Seroatlas · Human Serome Atlas

TEX15

Testis-expressed protein 15

Also known as: CT42, TEX15_HUMAN

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

Protein identityUniProt · HPA

UniProt accession
Q9BXT5
Gene
TEX15
Ensembl
ENSG00000133863
Chromosome
8
Canonical length
2789 aa
Protein class
Disease related genes, Human disease related genes, Predicted intracellular proteins
Subcellular location
Nucleoplasm,Cytosol

OverviewNCBI Gene

This gene encodes a protein that is required for DNA double-strand break repair, chromosome synapsis, and meiotic recombination in spermatocytes. Male mice with a knockout of the orthologous gene are viable but sterile. Loss-of-function mutations in the orthologous mouse gene cause early meiotic arrest in spermatocytes, before the mid-pachytene stage. Naturally occurring mutations in this gene are associated with nonobstructive azoospermia. [provided by RefSeq, Apr 2017]

Canonical amino-acid sequenceUniProt

2789 residues, UniProt reviewed canonical sequence.

>Q9BXT5|TEX15
     1  MPSDAKDSVN GDLLLNWTSL KNILSGLNAS FPLHNNTGSS TVTTSKSIKD PRLMRREESM
    61  GEQSSTAGLN EVLQFEKSSD NVNSEIKSTP SNSASSSEVV PGDCAVLTNG LDTPCFKTSV
   121  NDSQSWAHNM GSEDYDCIPP NKVTMAGQCK DQGNFSFPIS VSNVVSEVEN QNHSEEKAQR
   181  AQQESGNAYT KEYSSHIFQD SQSSDLKTIY QTGCQTSTVF PLKKKVSIDE YLQNTGKMKN
   241  FADLEDSSKH EEKQTSWKEI DNDFTNETKI SPIDNYIVLH QEYKESESHN SFGKSCDKIL
   301  ITQELEITKS STSTIKDKDE LDHLALEWQI TPSFESLSQK HPQHSVEYEG NIHTSLAIAQ
   361  KLMELKLGKI NQNYASIITE AFPKPKDIPQ AKEMFIDTVI SSYNIETAHD SSNCSITREH
   421  ICVHRKNENE PVSLENIQRD YKETAYVEDR GQDHNLFCNS QLSNDIWLNV NFKKQTDREN
   481  QNEAKENSAS CVENNIENIY GDKKQDSHTN ENFSNIDEKE DKNYHNIEIL SSEEFSTKFN
   541  LICREDNAVS AATALLESEE DTISAVKQKD TENTGRSVEH LASTTFPKTA SSSVCVASNA
   601  AIQIASATMP ALSLNNDDHQ IYQFKETCSS ESPDFGLLVK HRVSDCEIDT DKNKSQESFH
   661  QSINENLVLQ SIELESEIEI ELEDCDDAFI FQQDTHSHEN MLCEEFVTSY KALKSRISWE
   721  GLLALDNGEM EVLESTTGRE NSDQHYSKES NYFYSSTQNN ETELTSPILL PDLQIKITNI
   781  FRPGFSPTAD SLALKDSFCT HVTEATKPEI NKEDGEILGF DIYSQPFGEN ADYPCEDKVD
   841  NIRQESGPVS NSEISLSFDL SRNTDVNHTS ENQNSESLFT EPSNVTTIDD GSRCFFTKSK
   901  TDYNDTKNKK EVESRISKRK LHISSRDQNI PHKDLRRHKI YGRKRRLTSQ DSSECFSSLS
   961  QGRIKTFSQS EKHIKSVLNI LSDEASLCKS KCLSRKLDKA VVHLKKAHRR VHTSLQLITK
  1021  VGEERKGPLP KSYAIICNNF WESCDLQGYS SVSQRKYYST KHFSSKRKYD KRRKKRAPKA
  1081  DISKSLTHVS KHKSYKTSGE KKCLSRKSMA SSVSKSHPTT SHMGEFCNQE HPESQLPVSS
  1141  TSQSTSQSVY YNSSVSNPSL SEEHQPFSGK TAYLFSPDHS DEKLIEKENQ IDTAFLSSTS
  1201  KYEKLEKHSA NHNVKDATKE NSCDANEVIN ESNSVSLSCI KENINSSTGN DCDATCIGHT
  1261  KAKTDVLISV LDSNVKHFLN DLYQQGNLIL SDCKRNLEVK WTDPIERPKQ NIITGNFLMG
  1321  PLNLTLIASK KYSIPQLSAA AVTDSEGESS KSYLDKQRIL TVDSFAASST VPHCEQSCRE
  1381  KELLKTEQCS SGNCLHTDGN ETNVTENYEL DVASGTEEDK SYGENIVELS SSDSSLLLKD
  1441  NVKGSSSETC IVKKDTEDRI TWKVKQAEKA KDSVYKRSMT EGSTVNTEYK NQKNQISEES
  1501  CLNEKIITTN LIDSHLSTKN TTTESVPLKN TVSNPLNKRE KKGEIKVSKD SQSDLTLHSE
  1561  IAYISKPGIL GVNHTPILPA HSETCKVPTL LKKPASYVSD FKEKHCSANH TALIANLSQI
  1621  LQRADEASSL QILQEETKVC LNILPLFVEA FERKQECSVE QILISRELLV DQNLWNNCKH
  1681  TLKPCAVDTL VELQMMMETI QFIENKKRHL EGEPTLRSLL WYDETLYAEL LGKPRGFQQQ
  1741  SNFYPGFQGR LKYNAFCELQ TYHDQLVELL EETKREKNSY YVFLKYKRQV NECEAIMEHC
  1801  SDCFDFSLSV PFTCGVNFGD SLEDLEILRK STLKLINVCG DSPKVHSYPG KQDHLWIIIE
  1861  MISSKVNFIK NNEAVRVKIS LYGLEHIFFD AAKNLVWKER TQSFSKKYSQ KKDEERLLRV
  1921  NKCAFSKLQK IYDTLSKDLN NEPISPIGLE EDTIIASRKS DHPINEATIS IENSKFNSNL
  1981  LAHPDICCIS EILDQAEFAD LKKLQDLTLR CTDHLEILKK YFQMLQDNNM DNIFITEENV
  2041  LDVVINHSHE AIILKPEAIE MYIEIVMVSE TIHFLKNSIA KKLDKQRFRG MLWFDLSLLP
  2101  ELVQCQEKMA SFSFLKDNST DVCLWKVIET AVSELKKDLD IICKYNEAVN CSYAIHLLSR
  2161  ELQELSEIKK LLKKSKYFIS TYIDFVPYIA SINYGSTVTE LEYNYNQFST LLKNVMSAPR
  2221  KDLGKMAHIR KVMKTIEHMK MICTKNAELT ISFFLCQMLY NRRKILQLKR KEKMNIHIVK
  2281  PGENNNKFSI STMLPPVSEC INKNISNSSK KRPSTVDKCE DSQEQQQDTT VSSCKKLKVD
  2341  MKDVTKINRE KATFKHPRTT GSHPKSENKI VPSSCDSLKR NHLTPKKVEM QRSLPGSLLP
  2401  LENPKDTCAS KSESKIDLTV SSDHFSGQQE NLNSMKKRNV NFSAAETKSD KKDCAAFAIC
  2461  DQKSVHGTFS PDHGTLLQKF LKNSPDPTQK SCLSDINPET DVSLVPDASV LSKPIFCFVK
  2521  DVHPDLEMND TVFELQDNDI VNSSIKNSSC MTSPEPICIQ NKIPTLQINK LQPTETESED
  2581  KYMKDTLNPN TVHTFGASGH ITLNVNQGAE YSLSEQQNDK NSKVLMQNAA TYWNELPQSA
  2641  CNPTYNSSEH LFGTSYPYSA WCVYQYSNSN GNAITQTYQG ITSYEVQPSP SGLLTTVAST
  2701  AQGTHSNLLY SQYFTYFAGE PQANGFVPVN GYFQSQIPAS NFRQPIFSQY ASHQPLPQAT
  2761  YPYLPNRFVP PEVPWVYAPW HQESFHPGH

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against TEX15 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
11 nTPM

Expression across tissuesHPA

Tissue

  • testis: 11 nTPM
  • endometrium: 6.3 nTPM
  • smooth muscle: 4.9 nTPM
  • basal ganglia: 0.5 nTPM
  • cervix: 0.5 nTPM
  • pituitary gland: 0.5 nTPM

Single-cell type

  • early primary spermatocytes: 420 nCPM
  • differentiating spermatogonia: 179 nCPM
  • undifferentiated spermatogonia: 142 nCPM
  • early spermatids: 126 nCPM
  • late primary spermatocytes: 125 nCPM
  • ependymal cells: 89 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

  • basal ganglia: 3.1 nTPM
  • hippocampal formation: 2.1 nTPM
  • medulla oblongata: 2.1 nTPM
  • midbrain: 1.9 nTPM
  • cerebral cortex: 1.5 nTPM
  • amygdala: 1.4 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about TEX15.

Disease | AllUniProt

Conditions TEX15 is implicated in, by any mechanism.

Disease | GeneticClinVar

27 pathogenic / likely-pathogenic of 426 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

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)
0.78
gnomAD pLI
0
gnomAD missense Z
-1.15
DepMap mean gene effect
0.08
DepMap dependency class
none

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

Cellular components

Protein domainsUniProt · Pfam · InterPro

  • Testis-expressed sequence 15 protein
  • Testis expressed sequence 15 domain
  • Testis expressed sequence 15

KeywordsUniProt

InteractionsUniProt · HPA

Protein binding partners of TEX15 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 TEX15 as an antibody target. Whether an autoantibody or antibody against TEX15 could matter depends on whether native TEX15 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

TEX15 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 TEX15 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/TEX15. 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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