Seroatlas · Human Serome Atlas

NME3

Nucleoside diphosphate kinase 3

Also known as: DR-nm23, NDK3_HUMAN, NDPKC, NM23-H3

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

Protein identityUniProt · HPA

UniProt accession: Q13232
Gene: NME3
Ensembl: ENSG00000103024
Chromosome: 16
Canonical length: 169 aa
Protein class: Enzymes, Metabolic proteins, Plasma proteins, Predicted intracellular proteins
Secretome location: Intracellular and membrane
Quaternary structure: Homohexamer

OverviewNCBI Gene

Enables nucleoside diphosphate kinase activity. Involved in DNA repair; mitochondrial fusion; and nucleoside triphosphate biosynthetic process. Located in mitochondrial outer membrane. [provided by Alliance of Genome Resources, Jul 2025]

Canonical amino-acid sequenceUniProt

169 residues, UniProt reviewed canonical sequence.

>Q13232|NME3
     1  MICLVLTIFA NLFPAACTGA HERTFLAVKP DGVQRRLVGE IVRRFERKGF KLVALKLVQA
    61  SEELLREHYA ELRERPFYGR LVKYMASGPV VAMVWQGLDV VRTSRALIGA TNPADAPPGT
   121  IRGDFCIEVG KNLIHGSDSV ESARREIALW FRADELLCWE DSAGHWLYE

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against NME3 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: Other membrane
Secreted: No
Transmembrane segments: 0
Mean surface accessibility (rSASA): 0.31
Highest tissue expression: 106 nTPM

Expression across tissuesHPA

Tissue

adrenal gland: 106 nTPM
pituitary gland: 93 nTPM
cerebellum: 84 nTPM
basal ganglia: 81 nTPM
prostate: 80 nTPM
amygdala: 75 nTPM

Single-cell type

breast lactating cells: 277 nCPM
epididymal efferent duct absorptive cells: 207 nCPM
epididymal basal cells: 178 nCPM
breast myoepithelial cells: 168 nCPM
breast hormone-responsive cells: 156 nCPM
decidual stromal cells: 145 nCPM

Immune cell

plasmacytoid DC: 87 nTPM
non-classical monocyte: 66 nTPM
classical monocyte: 62 nTPM
intermediate monocyte: 61 nTPM
memory CD4 T-cell: 56 nTPM
myeloid DC: 54 nTPM

Brain region

white matter: 50 nTPM
medulla oblongata: 48 nTPM
thalamus: 46 nTPM
spinal cord: 45 nTPM
midbrain: 44 nTPM
basal ganglia: 44 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): 1.95
gnomAD pLI: 0
gnomAD missense Z: -0.69
DepMap mean gene effect: 0.07
DepMap dependency class: selective

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

apoptotic process
CTP biosynthetic process
DNA repair
dTTP biosynthetic process
GTP biosynthetic process
mitochondrial fusion
nucleoside triphosphate biosynthetic process
protein hexamerization
UTP biosynthetic process
mitochondrial outer membrane fusion

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

InteractionsUniProt · HPA

Protein binding partners of NME3 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 NME3 as an antibody target. Whether an autoantibody or antibody against NME3 could matter depends on whether native NME3 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

NME3 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 NME3 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

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