GINS3
DNA replication complex GINS protein PSF3
Also known as: FLJ13912, PSF3, PSF3_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q9BRX5
- Gene
- GINS3
- Ensembl
- ENSG00000181938
- Chromosome
- 16
- Canonical length
- 216 aa
- Protein class
- Predicted intracellular proteins
- Subcellular location
- Nucleoplasm
OverviewNCBI Gene
This gene encodes a protein subunit of the GINS heterotetrameric complex, which is essential for the initiation of DNA replication and replisome progression in eukaryotes. Alternatively spliced transcript variants encoding distinct isoforms have been described. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
216 residues, UniProt reviewed canonical sequence.
>Q9BRX5|GINS3
1 MSEAYFRVES GALGPEENFL SLDDILMSHE KLPVRTETAM PRLGAFFLER SAGAETDNAV
61 PQGSKLELPL WLAKGLFDNK RRILSVELPK IYQEGWRTVF SADPNVVDLH KMGPHFYGFG
121 SQLLHFDSPE NADISQSLLQ TFIGRFRRIM DSSQNAYNED TSALVARLDE MERGLFQTGQ
181 KGLNDFQCWE KGQASQITAS NLVQNYKKRK FTDMEDLocalizationUniProt · AlphaFold · HPA
Whether an antibody against GINS3 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)
- 0.36
- Highest tissue expression
- 8.9 nTPM
Expression across tissuesHPA
Tissue
- esophagus: 8.9 nTPM
- basal ganglia: 8.3 nTPM
- thymus: 8.2 nTPM
- bone marrow: 7.9 nTPM
- tonsil: 7.5 nTPM
- lymph node: 7.3 nTPM
Single-cell type
- astrocytes: 233 nCPM
- early spermatids: 118 nCPM
- late primary spermatocytes: 100 nCPM
- schwann cells: 85 nCPM
- oligodendrocyte progenitor cells: 76 nCPM
- ependymal cells: 69 nCPM
Immune cell
- plasmacytoid DC: 8.2 nTPM
- naive B-cell: 4.4 nTPM
- myeloid DC: 4.1 nTPM
- NK-cell: 4.1 nTPM
- memory CD8 T-cell: 2.9 nTPM
- memory B-cell: 2.5 nTPM
Brain region
- basal ganglia: 7.8 nTPM
- cerebellum: 6.7 nTPM
- midbrain: 6.5 nTPM
- thalamus: 5.8 nTPM
- medulla oblongata: 5.3 nTPM
- spinal cord: 4.9 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about GINS3.
Disease | GeneticClinVar
2 pathogenic / likely-pathogenic of 51 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Meier-Gorlin syndrome 9
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)
- 1.52
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.46
- DepMap mean gene effect
- -1.13
- DepMap dependency class
- common
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
- GINS subunit, domain A
- GINS, helical bundle-like domain superfamily
- GINS complex protein helical bundle domain
- GINS complex, subunit Psf3
- GINS complex, subunit Psf3 superfamily
- DNA replication complex GINS protein PSF3, N-terminal domain
- PSF3 N-terminal domain
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of GINS3 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 GINS3 as an antibody target. Whether an autoantibody or antibody against GINS3 could matter depends on whether native GINS3 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
GINS3 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 GINS3 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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