CA3
Carbonic anhydrase 3
Also known as: CAH3_HUMAN, CAIII, Car3
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P07451
- Gene
- CA3
- Ensembl
- ENSG00000164879
- Chromosome
- 8
- Canonical length
- 260 aa
- Protein class
- Enzymes, FDA approved drug targets, Metabolic proteins, Plasma proteins, Predicted intracellular proteins
OverviewNCBI Gene
Carbonic anhydrase III (CAIII) is a member of a multigene family (at least six separate genes are known) that encodes carbonic anhydrase isozymes. These carbonic anhydrases are a class of metalloenzymes that catalyze the reversible hydration of carbon dioxide and are differentially expressed in a number of cell types. The expression of the CA3 gene is strictly tissue specific and present at high levels in skeletal muscle and much lower levels in cardiac and smooth muscle. A proportion of carriers of Duchenne muscle dystrophy have a higher CA3 level than normal. The gene spans 10.3 kb and contains seven exons and six introns. [provided by RefSeq, Oct 2008]
Canonical amino-acid sequenceUniProt
260 residues, UniProt reviewed canonical sequence.
>P07451|CA3
1 MAKEWGYASH NGPDHWHELF PNAKGENQSP VELHTKDIRH DPSLQPWSVS YDGGSAKTIL
61 NNGKTCRVVF DDTYDRSMLR GGPLPGPYRL RQFHLHWGSS DDHGSEHTVD GVKYAAELHL
121 VHWNPKYNTF KEALKQRDGI AVIGIFLKIG HENGEFQIFL DALDKIKTKG KEAPFTKFDP
181 SCLFPACRDY WTYQGSFTTP PCEECIVWLL LKEPMTVSSD QMAKLRSLLS SAENEPPVPL
241 VSNWRPPQPI NNRVVRASFKLocalizationUniProt · AlphaFold · HPA
Whether an antibody against CA3 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)
- 0.24
- Highest tissue expression
- 4,942 nTPM
Expression across tissuesHPA
Tissue
- skeletal muscle: 4,942 nTPM
- tongue: 951 nTPM
- prostate: 84 nTPM
- esophagus: 61 nTPM
- adipose tissue: 41 nTPM
- lung: 23 nTPM
Single-cell type
- thymic myoid cells: 908 nCPM
- myonuclei: 590 nCPM
- enterocytes: 147 nCPM
- erythrocyte progenitors: 117 nCPM
- breast secretory cells: 108 nCPM
- salivary duct cells: 93 nCPM
Immune cell
- plasmacytoid DC: 0.2 nTPM
- naive CD8 T-cell: 0.1 nTPM
- basophil: 0 nTPM
- classical monocyte: 0 nTPM
- eosinophil: 0 nTPM
- gdT-cell: 0 nTPM
Brain region
- cerebral cortex: 5.9 nTPM
- medulla oblongata: 4.6 nTPM
- hypothalamus: 4.4 nTPM
- white matter: 4.1 nTPM
- cerebellum: 4 nTPM
- spinal cord: 3.7 nTPM
ReferencesPubMed · IEDB
Publications for CA3 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
3 publications
- Anti-carbonic anhydrase III autoantibodies in vasculitis syndrome.
2013 · Int J Rheum Dis · RCR 0.1 · 4 citations - The Relationship between Serum Carbonic Anhydrase I-II Autoantibody Levels and Diabetic Retinopathy in Type 1 Diabetes Patients.
2017 · Turk J Ophthalmol · RCR 0.1 · 2 citations - Carbonic anhydrase I-II autoantibodies and oxidative status in long-term follow-up of patients with Crimean-Congo haemorrhagic fever.
2018 · Arch Physiol Biochem · RCR 0 · 1 citations
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. 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)
- 0.85
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.55
- DepMap mean gene effect
- 0.09
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 3% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- cellular response to hypoxia
- cellular response to insulin stimulus
- cellular response to leptin stimulus
- liver regeneration
- negative regulation of intrinsic apoptotic signaling pathway in response to hydrogen peroxide
- negative regulation of reactive oxygen species biosynthetic process
- positive regulation of cell population proliferation
- response to bacterium
- response to ethanol
- response to lipid
- response to oxidative stress
- skeletal muscle contraction
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads CA3 as an antibody target. Whether an autoantibody or antibody against CA3 could matter depends on whether native CA3 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
CA3 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 CA3 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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