Seroatlas · Human Serome Atlas

POLR3GL

DNA-directed RNA polymerase III subunit RPC7-like

Also known as: flj32422, MGC3200, RPC7L_HUMAN

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

Protein identityUniProt · HPA

UniProt accession: Q9BT43
Gene: POLR3GL
Ensembl: ENSG00000121851
Chromosome: 1
Canonical length: 218 aa
Protein class: Disease related genes, Human disease related genes, Metabolic proteins, Predicted intracellular proteins, RNA polymerase related proteins

OverviewNCBI Gene

Predicted to enable chromatin binding activity. Involved in transcription by RNA polymerase III. Located in nucleus. Part of RNA polymerase III complex. [provided by Alliance of Genome Resources, Jul 2025]

Canonical amino-acid sequenceUniProt

218 residues, UniProt reviewed canonical sequence.

>Q9BT43|POLR3GL
     1  MASRGGGRGR GRGQLTFNVE AVGIGKGDAL PPPTLQPSPL FPPLEFRPVP LPSGEEGEYV
    61  LALKQELRGA MRQLPYFIRP AVPKRDVERY SDKYQMSGPI DNAIDWNPDW RRLPRELKIR
   121  VRKLQKERIT ILLPKRPPKT TEDKEETIQK LETLEKKEEE VTSEEDEEKE EEEEKEEEEE
   181  EEYDEEEHEE ETDYIMSYFD NGEDFGGDSD DNMDEAIY

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against POLR3GL 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): 0.62
Highest tissue expression: 133 nTPM

Expression across tissuesHPA

Tissue

skeletal muscle: 133 nTPM
heart muscle: 63 nTPM
tongue: 62 nTPM
liver: 52 nTPM
adipose tissue: 48 nTPM
blood vessel: 46 nTPM

Single-cell type

megakaryocytes: 105 nCPM
hepatocytes: 97 nCPM
thymic myoid cells: 86 nCPM
mast cells: 85 nCPM
hofbauer cells: 84 nCPM
parietal cells: 81 nCPM

Immune cell

eosinophil: 267 nTPM
basophil: 227 nTPM
T-reg: 180 nTPM
naive CD8 T-cell: 131 nTPM
naive CD4 T-cell: 127 nTPM
memory CD4 T-cell: 126 nTPM

Brain region

hypothalamus: 22 nTPM
medulla oblongata: 21 nTPM
cerebral cortex: 20 nTPM
thalamus: 20 nTPM
choroid plexus: 18 nTPM
basal ganglia: 18 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about POLR3GL.

Disease | AllUniProt

Conditions POLR3GL is implicated in, by any mechanism.

Short stature, oligodontia, dysmorphic facies, and motor delay (SOFM) MIM:619234

Disease | GeneticClinVar

3 pathogenic / likely-pathogenic of 48 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

Short stature, oligodontia, dysmorphic facies, and motor delay
Oligodontia
Abnormal facial shape
Short stature
Hyperostosis

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): 1.17
gnomAD pLI: 0
gnomAD missense Z: 0.34
DepMap mean gene effect: -0.09
DepMap dependency class: selective

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 6% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

transcription by RNA polymerase III

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

InteractionsUniProt · HPA

Protein binding partners of POLR3GL 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 POLR3GL as an antibody target. Whether an autoantibody or antibody against POLR3GL could matter depends on whether native POLR3GL is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

POLR3GL 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 POLR3GL as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

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