Seroatlas · Human Serome Atlas

APOH

Beta-2-glycoprotein 1

Also known as: APOH_HUMAN, B2G1, BG

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

Protein identityUniProt · HPA

UniProt accession
P02749
Gene
APOH
Ensembl
ENSG00000091583
Chromosome
17
Canonical length
345 aa
Protein class
Candidate cardiovascular disease genes, Plasma proteins, Predicted intracellular proteins, Predicted secreted proteins
Subcellular location
Golgi apparatus
Secretome location
Secreted to blood

OverviewNCBI Gene

Apolipoprotein H, also known as beta-2-glycoprotein I, is a component of circulating plasma lipoproteins. It has been implicated in a variety of physiologic pathways including lipoprotein metabolism, coagulation, hemostasis, and the production of antiphospholipid autoantibodies. APOH may be a required cofactor for anionic phospholipid binding by the antiphospholipid autoantibodies found in sera of many patients with lupus and primary antiphospholipid syndrome (APS). The anti-beta (2) glycoprotein I antibodies from APS patients, mediate inhibition of activated protein C which has anticoagulant properties. Because beta-2-GPI is the main autoantigen in patients with APS, the disruption of this pathway by autoantibodies may be an important mechanism for thrombosis in patients with APS.[provided by RefSeq, Dec 2019]

Canonical amino-acid sequenceUniProt

345 residues, UniProt reviewed canonical sequence.

>P02749|APOH
     1  MISPVLILFS SFLCHVAIAG RTCPKPDDLP FSTVVPLKTF YEPGEEITYS CKPGYVSRGG
    61  MRKFICPLTG LWPINTLKCT PRVCPFAGIL ENGAVRYTTF EYPNTISFSC NTGFYLNGAD
   121  SAKCTEEGKW SPELPVCAPI ICPPPSIPTF ATLRVYKPSA GNNSLYRDTA VFECLPQHAM
   181  FGNDTITCTT HGNWTKLPEC REVKCPFPSR PDNGFVNYPA KPTLYYKDKA TFGCHDGYSL
   241  DGPEEIECTK LGNWSAMPSC KASCKVPVKK ATVVYQGERV KIQEKFKNGM LHGDKVSFFC
   301  KNKEKKCSYT EDAQCIDGTI EVPKCFKEHS SLAFWKTDAS DVKPC

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against APOH 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
Secreted
Secreted
Yes
Transmembrane segments
0
Mean surface accessibility (rSASA)
0.35
Highest tissue expression
16,782 nTPM

Expression across tissuesHPA

Tissue

  • liver: 16,782 nTPM
  • kidney: 30 nTPM
  • pancreas: 10 nTPM
  • lung: 5.3 nTPM
  • spleen: 3.6 nTPM
  • stomach: 3.5 nTPM

Single-cell type

  • hepatocytes: 9,196 nCPM
  • pancreatic islet cells: 166 nCPM
  • cholangiocytes: 160 nCPM
  • kupffer cells: 113 nCPM
  • hepatic stellate cells: 58 nCPM
  • epididymal efferent duct absorptive cells: 42 nCPM

Immune cell

  • basophil: 0.2 nTPM
  • classical monocyte: 0.2 nTPM
  • gdT-cell: 0.2 nTPM
  • naive B-cell: 0.2 nTPM
  • eosinophil: 0.1 nTPM
  • MAIT T-cell: 0.1 nTPM

Brain region

  • choroid plexus: 1.4 nTPM
  • cerebral cortex: 1.3 nTPM
  • medulla oblongata: 1.3 nTPM
  • hippocampal formation: 1.2 nTPM
  • hypothalamus: 1.2 nTPM
  • spinal cord: 1.2 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about APOH.

Disease | ImmuneIEDB

Conditions an epitope on APOH was assayed in.

Disease | AutoantibodyPubMed

Conditions in which antibodies against APOH are reported. Each links to that disease's full target list.

Showing 20 of 81 — disease pages carrying at least 10 antigens.

ReferencesPubMed · IEDB

Publications for APOH from three distinct lines of evidence, kept separate because they answer different questions: whether antibodies are directed at the protein, whether a B-cell epitope has been mapped on it, and whether a T-cell epitope has. Each is labelled with its source.

Reference: AutoantibodyPubMed

1,254 publications

Show 20 more of 1,254 total

Reference: B cellIEDB

7 publications

Show 2 more

Reference: T cellIEDB

1 publication

Sources: PubMed — antigen-level antibody evidence from a custom retrieval. Records matching a controlled set of autoantibody terms (the MeSH descriptors Autoantibodies and Autoantigens, with title and abstract term variants) were obtained through NCBI E-utilities, and their titles and abstracts parsed for constructions that direct an antibody at a named protein rather than for co-occurrence. Captured names were resolved against UniProt nomenclature and each antigen adjudicated individually against the source text. IEDB — curated epitope assays from the Immune Epitope Database (Vita et al., Nucleic Acids Research 2019). Bibliographic records from PubMed and MeSH, U.S. National Library of Medicine; citation metrics from NIH iCite (Hutchins et al., PLoS Biology 2016). Titles link to PubMed; abstracts are not reproduced here. The NLM does not endorse this analysis.

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)
1.66
gnomAD pLI
0
gnomAD missense Z
0.28
DepMap mean gene effect
-0.08
DepMap dependency class
selective

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 2% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

Antibody and autoantibody relevanceSeroatlas analysis

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

APOH is annotated as secreted, so native APOH circulates and is directly accessible to antibodies. Secreted and cell-surface proteins are the autoantibody targets most likely to act like drugs, blocking or depleting the native protein.

Source-annotated serology context

The source annotations explicitly mention antibody, autoantibody, autoantigen, or autoimmune context. This is biological context, not study-specific reactivity.

  • It has been implicated in a variety of physiologic pathways including lipoprotein metabolism, coagulation, hemostasis, and the production of antiphospholipid autoantibodies.
  • APOH may be a required cofactor for anionic phospholipid binding by the antiphospholipid autoantibodies found in sera of many patients with lupus and primary antiphospholipid syndrome (APS).
  • Because beta-2-GPI is the main autoantigen in patients with APS, the disruption of this pathway by autoantibodies may be an important mechanism for thrombosis in patients with APS.[provided by RefSeq, Dec 2019]
  • The anti-beta (2) glycoprotein I antibodies from APS patients, mediate inhibition of activated protein C which has anticoagulant properties.

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