Affinage

CRYAA

Alpha-crystallin A chain · UniProt P02489

Length
173 aa
Mass
19.9 kDa
Annotated
2026-06-09
44 papers in source corpus 17 papers cited in narrative 17 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CRYAA (alphaA-crystallin/HspB4) is a lens-predominant small heat-shock protein whose core function is molecular chaperone activity that prevents protein aggregation to maintain lens transparency, with additional context-dependent cytoprotective and immunomodulatory roles in cornea and retina (PMID:18407550, PMID:22359280). Within the lens it suppresses substrate aggregation, and the disease-causing R116H substitution increases protein hydrophobicity, raises lysozyme-binding affinity, and abolishes chaperone activity, defining loss of chaperone function as one molecular route to cataract (PMID:18407550). CRYAA participates in mixed oligomers, forming hetero-complexes with HspB5/alphaB-crystallin that display distinct chaperone-like activity and slower subunit exchange than other small-HSP pairs (PMID:22210387). Multiple dominant cataract mutations act through gain-of-toxicity mechanisms rather than simple loss of chaperoning: R12L drives accumulation of insoluble protein and cytoplasmic aggresomes (PMID:30340470), Y118D triggers ER-stress/unfolded-protein-response activation and proteotoxic death in lens fibers (PMID:33929105), and E156K induces epithelial-mesenchymal transition in lens epithelial cells via FAK/Src and Wnt/beta-catenin signaling (PMID:38187316). CRYAA itself is required for lens epithelial homeostasis, restraining apoptosis and autophagy (PMID:37253645), and its expression is silenced in age-related cataract by CpG hypermethylation of its promoter, which reduces Sp1 binding and transcription (PMID:22889833, PMID:27507241). Outside the lens, CRYAA released from injured keratocytes functions as a DAMP that activates resident macrophages through a TLR2/NF-kappaB axis to drive sterile corneal inflammation (PMID:22359280). In the retina, mTORC2-mediated phosphorylation of CRYAA at T148 confers anti-inflammatory, anti-apoptotic, and neuroprotective activity, including suppression of NLRP3/NF-kappaB signaling (PMID:34071438, PMID:39682748) and phosphorylation-dependent binding and stabilization of the pro-survival factor FAIM2 to protect photoreceptors (PMID:39311341). The R116C mutation in CRYAA causes autosomal dominant congenital cataract (PMID:9467006).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1998 Medium

    Established CRYAA as a disease gene by linking a specific missense mutation to inherited lens opacity, answering whether crystallin genes themselves cause cataract.

    Evidence Linkage analysis and gene sequencing in an autosomal dominant congenital cataract family

    PMID:9467006

    Open questions at the time
    • No in vitro functional assay to show how R116C alters protein behavior
    • Did not distinguish loss-of-function from gain-of-toxicity
  2. 2008 High

    Resolved the molecular basis of mutation-driven cataract by showing the disease substitution abolishes chaperone activity and increases hydrophobicity, defining a loss-of-chaperone mechanism.

    Evidence Recombinant R116H protein with RP-HPLC, FPLC binding, and insulin-aggregation chaperone assays

    PMID:18407550

    Open questions at the time
    • In vitro assays do not establish in vivo lens consequences
    • Tested R116H rather than the original R116C allele
  3. 2008 Medium

    Identified the genomic regulatory element controlling lens-specific CRYAA expression, addressing how the gene is restricted to differentiating fiber cells.

    Evidence BAC transgenic mice with EGFP reporter and deletion of the DCR3 distal enhancer

    PMID:18803847

    Open questions at the time
    • Trans-acting factors binding DCR3 not identified
    • Single transgenic system
  4. 2011 Medium

    Defined CRYAA's oligomeric biology by showing it forms hetero-complexes with HspB5 with distinct properties, refining what the functional chaperone species actually is.

    Evidence SEC, SAXS, subunit-exchange kinetics, and in vitro chaperone assays of HspB4/HspB5 complexes

    PMID:22210387

    Open questions at the time
    • In vivo relevance of hetero-complex stoichiometry not established
    • Single lab biophysical study
  5. 2012 High

    Revealed an unexpected extracellular, pro-inflammatory role by showing released CRYAA acts as a DAMP driving sterile corneal inflammation through TLR2/NF-kappaB.

    Evidence HSPB4-/- and TLR2-/- mice, anti-HSPB4 antibody blockade, and NF-kappaB pathway analysis

    PMID:22359280

    Open questions at the time
    • Direct CRYAA-TLR2 binding not structurally defined
    • Receptor co-factors not yet mapped
  6. 2012 Medium

    Explained age-related loss of CRYAA expression by demonstrating promoter CpG hypermethylation represses transcription and is reversible by demethylation.

    Evidence Bisulfite sequencing, RT-PCR, Western blot, and zebularine rescue in cataract lens epithelia

    PMID:22889833

    Open questions at the time
    • Did not identify the transcription factor affected by methylation
    • Correlative human-tissue data
  7. 2016 Medium

    Provided the mechanistic link for methylation-driven silencing by showing methylated CpG sites reduce Sp1 binding to the CRYAA promoter.

    Evidence EMSA with methylated vs unmethylated probes plus demethylation/qRT-PCR

    PMID:27507241

    Open questions at the time
    • Other transcription factors at the promoter not excluded
    • Single-lab EMSA evidence
  8. 2018 Medium

    Showed that not all cataract mutations act by loss of chaperoning, identifying R12L as a gain-of-toxicity allele that drives insoluble aggregation and aggresome formation.

    Evidence Transfection of WT/R12L in HEK293T and HeLa cells with solubility fractionation and immunofluorescence

    PMID:30340470

    Open questions at the time
    • Aggregation shown in non-lens cell lines
    • Chaperone activity of R12L not directly measured
  9. 2018 Medium

    Tested the structural role of the conserved N-terminal Arg motif, showing CRYAA differs from other small HSPs and that this residue has a context-dependent role.

    Evidence Biophysical characterization of Arg-to-Ala mutants (thermal stability, fluorescence, SEC)

    PMID:30036999

    Open questions at the time
    • Did not connect motif perturbation to disease phenotype
    • Single-lab biophysics
  10. 2021 Medium

    Established a phosphorylation switch by showing T148 phosphorylation governs CRYAA's anti-inflammatory activity in retinal Muller glia.

    Evidence Phosphomimetic T148D vs T148A in primary HSPB4-knockout Muller cells with inflammatory marker qPCR and NF-kappaB/NLRP3 readouts

    PMID:34071438

    Open questions at the time
    • The responsible kinase was not yet identified
    • Single cell-type model
  11. 2021 Medium

    Connected a cataract mutation to a proteostasis stress pathway in vivo, showing Y118D activates ER-stress/UPR leading to proteotoxic fiber cell death.

    Evidence Y118D knock-in mouse with histology and transcriptome pathway analysis

    PMID:33929105

    Open questions at the time
    • Causal versus consequential role of UPR not separated
    • Single mutant allele studied
  12. 2023 Low

    Demonstrated CRYAA is required for lens epithelial homeostasis by showing its loss elevates apoptosis and autophagy.

    Evidence siRNA knockdown in HLEB3 cells with apoptosis/autophagy markers, flow cytometry, and viability assay

    PMID:37253645

    Open questions at the time
    • Single knockdown approach with limited pathway resolution
    • No rescue control reported
    • Mechanism linking CRYAA to autophagy unresolved
  13. 2023 Medium

    Identified a non-chaperone disease mechanism by which the E156K mutation drives EMT in lens epithelium through FAK/Src and Wnt/beta-catenin signaling.

    Evidence Knockdown-replacement of WT vs E156K in HLECs with EMT markers, migration assays, and pathway inhibitors

    PMID:38187316

    Open questions at the time
    • How E156K engages FAK/Src or Wnt is not defined
    • Single-lab cell model
  14. 2023 Low

    Refined the corneal DAMP mechanism by establishing CD14 as a required co-receptor for CRYAA-driven TLR2 activation and identifying DOPG as an inhibitor.

    Evidence In vitro TLR2 activation assay with CD14 knockdown/inhibition and DOPG treatment

    PMID:36982926

    Open questions at the time
    • Single in vitro assay with CD14 requirement inferred from inhibition
    • Not confirmed in vivo
  15. 2024 Medium

    Identified the kinase for the T148 phosphoswitch, showing mTORC2 phosphorylates CRYAA in vitro and that chaperone function reinforces the interaction.

    Evidence In vitro kinome profiling, chemoproteomics, and in vitro kinase assay

    PMID:39682748

    Open questions at the time
    • T148 phosphorylation by mTORC2 confirmed only in vitro
    • Cellular and in vivo regulation not yet validated
  16. 2024 Medium

    Linked the T148 phosphoswitch to a concrete neuroprotective output by showing phospho-dependent binding and stabilization of FAIM2 to promote photoreceptor survival.

    Evidence Reciprocal Co-IP, retinal detachment model, TUNEL, and phosphomimetic mutants in FasL-induced photoreceptor death

    PMID:39311341

    Open questions at the time
    • Mechanism by which CRYAA stabilizes FAIM2 not resolved
    • Single-lab model
  17. 2025 Medium

    Defined a cytoprotective signaling axis in retinal pigment epithelium whereby CRYAA lowers miR-155-5p to de-repress SIRT1 and activate PI3K/AKT against oxidative apoptosis.

    Evidence ARPE-19 overexpression, dual-luciferase miR-155-5p/SIRT1 binding, pathway Western blots, SIRT1-silencing rescue, and AAV-Cryaa in vivo model

    PMID:40350053

    Open questions at the time
    • How CRYAA regulates miR-155-5p levels is unknown
    • Single-lab study

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CRYAA's intracellular chaperone activity, its phosphorylation-dependent signaling roles, and its extracellular DAMP function are integrated within a single tissue context remains unresolved.
  • No structural model of how T148 phosphorylation alters oligomer or partner binding
  • Relationship between hetero-complex composition and tissue-specific function unclear
  • Whether non-chaperone disease mechanisms (aggregation, EMT, UPR) share a common upstream trigger is unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0044183 protein folding chaperone 2 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005576 extracellular region 1 GO:0005829 cytosol 1
Pathway
R-HSA-168256 Immune System 2 R-HSA-392499 Metabolism of proteins 2 R-HSA-5357801 Programmed Cell Death 2
Partners
CD14CRYABFAIM2MTORC2SP1TLR2
Complex memberships
HspB4-HspB5 (alphaA/alphaB-crystallin) hetero-oligomer

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 A missense mutation R116C in CRYAA (alphaA-crystallin) is associated with autosomal dominant congenital cataract, establishing CRYAA as a causative gene for hereditary lens opacity. Linkage analysis and gene sequencing in an ADCC family Human molecular genetics Medium 9467006
2008 The R116H mutation in alphaA-crystallin increases hydrophobicity of the protein, abolishes chaperone activity in a DTT-induced insulin aggregation assay, and increases binding affinity to lysozyme, indicating loss of normal chaperone function as the molecular basis for cataract formation. Recombinant protein expression in E. coli, RP-HPLC (hydrophobicity), FPLC (binding affinity), in vitro chaperone activity assay (insulin aggregation) Human mutation High 18407550
2012 CRYAA released from injured keratocytes acts as a DAMP and activates resident macrophages via the TLR2/NF-κB signaling pathway, triggering Phase II sterile corneal inflammation responsible for vision-threatening opacity. This was suppressed in HSPB4-knockout or TLR2-knockout mice, and by anti-HSPB4 antibodies. Mouse knockout models (HSPB4-/-, TLR2-/-), antibody inhibition, temporal kinetic analysis of neutrophil infiltration, NF-κB pathway analysis EMBO molecular medicine High 22359280
2012 CRYAA expression is epigenetically repressed in age-related nuclear cataract lens epithelia via CpG island hypermethylation of the CRYAA promoter; treatment with the demethylating agent zebularine restores CRYAA mRNA and protein expression. Bisulfite genomic sequencing, RT-PCR, Western blot, demethylating agent treatment (zebularine) FASEB journal Medium 22889833
2016 Methylation of CpG sites in the CRYAA promoter directly reduces binding of transcription factor Sp1, providing the mechanistic link between promoter hypermethylation and transcriptional silencing of CRYAA. Electrophoretic mobility shift assay (EMSA) with methylated vs. unmethylated probes, demethylating agent treatment with qRT-PCR BMC ophthalmology Medium 27507241
2011 HspB4 (CRYAA) forms hetero-complexes with HspB5 (alphaB-crystallin), and subunit exchange kinetics between HspB4 and HspB5 are slower than between HspB1 and HspB5. HspB4-HspB5 hetero-complexes exhibit distinct chaperone-like activity and structural properties compared to either homo-oligomer, suggesting that hetero-complex formation expands functional range. Biochemical and biophysical characterization (size exclusion chromatography, small-angle X-ray scattering), subunit exchange kinetics, in vitro chaperone activity assays Biochimie Medium 22210387
2018 Substitution of the conserved Arg in the N-terminal RLFDQxFG motif of HspB4 (R12 equivalent region) induces only minor changes in thermal stability and oligomeric structure compared to the larger effects seen in HspB1 and HspB8, indicating that this motif plays a distinct, context-dependent structural role in HspB4. Biophysical characterization (thermal stability, intrinsic fluorescence, size exclusion chromatography) of recombinant Arg-to-Ala mutant proteins International journal of molecular sciences Medium 30036999
2021 HspB4/αA-crystallin phosphorylation at T148 regulates its anti-inflammatory function in retinal Müller glial cells: phosphomimetic T148D mutant significantly reduced expression of pro-inflammatory cytokines (IL-6, IL-1β, MCP-1, IL-18), suppressed NLRP3 inflammasome components, and nearly abolished NF-κB induction, whereas non-phosphorylatable T148A mutant was ineffective. Primary Müller glial cells from HSPB4 knockout mice, transfection with WT/T148D/T148A plasmids, qPCR for inflammatory markers, Western blot for NF-κB and NLRP3 subcellular localization Journal of clinical medicine Medium 34071438
2024 αA-crystallin (HSPB4) interacts with the neuroprotective protein FAIM2, and this interaction requires phosphorylation of αA-crystallin at T148. During retinal detachment, FAIM2 is induced and co-immunoprecipitates with αA-crystallin, and αA-crystallin stabilizes FAIM2 to promote photoreceptor survival. Co-immunoprecipitation, immunohistochemistry, immunoblotting, TUNEL staining, cell culture model with FasL-induced photoreceptor death, phosphomimetic/non-phosphorylatable mutants Neurology international Medium 39311341
2024 mTORC2 is identified as a kinase that phosphorylates HSPB4 at T148 in vitro; additionally, the chaperone function of HSPB4 further strengthens the interaction with mTORC2, suggesting a multi-faceted regulatory relationship. In vitro kinome profiling, bioinformatics analysis, chemoproteomics, in vitro kinase assay Cells Medium 39682748
2018 The R12L mutation in CRYAA causes aggregation of the mutant protein in the insoluble fraction, forms large cytoplasmic aggregates and aggresomes in HeLa cells, and increases overall CRYAA protein expression levels, suggesting that mutation-induced aggregation underlies cataract pathogenesis. Transfection of WT and R12L-CRYAA in HEK293T and HeLa cells, Western blotting (solubility), immunofluorescence (aggresome formation) BMC medical genetics Medium 30340470
2021 In a CRYAA Y118D mutant mouse model, cataract formation is associated with activation of the endoplasmic reticulum stress-unfolded protein response (ERS-UPR) pathway, with up-regulated ERS-UPR genes; prolonged UPR activation leads to proteotoxic cell death in lens fibers. Knock-in mouse model, histological analysis, transcriptome analysis, key pathway analysis Zoological research Medium 33929105
2023 Silencing of CRYAA in HLEB3 lens epithelial cells increases apoptosis and autophagy, demonstrating that CRYAA is required to suppress apoptotic and autophagic pathways in lens epithelial cell homeostasis. siRNA knockdown, Western blotting for apoptosis and autophagy markers, flow cytometry, CCK-8 viability assay Aging Low 37253645
2025 CRYAA overexpression in RPE cells reduces miR-155-5p levels, which in turn de-represses SIRT1 (confirmed by dual luciferase assay showing miR-155-5p binds SIRT1 3'-UTR), leading to activation of the PI3K/AKT signaling pathway and protection from H2O2-induced apoptosis. Stable overexpression in ARPE-19 cells, RT-qPCR, dual luciferase reporter assay, Western blotting for PI3K/AKT pathway, flow cytometry for apoptosis, in vivo mouse retinal degeneration model with AAV-Cryaa injection Archives of biochemistry and biophysics Medium 40350053
2023 The E156K mutation in CRYAA induces epithelial-mesenchymal transition (EMT) in human lens epithelial cells, increasing mesenchymal markers (N-cadherin, vimentin) and decreasing epithelial marker (E-cadherin), with enhanced cell migration via activation of FAK/Src and Wnt/β-catenin signaling pathways. Knockdown and replacement with WT or E156K-mutant CRYAA in HLECs, Western blotting for EMT markers, rhodamine cytoskeleton staining, migration assay, β-catenin inhibitor (ICG001) and FAK/Src inhibitor treatments Heliyon Medium 38187316
2008 A 148 kb BAC transgene containing the Cryaa locus recapitulates endogenous alphaA-crystallin expression pattern in the lens. Deletion of the distal control region DCR3 from either the BAC or a 15 kb Cryaa fragment shows that DCR3 functions as a distal enhancer active during late primary lens fiber cell differentiation. BAC transgenic mice, standard transgenic mice, EGFP reporter, temporal/spatial expression analysis by fluorescence imaging BMC developmental biology Medium 18803847
2023 HSPB4 (CRYAA) activates TLR2 signaling in corneal cells acting as a DAMP; dioleoylphosphatidylglycerol (DOPG) inhibits TLR2 activation induced by HSPB4 in vitro, and this TLR2 activation requires the co-receptor CD14. In vitro TLR2 activation assay, CD14 co-receptor requirement established by knockdown/inhibition International journal of molecular sciences Low 36982926

Source papers

Stage 0 corpus · 44 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1998 Autosomal dominant congenital cataract associated with a missense mutation in the human alpha crystallin gene CRYAA. Human molecular genetics 386 9467006
2000 A nonsense mutation (W9X) in CRYAA causes autosomal recessive cataract in an inbred Jewish Persian family. Investigative ophthalmology & visual science 157 11006246
2007 Genetic heterogeneity in microcornea-cataract: five novel mutations in CRYAA, CRYGD, and GJA8. Investigative ophthalmology & visual science 123 17724170
2018 Circular RNA HIPK3 regulates human lens epithelial cells proliferation and apoptosis by targeting the miR-193a/CRYAA axis. Biochemical and biophysical research communications 86 29959922
2014 HspB1, HspB5 and HspB4 in Human Cancers: Potent Oncogenic Role of Some of Their Client Proteins. Cancers 77 24514166
2006 Identification of a novel, putative cataract-causing allele in CRYAA (G98R) in an Indian family. Molecular vision 66 16862070
2006 Congenital cataract and macular hypoplasia in humans associated with a de novo mutation in CRYAA and compound heterozygous mutations in P. Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie 63 16453125
2012 Down-regulation and CpG island hypermethylation of CRYAA in age-related nuclear cataract. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 62 22889833
2007 Recessive congenital total cataract with microcornea and heterozygote carrier signs caused by a novel missense CRYAA mutation (R54C). American journal of ophthalmology 57 17937925
2009 Mutation analysis of CRYAA, CRYGC, and CRYGD associated with autosomal dominant congenital cataract in Brazilian families. Molecular vision 56 19390652
2018 The small heat shock proteins, especially HspB4 and HspB5 are promising protectants in neurodegenerative diseases. Neurochemistry international 52 29425965
2012 Identification of the HSPB4/TLR2/NF-κB axis in macrophage as a therapeutic target for sterile inflammation of the cornea. EMBO molecular medicine 50 22359280
2008 A novel mutation in AlphaA-crystallin (CRYAA) caused autosomal dominant congenital cataract in a large Chinese family. Human mutation 50 18407550
1987 Confirmation of assignment of the human alpha 1-crystallin gene (CRYA1) to chromosome 21 with regional localization to q22.3. Human genetics 48 3610158
2006 A novel fan-shaped cataract-microcornea syndrome caused by a mutation of CRYAA in an Indian family. Molecular vision 47 16735993
2008 Clinical variability of autosomal dominant cataract, microcornea and corneal opacity and novel mutation in the alpha A crystallin gene (CRYAA). American journal of medical genetics. Part A 40 18302245
2007 New phenotype associated with an Arg116Cys mutation in the CRYAA gene: nuclear cataract, iris coloboma, and microphthalmia. Archives of ophthalmology (Chicago, Ill. : 1960) 36 17296897
2011 Structural and functional specificity of small heat shock protein HspB1 and HspB4, two cellular partners of HspB5: role of the in vitro hetero-complex formation in chaperone activity. Biochimie 28 22210387
2018 The Role of the Arginine in the Conserved N-Terminal Domain RLFDQxFG Motif of Human Small Heat Shock Proteins HspB1, HspB4, HspB5, HspB6, and HspB8. International journal of molecular sciences 25 30036999
2016 CpG site methylation in CRYAA promoter affect transcription factor Sp1 binding in human lens epithelial cells. BMC ophthalmology 20 27507241
2013 A R54L mutation of CRYAA associated with autosomal dominant nuclear cataracts in a Chinese family. Current eye research 20 24074001
2008 Transcriptional regulation of mouse alpha A-crystallin gene in a 148kb Cryaa BAC and its derivates. BMC developmental biology 17 18803847
2018 A novel mutation in the CRYAA gene associated with congenital cataract and microphthalmia in a Chinese family. BMC medical genetics 16 30340470
2012 A novel mutation in CRYAA is associated with autosomal dominant suture cataracts in a Chinese family. Molecular vision 16 23288997
2010 Autosomal dominant congenital nuclear cataracts caused by a CRYAA gene mutation. Current eye research 15 20465443
2021 HspB4/αA-Crystallin Modulates Neuroinflammation in the Retina via the Stress-Specific Inflammatory Pathways. Journal of clinical medicine 14 34071438
2015 A novel 3-base pair deletion of the CRYAA gene identified in a large Chinese pedigree featuring autosomal dominant congenital perinuclear cataract. Genetics and molecular research : GMR 13 25729975
2021 Cataract-causing allele in CRYAA (Y118D) proceeds through endoplasmic reticulum stress in mouse model. Zoological research 11 33929105
2020 Expanding the phenotype of CRYAA nucleotide variants to a complex presentation of anterior segment dysgenesis. Orphanet journal of rare diseases 11 32791987
2017 Correlations of single nucleotide polymorphisms of CRYAA and CRYAB genes with the risk and clinicopathological features of children suffering from congenital cataract. Medicine 8 28640093
2023 Expression of αA-crystallin (CRYAA) in vivo and in vitro models of age-related cataract and the effect of its silencing on HLEB3 cells. Aging 6 37253645
2011 Congenital anterior polar cataract associated with a missense mutation in the human alpha crystallin gene CRYAA. Molecular vision 6 22065922
1990 Regional assignment of the mouse alpha A2-crystallin gene (Crya-1) to chromosome 17A3----B by in situ hybridization. Cytogenetics and cell genetics 6 2369847
2024 HSPB4/CRYAA Protect Photoreceptors during Retinal Detachment in Part through FAIM2 Regulation. Neurology international 4 39311341
2025 CRYAA activates the SIRT1-pi3K/AKT signaling pathway by suppressing mir-155-5p to protect the RPE. Archives of biochemistry and biophysics 3 40350053
2023 Dioleoylphosphatidylglycerol Inhibits Heat Shock Protein B4 (HSPB4)-Induced Inflammatory Pathways In Vitro. International journal of molecular sciences 3 36982926
1990 PvuII and XhoI/EcoRV polymorphisms adjacent to the alpha A-crystallin (CRYA1) gene on human chromosome 21. Nucleic acids research 3 1974046
2024 Novel mTORC2/HSPB4 Interaction: Role and Regulation of HSPB4 T148 Phosphorylation. Cells 2 39682748
2022 Association of single nucleotide polymorphism variations in CRYAA and CRYAB genes with congenital cataract in Pakistani population. Saudi journal of biological sciences 2 35531184
2023 CRYAA and GJA8 promote visual development after whisker tactile deprivation. Heliyon 1 36915480
2021 Polymorphisms in CRYAA Promoter with Susceptibility to Cataract: A Meta-Analysis. Seminars in ophthalmology 1 34010109
2011 [CRYAA gene mutation study in a family with autosomal dominant congenital cataract combined with microcornea]. [Zhonghua yan ke za zhi] Chinese journal of ophthalmology 1 21612679
2023 Mutational analysis of CRYAA gene of cataract and investigating risk assessment factors responsible for eye diseases in district buner, KPK, Pakistan. Cellular and molecular biology (Noisy-le-Grand, France) 0 37807341
2023 The E156K mutation in the CRYAA gene affects the epithelial-mesenchymal transition and migration of human lens epithelial cells. Heliyon 0 38187316

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