Seroatlas · Human Serome Atlas

CRYAA

Alpha-crystallin A chain

Also known as: CRYA1, CRYAA_HUMAN, HSPB4

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

Protein identityUniProt · HPA

UniProt accession
P02489
Gene
CRYAA
Ensembl
ENSG00000160202
Chromosome
21
Canonical length
173 aa
Protein class
Disease related genes, Human disease related genes, Plasma proteins, Potential drug targets, Predicted intracellular proteins, Transporters
Subcellular location
Nucleoplasm,Cytosol
Quaternary structure
Homotetramer

OverviewNCBI Gene

Mammalian lens crystallins are divided into alpha, beta, and gamma families. Alpha crystallins are composed of two gene products: alpha-A and alpha-B, for acidic and basic, respectively. Alpha crystallins can be induced by heat shock and are members of the small heat shock protein (HSP20) family. They act as molecular chaperones although they do not renature proteins and release them in the fashion of a true chaperone; instead they hold them in large soluble aggregates. Post-translational modifications decrease the ability to chaperone. These heterogeneous aggregates consist of 30-40 subunits; the alpha-A and alpha-B subunits have a 3:1 ratio, respectively. Two additional functions of alpha crystallins are an autokinase activity and participation in the intracellular architecture. The encoded protein has been identified as a moonlighting protein based on its ability to perform mechanistically distinct functions. Alpha-A and alpha-B gene products are differentially expressed; alpha-A is preferentially restricted to the lens and alpha-B is expressed widely in many tissues and organs. Defects in this gene cause autosomal dominant congenital cataract (ADCC). [provided by RefSeq, Jan 2014]

Canonical amino-acid sequenceUniProt

173 residues, UniProt reviewed canonical sequence.

>P02489|CRYAA
     1  MDVTIQHPWF KRTLGPFYPS RLFDQFFGEG LFEYDLLPFL SSTISPYYRQ SLFRTVLDSG
    61  ISEVRSDRDK FVIFLDVKHF SPEDLTVKVQ DDFVEIHGKH NERQDDHGYI SREFHRRYRL
   121  PSNVDQSALS CSLSADGMLT FCGPKIQTGL DATHAERAIP VSREEKPTSA PSS

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against CRYAA 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)
0.44
Highest tissue expression
104 nTPM

Expression across tissuesHPA

Tissue

  • kidney: 104 nTPM
  • retina: 96 nTPM
  • liver: 12 nTPM
  • thymus: 0.6 nTPM
  • duodenum: 0.4 nTPM
  • small intestine: 0.4 nTPM

Single-cell type

  • müller glia: 1.5 nCPM
  • hepatocytes: 0.1 nCPM
  • adipocytes: 0 nCPM
  • adrenal cortex cells: 0 nCPM
  • adrenal medulla cells: 0 nCPM
  • alveolar cells type 1: 0 nCPM

Immune cell

  • basophil: 0 nTPM
  • classical monocyte: 0 nTPM
  • eosinophil: 0 nTPM
  • gdT-cell: 0 nTPM
  • intermediate monocyte: 0 nTPM
  • MAIT T-cell: 0 nTPM

Brain region

  • white matter: 1.1 nTPM
  • cerebral cortex: 0.7 nTPM
  • hippocampal formation: 0.6 nTPM
  • hypothalamus: 0.5 nTPM
  • medulla oblongata: 0.5 nTPM
  • thalamus: 0.5 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about CRYAA.

Disease | AllUniProt

Conditions CRYAA is implicated in, by any mechanism.

Disease | GeneticClinVar

11 pathogenic / likely-pathogenic of 115 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

  • Cataract 9 multiple types
  • Developmental cataract
  • Cataract 9, multiple types, with microcornea
  • CRYAA-related disorder
  • Cataract 9, autosomal recessive

Disease | ImmuneIEDB

Conditions an epitope on CRYAA was assayed in.

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)
0.99
gnomAD pLI
0.17
gnomAD missense Z
0.35
DepMap mean gene effect
0.07
DepMap dependency class
none

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

InteractionsUniProt · HPA

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

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

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