Seroatlas · Human Serome Atlas

NBPF10

NBPF family member NBPF10

Also known as: AG1, NBPFA_HUMAN

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

Protein identityUniProt · HPA

UniProt accession
Q6P3W6
Gene
NBPF10
Ensembl
ENSG00000271425
Chromosome
1
Canonical length
3795 aa
Protein class
Cancer-related genes, Predicted intracellular proteins
Subcellular location
Golgi apparatus,Vesicles,Microtubules,Cytokinetic bridge,Primary cilium,Cytosol,Mid piece,Principal piece,End piece

OverviewNCBI Gene

This gene is a member of the neuroblastoma breakpoint family (NBPF) which consists of dozens of recently duplicated genes primarily located in segmental duplications on human chromosome 1. This gene family has experienced its greatest expansion within the human lineage and has expanded, to a lesser extent, among primates in general. Members of this gene family are characterized by tandemly repeated copies of DUF1220 protein domains. Gene copy number variations in the human chromosomal region 1q21.1, where most DUF1220 domains are located, have been implicated in a number of developmental and neurogenetic diseases such as microcephaly, macrocephaly, autism, schizophrenia, cognitive disability, congenital heart disease, neuroblastoma, and congenital kidney and urinary tract anomalies. Altered expression of some gene family members is associated with several types of cancer. This gene family contains numerous pseudogenes. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Oct 2014]

Canonical amino-acid sequenceUniProt

3795 residues, UniProt reviewed canonical sequence.

>Q6P3W6|NBPF10
     1  MVVSAGPWSS EKAEMNILEI NETLRPQLAE KKQQFRSLKE KCFLTQLAGF LANRQKKYKY
    61  EECKDLIKFM LRNERQFKEE KLAEQLKQAE ELRQYKVLVH SQERELTQLR EKLREGRDAS
   121  RSLYEHLQAL LTPDEPDKSQ GQDLQEQLAE GCRLAQHLVQ KLSPENDEDE DEDVQVEEAE
   181  KVLESSAPRE VQKAEESKVP EDSLEECAIT CSNSHGPCDS NQPHKNIKIT FEEDEVNSTL
   241  VVDRESSHDE CQDALNILPV PGPTSSATNV SMVVSAGPLS SEKAEMNILE INEKLRPQLA
   301  EKKQQFRNLK EKCFLTQLSG FLANQQKKYK YEECKDLIKF MLRNERQFKE EKLAEQLKQA
   361  EELRQYKVLV HAQERELTQL KEKLREGRDA SRSLNEHLQA LLTPYEPDKS QGQDLQEQLA
   421  EGCRLAQHLV QKLSPENDND DDEDVQVEVA EKVQKSSAPR EMQKAEEKEV PEDSLEECAI
   481  TYSNSHGSYD SNQPHRKTKI TFEEDKVDST LIGSSSHVEW EDAVHIIPEN ESDDEEEEEK
   541  GPVSPRNLQE SEEEEVPQES WDEGYSTLSI PPEMLASYQS YSSTFHSLEE QQVCMAVDIG
   601  RHRWDQVKKE DQEATGPRLS RELLDEKGPE VLQDSQDRCY STPSGCLELT DSCQPYRSAF
   661  YILEQQRVGL AIDMDEIEKY QEVEEDQDPS CPRLSRELLD EKEPEVLQDS LDRCYSTPSG
   721  YLELPDLGQP YSSAVYSLEE QYLGLALDVD RIKKDQEEEE DQGPPCPRLS RELLEVVEPE
   781  VLQDSLDRCY STPSSCLEQP DSCQPYGSSF YALEEKHVGF SLDVGEIEKK GKGKKRRGRR
   841  SKKERRRGRK EGEEDQNPPC PRLSRELLDE KGPEVLQDSL DRCYSTPSGC LELTDSCQPY
   901  RSAFYVLEQQ RVGFAFDMDE IEKYQEVEED QDPSCPRLSR ELLDEKEPEV LQDSLDRCYS
   961  TPSGYLELPD LGQPYSSAVY SLEEQYLGLA LDVDRIKKDE EEEEDQDPPC PRLSRELLEV
  1021  VEPEVLQDSL DRCYSTPSSC LEQPDSCQPY GSSFYALEEN HVGFSLDVGE IEKKGKGKKR
  1081  RGRRSKKERR RGRKEGEEDQ NPPCPRLSRE LLEEKGPEVL QDSLDRCYST PSGCLELTDS
  1141  CQPYRSAFYV LEQQRVGFAV DMDEIEKYQE VEEDQDPSCP RLSRELLDEK EPEVLQDSLD
  1201  RCYSTPSGYL ELPDLGQPYS SAVYSLEEQY LGLALDVDRI KKDEEEEEDQ DPPCPRLSRE
  1261  LLEVVEPEVL QDSLDRCYST PSSCLEQPDS CQPYGSSFYA LEEKHVGFSL DVGEIEKKGK
  1321  GKKRRGRRSK KERRRGRKEG EEDQNPPCPR LSRELLEEKG PEVLQDSLDR CYSTPSGCLE
  1381  LTDSCQPYRS AFYVLEQQRV GFAVDMDEIE KYQEVEEDQD PSCPRLSREL LDEKEPEVLQ
  1441  DSLDRCYSTP SGYLELPDLG QPYSSAVYSL EEQYLGLALD VDRIKKDEEE EEDQDPPCPR
  1501  LSRELLEVVE PEVLQDSLDR CYSTPSSCLE QPDSCQPYGS SFYALEEKHV GFSLDVGEIE
  1561  KKGKGKKRRG RRSKKERRRG RKEGEEDQNP PCPRLSRELL DEKGPEVLQD SLDRCYSTPS
  1621  GCLELTDSCQ PYRSAFYVLE QQHVGLAVDM DEIEKYQEVE EDQDPSCPRL SRELLDEKEP
  1681  EVLQDSLDRC YSTPSGYLEL PDLGQPYSSA VYSLEEQYLG LALDVDRIKK DQEEEEDQGP
  1741  PCPRLSRELL EVVEPEVLQD SLDRCYSTPS SCLEQPDSCQ PYGSSFYALE EKHVGFSLDV
  1801  GEIEKKGKGK KRRGRRSKKE RRRGRKEGEE DQNPPCPRLS RELLDEKGPE VLQDSLDRCY
  1861  STPSGCLELT DSCQPYRSAF YVLEQQHVGL AVDMDEIEKY QEVEEDQDPS CPRLSRELLD
  1921  EKEPEVLQDS LDRCYSTPSG YLELPDLGQP YSSAVYSLEE QYLGLALDVD RIKKDQEEEE
  1981  DQGPPCPRLS RELLEVVEPE VLQDSLDRCY STPSSCLEQP DSCQPYGSSF YALEEKHVGF
  2041  SLDVGEIEKK GKGKKRRGRR SKKERRRGRK EGEEDQNPPC PRLSRELLDE KGPEVLQDSL
  2101  DRCYSTPSGC LELTDSCQPY RSAFYVLEQQ HVGLAVDMDE IEKYQEVEED QDPSCPRLSR
  2161  ELLDEKEPEV LQDSLDRCYS TPSGYLELPD LGQPYSSAVY SLEEQYLGLA LDVDRIKKDQ
  2221  EEEEDQGPPC PRLSRELLEV VEPEVLQDSL DRCYSTPSSC LEQPDSCQPY GSSFYALEEK
  2281  HVGFSLDVGE IEKKGKGKKR RGRRSKKERR RGRKEGEEDQ NPPCPRLSRE LLDEKGPEVL
  2341  QDSLDRCYST PSGCLELTDS CQPYRSAFYV LEQQHVGLAV DMDEIEKYQE VEEDQDPSCP
  2401  RLSRELLDEK EPEVLQDSLD RCYSTPSGYL ELPDLGQPYS SAVYSLEEQY LGLALDVDRI
  2461  KKDQEEEEDQ DPPCPRLSRE LLEVVEPEVL QDSLDRCYST PSSCLEQPDS CQPYGSSFYA
  2521  LEEKHVGFSL DVGEIEKKGK GKKRRGRRSK KERRRGRKEG EEDQNPPCPR LSRELLDEKG
  2581  PEVLQDSLDR CYSTPSGCLE LTDSCQPYRS AFYVLEQQHV GLAVDMDEIE KYQEVEEDQD
  2641  PSCPRLSREL LDEKEPEVLQ DSLDRCYSTP SGYLELPDLG QPYSSAVYSL EEQYLGLALD
  2701  VDRIKKDQEE EEDQGPPCPR LSRELLEVVE PEVLQDSLDR CYSTPSSCLE QPDSCQPYGS
  2761  SFYALEEKHV GFSLDVGEIE KKGKGKKRRG RRSKKERRRG RKEGEEDQNP PCPRLSRELL
  2821  DEKGPEVLQD SLDRCYSTPS GCLELTDSCQ PYRSAFYVLE QQHVGLAVDM DEIEKYQEVE
  2881  EDQDPSCPRL SRELLDEKEP EVLQDSLDRC YSTPSGYLEL PDLGQPYSSA VYSLEEQYLG
  2941  LALDVDRIKK DQEEEEDQGP PCPRLSRELL EVVEPEVLQD SLDRCYSTPS SCLEQPDSCQ
  3001  PYGSSFYALE EKHVGFSLDV GEIEKKGKGK KRRGRRSKKE RRRGRKEGEE DQNPPCPRLS
  3061  RELLDEKGPE VLQDSLDRCY STPSGCLELT DSCQPYRSAF YVLEQQHVGL AVDMDEIEKY
  3121  QEVEEDQDPS CPRLSRELLD EKEPEVLQDS LDRCYSTPSG YLELPDLGQP YSSAVYSLEE
  3181  QYLGLALDVD RIKKDEEEEE DQDPPCPRLS RELLEVVEPE VLQDSLDRCY STPSSCLEQP
  3241  DSCQPYGSSF YALEEKHVGF SLDVGEIEKK GKGKKRRGRR SKKERRRGRK EGEEDQNPPC
  3301  PRLSRELLDE KGPEVLQDSL DRCYSTPSGY LELTDSCQPY RSAFYVLEQQ HVGLAVDMDE
  3361  IEKYQEVEED QDPSCPRLSR ELLDEKEPEV LQDSLDRCYS TPSGYLELPD LGQPYSSAVY
  3421  SLEEQYLGLA LDVDRIKKDQ EEEEDQGPPC PRLSRELLEV VEPEVLQDSL DRCYSTPSSC
  3481  LEQPDSCQPY GSSFYALEEK HVGFSLDVGE IEKKGKGKKR RGRRSKKERR RGRKEGEEDQ
  3541  NPPCPRLSRE LLDEKGPEVL QDSLDRCYST PSGCLELCDS CQPYRSAFYV LEQQRVGLAV
  3601  DMDEIEKYQE VEEDQDPSCP RLSRELLDEK EPEVLQDSLD RCYSTPSGYL ELPDLGQPYS
  3661  SAVYSLEEQY LGLALDVDKI EKKGKGKKRR GRRSKKERRR GRKEGEEDQN PPCPRLNGVL
  3721  MEVEEREVLQ DSLDRCYSTP SMYFELPDSF QHYRSVFYSF EEQHISFALY VDNRFFTLTV
  3781  TSLHLVFQMG VIFPQ

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against NBPF10 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)
0.6
Highest tissue expression
7.1 nTPM

Expression across tissuesHPA

Tissue

  • bone marrow: 7.1 nTPM
  • skin: 7 nTPM
  • ovary: 5.1 nTPM
  • cervix: 4.7 nTPM
  • retina: 4.3 nTPM
  • breast: 4.1 nTPM

Single-cell type

  • sertoli cells: 36 nCPM
  • neutrophils: 32 nCPM
  • paneth cells: 31 nCPM
  • leydig cells: 24 nCPM
  • monocytes: 23 nCPM
  • bergmann glia: 21 nCPM

Immune cell

  • neutrophil: 5.6 nTPM
  • eosinophil: 2.8 nTPM
  • non-classical monocyte: 2.3 nTPM
  • plasmacytoid DC: 2.3 nTPM
  • classical monocyte: 2 nTPM
  • memory B-cell: 1.9 nTPM

Brain region

  • choroid plexus: 21 nTPM
  • cerebral cortex: 18 nTPM
  • thalamus: 15 nTPM
  • white matter: 13 nTPM
  • medulla oblongata: 13 nTPM
  • hippocampal formation: 12 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)
1.99
gnomAD pLI
0
gnomAD missense Z
-12

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

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads NBPF10 as an antibody target. Whether an autoantibody or antibody against NBPF10 could matter depends on whether native NBPF10 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

NBPF10 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 NBPF10 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/NBPF10. Study-independent annotations aggregated from UniProt, Human Protein Atlas, PubMed, IEDB, Pfam, InterPro, Gene Ontology, AlphaFold, gnomAD, DepMap, ClinVar, TCGA. Catalog release seroatlas-reviewed-human-uniprot-20260313.

Seroatlas is the reference for exploring autoantibody and antibody serology at the human-protein level: the autoreactome and human serome, multiplex serology (HuProt, HuScan, VirScan, PhIP-Seq).

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