ADAP2
Arf-GAP with dual PH domain-containing protein 2
Also known as: ADAP2_HUMAN, CENTA2
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q9NPF8
- Gene
- ADAP2
- Ensembl
- ENSG00000184060
- Chromosome
- 17
- Canonical length
- 381 aa
- Protein class
- Predicted intracellular proteins
OverviewNCBI Gene
The protein encoded by this gene binds beta-tubulin and increases the stability of microtubules. The encoded protein can also translocate to the cell membrane and bind phosphatidylinositol 3,4,5-trisphosphate (PtdInsP3) and inositol 1,3,4,5-tetrakisphosphate (InsP4). In addition, this protein is a GTPase-activating protein for ADP ribosylation factor 6 and may be able to block the entry of some RNA viruses. [provided by RefSeq, Oct 2016]
Canonical amino-acid sequenceUniProt
381 residues, UniProt reviewed canonical sequence.
>Q9NPF8|ADAP2
1 MGDRERNKKR LLELLRAPDT GNAHCADCGA ADPDWASYKL GIFICLNCCG VHRNFPDISR
61 VKSVRLDFWD DSIVEFMIHN GNLRVKAKFE ARVPAFYYIP QANDCLVLKE QWIRAKYERR
121 EFMADGETIS LPGNREGFLW KRGRDNSQFL RRKFVLLARE GLLKYFTKEQ GKSPKAVISI
181 KDLNATFQTE KIGHPHGLQI TYRRDGHTRN LFVYHESGKE IVDWFNALRA ARLQYLKMAF
241 PELPESELVP FLTRNYLKQG FMEKTGPKQK EPFKKRWFAL DCHERRLLYY KNPLDAFEQG
301 QVFLGNKEQG YEAYEDLPKG IRGNRWKAGL TIVTPERRFV LTCPSEKEQQ EWLESLRGVL
361 SSPLTPLNRL TASTESGRSS RLocalizationUniProt · AlphaFold · HPA
Whether an antibody against ADAP2 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
- Cell surface
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.26
- Highest tissue expression
- 21 nTPM
Expression across tissuesHPA
Tissue
- spleen: 21 nTPM
- placenta: 19 nTPM
- appendix: 14 nTPM
- adipose tissue: 11 nTPM
- liver: 10 nTPM
- lung: 9.2 nTPM
Single-cell type
- kupffer cells: 470 nCPM
- hofbauer cells: 334 nCPM
- macrophages: 245 nCPM
- microglia: 227 nCPM
- extravillous trophoblasts: 144 nCPM
- monocytes: 108 nCPM
Immune cell
- non-classical monocyte: 44 nTPM
- intermediate monocyte: 34 nTPM
- classical monocyte: 23 nTPM
- myeloid DC: 13 nTPM
- total PBMC: 6.7 nTPM
- memory B-cell: 3 nTPM
Brain region
- thalamus: 28 nTPM
- white matter: 24 nTPM
- medulla oblongata: 23 nTPM
- pons: 20 nTPM
- choroid plexus: 17 nTPM
- cerebral cortex: 16 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)
- 1.08
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.8
- DepMap mean gene effect
- -0.15
- DepMap dependency class
- selective
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
Molecular functions
- GTPase activator activity
- inositol 1,3,4,5 tetrakisphosphate binding
- phosphatidylinositol-3,4,5-trisphosphate binding
- phosphatidylinositol-3,4-bisphosphate binding
- phosphatidylinositol-4,5-bisphosphate binding
- protein-macromolecule adaptor activity
- zinc ion binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads ADAP2 as an antibody target. Whether an autoantibody or antibody against ADAP2 could matter depends on whether native ADAP2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
ADAP2 is annotated at the cell surface, where native ADAP2 is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.
Annotation status
The present source text does not explicitly label ADAP2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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