEQLK TDLKENIEMT
1081 IENQEELRLL GDELKKQQEI VAQEKNHAIK KEGELSRTCD RLAEVEEKLK EKSQQLQEKQ
1141 QQLLNVQEEM SEMQKKINEI ENLKNELKNK ELTLEHMETE RLELAQKLNE NYEEVKSITK
1201 ERKVLKELQK SFETERDHLR GYIREIEATG LQTKEELKIA HIHLKEHQET IDELRRSVSE
1261 KTAQIINTQD LEKSHTKLQE EIPVLHEEQE LLPNVKEVSE TQETMNELEL LTEQSTTKDS
1321 TTLARIEMER LRLNEKFQES QEEIKSLTKE RDNLKTIKEA LEVKHDQLKE HIRETLAKIQ
1381 ESQSKQEQSL NMKEKDNETT KIVSEMEQFK PKDSALLRIE IEMLGLSKRL QESHDEMKSV
1441 AKEKDDLQRL QEVLQSESDQ LKENIKEIVA KHLETEEELK VAHCCLKEQE ETINELRVNL
1501 SEKETEISTI QKQLEAINDK LQNKIQEIYE KEEQFNIKQI SEVQEKVNEL KQFKEHRKAK
1561 DSALQSIESK MLELTNRLQE SQEEIQIMIK EKEEMKRVQE ALQIERDQLK ENTKEIVAKM
1621 KESQEKEYQF LKMTAVNETQ EKMCEIEHLK EQFETQKLNL ENIETENIRL TQILHENLEE
1681 MRSVTKERDD LRSVEETLKV ERDQLKENLR ETITRDLEKQ EELKIVHMHL KEHQETIDKL
1741 RGIVSEKTNE ISNMQKDLEH SNDALKAQDL KIQEELRIAH MHLKEQQETI DKLRGIVSEK
1801 TDKLSNMQKD LENSNAKLQE KIQELKANEH QLITLKKDVN ETQKKVSEME QLKKQIKDQS
1861 LTLSKLEIEN LNLAQKLHEN LEEMKSVMKE RDNLRRVEET LKLERDQLKE SLQETKARDL
1921 EIQQELKTAR MLSKEHKETV DKLREKISEK TIQISDIQKD LDKSKDELQK KIQELQKKEL
1981 QLLRVKEDVN MSHKKINEME QLKKQFEAQN LSMQSVRMDN FQLTKKLHES LEEIRIVAKE
2041 RDELRRIKES LKMERDQFIA TLREMIARDR QNHQVKPEKR LLSDGQQHLT ESLREKCSRI
2101 KELLKRYSEM DDHYECLNRL SLDLEKEIEF QKELSMRVKA NLSLPYLQTK HIEKLFTANQ
2161 RCSMEFHRIM KKLKYVLSYV TKIKEEQHES INKFEMDFID EVEKQKELLI KIQHLQQDCD
2221 VPSRELRDLK LNQNMDLHIE EILKDFSESE FPSIKTEFQQ VLSNRKEMTQ FLEEWLNTRF
2281 DIEKLKNGIQ KENDRICQVN NFFNNRIIAI MNESTEFEER SATISKEWEQ DLKSLKEKNE
2341 KLFKNYQTLK TSLASGAQVN PTTQDNKNPH VTSRATQLTT EKIRELENSL HEAKESAMHK
2401 ESKIIKMQKE LEVTNDIIAK LQAKVHESNK CLEKTKETIQ VLQDKVALGA KPYKEEIEDL
2461 KMKLVKIDLE KMKNAKEFEK EISATKATVE YQKEVIRLLR ENLRRSQQAQ DTSVISEHTD
2521 PQPSNKPLTC GGGSGIVQNT KALILKSEHI RLEKEISKLK QQNEQLIKQK NELLSNNQHL
2581 SNEVKTWKER TLKREAHKQV TCENSPKSPK VTGTASKKKQ ITPSQCKERN LQDPVPKESP
2641 KSCFFDSRSK SLPSPHPVRY FDNSSLGLCP EVQNAGAESV DSQPGPWHAS SGKDVPECKT
2701 QLocalizationUniProt · AlphaFold · HPA
Whether an antibody against CENPE 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
- 9.4 nTPM
Expression across tissuesHPA
Tissue
- bone marrow: 9.4 nTPM
- thymus: 8.6 nTPM
- lymph node: 5.2 nTPM
- tonsil: 4.6 nTPM
- testis: 3.9 nTPM
- appendix: 2.5 nTPM
Single-cell type
- monocyte progenitors: 281 nCPM
- erythrocyte progenitors: 238 nCPM
- megakaryocyte progenitors: 160 nCPM
- neutrophil progenitors: 108 nCPM
- early primary spermatocytes: 95 nCPM
- differentiating spermatogonia: 80 nCPM
Immune cell
- basophil: 2.9 nTPM
- non-classical monocyte: 1.5 nTPM
- T-reg: 0.6 nTPM
- eosinophil: 0.3 nTPM
- NK-cell: 0.3 nTPM
- intermediate monocyte: 0.2 nTPM
Brain region
- pons: 2.1 nTPM
- hypothalamus: 1.3 nTPM
- thalamus: 1.3 nTPM
- white matter: 1.2 nTPM
- cerebral cortex: 1.1 nTPM
- medulla oblongata: 1.1 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about CENPE.
Disease | AllUniProt
Conditions CENPE is implicated in, by any mechanism.
- Microcephaly 13, primary, autosomal recessive (MCPH13) MIM:616051
Disease | GeneticClinVar
5 pathogenic / likely-pathogenic of 590 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Microcephaly 13, primary, autosomal recessive
Disease | ImmuneIEDB
Conditions an epitope on CENPE was assayed in.
- systemic scleroderma B 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)
- 0.31
- gnomAD pLI
- 0.24
- gnomAD missense Z
- 1.27
- DepMap mean gene effect
- -0.96
- DepMap dependency class
- common
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 5% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- attachment of mitotic spindle microtubules to kinetochore
- cell division
- chromosome segregation
- kinetochore assembly
- metaphase chromosome alignment
- microtubule-based movement
- mitotic cell cycle
- mitotic chromosome movement towards spindle pole
- mitotic metaphase chromosome alignment
- mitotic spindle organization
- positive regulation of protein kinase activity
- regulation of mitotic metaphase/anaphase transition
- lateral attachment of mitotic spindle microtubules to kinetochore
- microtubule plus-end directed mitotic chromosome migration
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of CENPE 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 CENPE as an antibody target. Whether an autoantibody or antibody against CENPE could matter depends on whether native CENPE is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
CENPE 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 CENPE as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
Loading the interactive Seroatlas protein explorer...