Affinage

CRYAB

Alpha-crystallin B chain · UniProt P02511

Length
175 aa
Mass
20.2 kDa
Annotated
2026-06-09
100 papers in source corpus 32 papers cited in narrative 32 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CRYAB (αB-crystallin/HSPB5) is an ATP-independent small heat-shock protein chaperone whose 'holdase' activity is gated by reversible transitions between low-activity nonactivated and high-activity activated oligomeric states, controlled by accessibility of the disordered N-terminal region and integrity of the α-crystallin domain (ACD) dimer interface (PMID:40377988). A conserved histidine (His-104) in the ACD dimer interface senses acidosis: its destabilization or mutation shifts the ACD from dimer toward monomer, expands oligomers, and produces constitutively activated holdase complexes (PMID:25962097), while disease mutants R120G and D109H mimic this constitutive NTR exposure and raise coaggregation propensity (PMID:40377988). CRYAB delays client aggregation through transient early-pathway interactions in the nonactivated state and engages later aggregation stages once activated (PMID:30567736), and it suppresses aggregation of clients including α-synuclein (PMID:28337642) and itself forms hetero-oligomers with HSPB1/HSPB4 via subunit exchange to modulate activity (PMID:22210387). Aggregation-prone CRYAB mutants (R120G, frameshift variants) form toxic amyloid oligomers that are countered by other small HSPs through competitive hetero-oligomer incorporation and ubiquitin-proteasomal clearance (PMID:17092938, PMID:20863832, PMID:25961584). Beyond protein quality control, CRYAB preserves cytoskeletal and sarcomeric integrity through a conserved actin-binding domain and physical interaction with the filamin/Cheerio actin crosslinker (PMID:25715399), translocates to the nucleus under heat stress to reduce F-actin aggregation and caspase-3 apoptosis (PMID:30246229), and protects cardiac contractile/diastolic mechanical function (PMID:17846079). It acts as an antiapoptotic mitochondrial chaperone by interacting with cytochrome c and VDAC to support OXPHOS assembly (PMID:39561005) and limits ferroptosis by stabilizing ferritin heavy chain FTH1 against proteasomal degradation (PMID:38787373). CRYAB modulates multiple signaling pathways: it stabilizes β-catenin against ubiquitination to promote canonical Wnt signaling (PMID:22158051, PMID:31638302), inhibits IKKβ-mediated canonical NF-κB signaling (PMID:31481750, PMID:32532961), suppresses STAT3 DNA-binding activity upon nuclear translocation (PMID:27724964), promotes SMAD4 nuclear translocation in TGF-β1 signaling (PMID:37259327), and supports degradation of mutant p53 via the Fbx4 ubiquitin ligase under HSF1 control (PMID:19343786). Phosphorylation at Ser45/Ser59 is required for its dendrite-protective function (PMID:27085702), while phosphorylation negatively regulates its O-GlcNAcylation-dependent non-classical secretion via exosomes (PMID:26620801). Recessive loss-of-function (343delT) causes myopathy through protein insolubility rescuable by wild-type co-expression (PMID:27226619), and CRYAB function is therapeutically targetable by stereoselective small-molecule binding to its dimer to reverse cataract (PMID:31369034).

Mechanistic history

Synthesis pass · year-by-year structured walk · 30 steps
  1. 2007 High

    Established that CRYAB protects the specifically mechanical (contractile/diastolic) properties of the heart, distinguishing its in vivo physiological role from energetic protection by HSPB2.

    Evidence Genetic mouse models (DKO, mCryAB transgenic) with ischemia/reperfusion, 31P NMR cardiac energetics, contractile measurement

    PMID:17846079

    Open questions at the time
    • Molecular basis linking chaperone activity to mechanical protection not defined
    • Does not identify the cardiac client proteins involved
  2. 2009 Medium

    Showed CRYAB acts as a degradation cofactor by linking mutant p53 to the Fbx4 ubiquitin ligase, connecting chaperone function to targeted proteolysis under HSF1 control.

    Evidence Reciprocal Co-IP of p53R175H with CRYAB and Fbx4, hsf1-/- and alphaBcry-/- MEFs, ectopic Fbx4 stability assays

    PMID:19343786

    Open questions at the time
    • Whether CRYAB is a general adaptor for Fbx4 substrates unknown
    • Structural basis of the p53-CRYAB-Fbx4 ternary interaction not resolved
  3. 2006 High

    Defined that the disease mutant R120G forms toxic amyloid oligomers and that other small HSPs can interrupt this to restore proteostasis and viability.

    Evidence Recombinant protein assays, native PAGE, anti-oligomer antibody, adenoviral cardiomyocyte expression, proteasome activity assay

    PMID:17092938

    Open questions at the time
    • Atomic structure of the toxic oligomer not determined
    • How HSP22/HSP25 physically block oligomerization unresolved
  4. 2010 High

    Demonstrated that aggregate-prone CRYAB mutants are cleared by the ubiquitin-proteasome system, with HSPB1 directing this degradation.

    Evidence Co-expression in H9c2 cells, HSPB1 overexpression/knockdown, proteasome inhibitor, ubiquitin conjugate immunoblot

    PMID:20863832

    Open questions at the time
    • E3 ligase mediating mutant ubiquitination not identified
    • Selectivity for mutant over wild-type not mechanistically explained
  5. 2011 Medium

    Mapped CRYAB engagement of adherens junctions, showing its core domain binds E-cadherin and β-catenin to retain β-catenin at the membrane and suppress Wnt target genes.

    Evidence Reciprocal Co-IP of endogenous E-cadherin/β-catenin with CRYAB, domain mapping, NPC xenograft assay

    PMID:22158051

    Open questions at the time
    • Reconciliation with later report that CRYAB promotes Wnt signaling not addressed
    • Direct vs indirect nature of the β-catenin interaction not fully separated
  6. 2011 Medium

    Showed CRYAB forms hetero-oligomers with HSPB1 and HSPB4 with distinct exchange kinetics and chaperone activities, establishing oligomeric plasticity as a regulatory feature.

    Evidence Biochemical reconstitution, SAXS, subunit exchange kinetics, chaperone activity assays

    PMID:22210387

    Open questions at the time
    • In vivo stoichiometry of hetero-oligomers unknown
    • Functional consequences in tissue not tested
  7. 2013 Medium

    Revealed a context-dependent role in NF-κB signaling, where CRYAB enhances TNF-α-induced NF-κB and adhesion molecule expression in endothelium.

    Evidence Ectopic expression and αB-crystallin-deficient endothelial cells, IκB measurement, in vivo leukocyte rolling

    PMID:23929007

    Open questions at the time
    • Opposite (inhibitory) effect on NF-κB in epithelial contexts not reconciled
    • Direct molecular target in the NF-κB cascade not identified here
  8. 2007 Medium

    Identified transcriptional control of CRYAB by BRG1/SWI-SNF acting through a nucleosome-positioned response element requiring HMGA1.

    Evidence Promoter deletion, ChIP for HMGA1 in vivo, in vitro binding, luciferase reporter

    PMID:17723105

    Open questions at the time
    • Physiological stimuli driving this regulation not defined
    • Tissue specificity of the element unclear
  9. 2015 High

    Defined His-104 in the ACD dimer interface as a pH sensor that toggles oligomer state and holdase activity, providing a structural basis for stress-activation.

    Evidence In vitro biochemistry, mutagenesis, dimer-interface structural analysis, pH-range chaperone assays

    PMID:25962097

    Open questions at the time
    • In-cell relevance of His-104 pH sensing not demonstrated
    • Identity of physiological clients of the activated state not mapped
  10. 2015 High

    Established the conserved actin/sarcomere role: CryAB localizes to Z-bands and binds the filamin orthologue Cheerio, and R120G disrupts myofibrillar integrity in vivo.

    Evidence Mass spectrometry, Co-IP, muscle RNAi, transgenic R120G expression, sarcomere imaging, cardiac phenotyping in Drosophila

    PMID:25715399

    Open questions at the time
    • Direct F-actin vs filamin contribution not fully separated
    • Whether human CRYAB binds filamin in muscle not directly tested
  11. 2015 Medium

    Showed phosphorylation negatively regulates non-classical exosomal secretion of CryAB, with O-GlcNAcylation required for packaging.

    Evidence YFP phosphomimetic constructs, CD63/Rab27 colocalization, exosome isolation and immunoblot

    PMID:26620801

    Open questions at the time
    • Kinase responsible in this context not identified
    • Functional role of secreted CryAB not addressed
  12. 2016 Medium

    Demonstrated that Ser45/Ser59 phosphorylation is specifically required for CRYAB-mediated enhancement of dendritic complexity.

    Evidence Phospho-mutant/phosphomimetic constructs in hippocampal neurons and in utero electroporation, Sholl analysis

    PMID:27085702

    Open questions at the time
    • Mechanism linking phosphorylation to dendrite morphology unknown
    • Relevant client/cytoskeletal effectors not identified
  13. 2016 Medium

    Placed CRYAB in anti-inflammatory signaling as a STAT3 partner that translocates to the nucleus and blocks STAT3 DNA binding.

    Evidence Co-IP with STAT3, EMSA, immunofluorescence, siRNA of DRD2/CRYAB in astrocytes

    PMID:27724964

    Open questions at the time
    • Direct vs scaffold-mediated inhibition of STAT3 unresolved
    • How nuclear translocation is triggered not defined
  14. 2016 Medium

    Identified KLF4 as a direct transcriptional activator of CRYAB driving osteosarcoma proliferation and migration.

    Evidence ChIP at CRYAB promoter, luciferase reporter, KLF4 gain/loss with CRYAB readout

    PMID:27105535

    Open questions at the time
    • Downstream CRYAB effectors in tumor cells not mapped
    • Generality across cancers untested
  15. 2016 Medium

    Supported a recessive loss-of-function disease model by showing the 343delT mutant is insoluble and rescued in solubility by direct interaction with wild-type CRYAB.

    Evidence Patient iPSC-derived myotubes/cardiomyocytes, HSPB5-null BHK21 cells, in vitro refolding, Co-IP

    PMID:27226619

    Open questions at the time
    • Native fold/structure of 343delT not characterized
    • Tissue-specific thresholds for pathology unclear
  16. 2017 Medium

    Confirmed CRYAB suppresses intracellular aggregation of α-synuclein, extending its anti-aggregation chaperone activity to a neurodegeneration-relevant client.

    Evidence Bicistronic constructs in Neuro-2a cells, quantification of α-syn inclusions

    PMID:28337642

    Open questions at the time
    • Whether interaction is direct and stoichiometric not shown
    • In vivo neuronal relevance not tested
  17. 2018 Medium

    Resolved state-dependent chaperone mechanism: nonactivated WT acts only early in aggregation, while activated mutant forms can also intervene at late stages.

    Evidence In vitro chaperone assays with α-lactalbumin, WT vs stress-mimicking mutants

    PMID:30567736

    Open questions at the time
    • Single defined client limits generalization
    • Structural snapshots of late-stage engagement absent
  18. 2018 Medium

    Linked nuclear translocation under heat stress to cytoskeletal protection and apoptosis suppression in cardiomyocytes.

    Evidence Stable CRYAB-overexpressing H9C2 cells, immunofluorescence of CRYAB/F-actin, cleaved caspase-3, flow cytometry

    PMID:30246229

    Open questions at the time
    • Nuclear import mechanism unknown
    • Direct vs indirect effect on caspase-3 unresolved
  19. 2019 Medium

    Reframed the CRYAB-β-catenin interaction as protective, stabilizing β-catenin against ubiquitination to promote Wnt-driven osteogenesis.

    Evidence Co-IP, in vitro ubiquitination, Wnt luciferase reporter, gain/loss in BMSCs, in vivo bone formation

    PMID:31638302

    Open questions at the time
    • Contradiction with adherens-junction sequestration model not reconciled
    • Mechanism by which CRYAB blocks β-catenin ubiquitination undefined
  20. 2019 Medium

    Defined CRYAB inhibition of canonical NF-κB by blocking IKK complex formation, with anti-inflammatory protection in colitis models.

    Evidence Lentiviral overexpression and CRISPR knockout, IKK complex immunoblot, cytokine assays, TAT-CRYAB in DSS/TNBS colitis

    PMID:31481750

    Open questions at the time
    • Direct CRYAB-IKKβ binding not structurally shown
    • Reconciliation with endothelial pro-NF-κB role missing
  21. 2019 Medium

    Showed the ACD mediates direct membrane interaction by embedding within liposomes, a feature relevant to non-classical secretion.

    Evidence Liposome binding, proteinase K protection, MS of protected domains

    PMID:31338686

    Open questions at the time
    • Membrane topology in cells not confirmed
    • Link to a specific secretion route not established
  22. 2019 High

    Established CRYAB dimers as a druggable target, with stereoselective oxysterol binding required to reverse lens opacity.

    Evidence In silico docking, DSF, MST, topical treatment of R120G and aged cataract mice, TEM

    PMID:31369034

    Open questions at the time
    • Co-structure of CRYAB-ligand complex not solved
    • Whether binding reactivates physiological chaperone function unclear
  23. 2020 Medium

    Extended NF-κB suppression to hepatic I/R injury and added Akt1/mTOR-driven M2 macrophage polarization as a parallel protective mechanism.

    Evidence IKKβ/IKKα pathway immunoblot/IF, Akt1/mTOR analysis, miR-450b-5p inhibition, in vivo hepatic IRI

    PMID:32532961

    Open questions at the time
    • Whether macrophage effect is cell-autonomous or secreted-CRYAB mediated unclear
    • Direct IKKβ engagement not shown structurally
  24. 2020 Medium

    Showed phosphomimetic HspB5 enhances plasma membrane trafficking and stability of F508del-CFTR, indicating phosphorylation-state-dependent client handling.

    Evidence Phospho-mutant expression, CFTR surface biotinylation, electrophysiology, Co-IP

    PMID:32650630

    Open questions at the time
    • Direct CRYAB-CFTR binding interface undefined
    • In vivo relevance to cystic fibrosis untested
  25. 2022 Medium

    Identified CRYAB as a senescence-induced survival gene whose chemical inhibition triggers senolysis.

    Evidence Single-cell RNA-seq, chemical inhibitor (25HC), in vitro/in vivo skeletal muscle validation

    PMID:35198901

    Open questions at the time
    • Molecular survival pathway protected by CRYAB in senescent cells not defined
    • Selectivity of 25HC for CRYAB incomplete
  26. 2023 Medium

    Connected HSPB5 to TGF-β1 signaling by promoting SMAD4 nuclear translocation, with druggable disruption reducing fibrosis.

    Evidence Co-IP with SMAD4, SMAD4 nuclear IF, NCI-41356 inhibitor, bleomycin mouse model, collagen quantification

    PMID:37259327

    Open questions at the time
    • Whether interaction is direct unconfirmed
    • Mechanism of SMAD4 import facilitation unknown
  27. 2023 Medium

    Identified NUAK kinase as an upstream regulator phosphorylating conserved serines on CryAB to prevent its aggregation in muscle.

    Evidence CRISPR kinase-dead mutation, yeast 2-hybrid, phospho-mimetic NUAK, phosphosite mutagenesis, Drosophila muscle phenotype

    PMID:37713608

    Open questions at the time
    • Direct in vitro phosphorylation by NUAK not shown
    • Whether human NUAK phosphorylates human CRYAB at these sites untested
  28. 2024 Medium

    Defined CRYAB as a mitochondrial antiapoptotic chaperone binding cytochrome c and VDAC to support OXPHOS, with a disease mutation impairing these interactions.

    Evidence Co-IP of WT and p.E105K with cytochrome c/VDAC, OXPHOS activity assays, Cryab knock-in/knockout mouse retinal phenotyping

    PMID:39561005

    Open questions at the time
    • Whether CRYAB resides inside mitochondria or at the outer membrane unresolved
    • Stoichiometry of cytochrome c/VDAC binding undefined
  29. 2024 Medium

    Showed CRYAB stabilizes ferritin heavy chain FTH1 against proteasomal degradation in a lactylation-dependent manner to suppress ferroptosis.

    Evidence IP-MS, Co-IP of CRYAB-FTH1, knockdown with Fe/ROS and ferroptosis assays in BMSCs

    PMID:38787373

    Open questions at the time
    • How lactylation controls the interaction mechanistically unclear
    • Whether CRYAB directly blocks FTH1 ubiquitination untested
  30. 2024 Medium

    Placed CRYAB in a LBH-CRYAB axis that inhibits both apoptosis and ferroptosis through a shared p53 effector in cardiac I/R injury.

    Evidence Inhibitors, ectopic expression, LBH/CRYAB knockout mice, apoptosis and ferroptosis assays

    PMID:38660406

    Open questions at the time
    • Direct CRYAB-p53 regulation in this context not mapped
    • Mechanism converging two death pathways on p53 unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CRYAB's reversible oligomeric activation state is selectively coupled to its many divergent and sometimes opposite client and signaling functions in vivo remains unresolved.
  • No unified model linking activation state to specific client/pathway selection
  • Opposing NF-κB and Wnt effects across tissues not mechanistically reconciled
  • Atomic structures of client-bound activated complexes lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0044183 protein folding chaperone 5 GO:0140313 molecular sequestering activity 4 GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005886 plasma membrane 3 GO:0005634 nucleus 2 GO:0005829 cytosol 2 GO:0005856 cytoskeleton 2 GO:0005739 mitochondrion 1
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-392499 Metabolism of proteins 4 R-HSA-5357801 Programmed Cell Death 3 R-HSA-8953897 Cellular responses to stimuli 3 R-HSA-397014 Muscle contraction 2
Partners
CTNNB1CYCSFLNAFTH1HSPB1SMAD4STAT3VDAC

Evidence

Reading pass · 32 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2015 A conserved histidine (His-104) in the ACD dimer interface of HSPB5 controls oligomer structure and chaperone activity in response to acidosis. Destabilization by pH or His-104 mutation shifts the ACD from dimer to monomer and expands oligomer states, producing constitutively activated holdase chaperones that reorganize into structurally distinct client-bound complexes. In vitro biochemical assays, mutagenesis, structural analysis of dimer interface, chaperone activity assays across pH range eLife High 25962097
2025 HSPB5 wild-type exists in reversible nonactivated (low activity) and activated (high activity) states; disease mutants R120G and D109H are constitutively activated chaperones. The disordered N-terminal regions (NTR) are sequestered from solvent in nonactivated states; mutation or acidic pH causes rearrangements that expose the NTR to enable client binding. Constitutive NTR exposure in mutants leads to increased coaggregation propensity and early cataract. Hydrogen-deuterium exchange mass spectrometry, native mass spectrometry, chaperone activity assays, mutagenesis of R120G and D109H variants Proceedings of the National Academy of Sciences of the United States of America High 40377988
2018 Under non-stress conditions, wild-type HSPB5 delays client aggregation solely through transient interactions early in the aggregation pathway, whereas HSPB5 mutants mimicking stress-activated states can also intervene at later aggregation stages, demonstrating state-dependent mechanistic differences in chaperone engagement. In vitro chaperone activity assays with α-lactalbumin as client, comparison of WT and stress-mimicking mutants under varying conditions The Journal of biological chemistry Medium 30567736
2006 The R120G mutant CryAB forms toxic amyloid oligomers (~240–480 kDa) detected by anti-oligomer antibody, whereas wild-type forms only high-molecular-mass species. HSP22 and HSP25 directly interrupt oligomer formation by CryAB R120G; blockade of oligomer formation recovered ubiquitin-proteasomal activity and cellular viability in cardiomyocytes. In vitro recombinant protein assay, native PAGE, anti-oligomer immunoreactivity, adenoviral transfection in cardiomyocytes, proteasome activity assay The Journal of biological chemistry High 17092938
2010 HSPB1 (Hsp27) selectively degrades aggregate-prone CryAB mutants (R120G, 450delA, 464delCT) via the ubiquitin-proteasome system. Evidence includes: proteasome inhibitor accumulates mutants; R120G and 450delA accumulate ubiquitin conjugates; HSPB1 knockdown increases polyubiquitin conjugates; HSPB1 overexpression rescue of 464delCT is blocked by proteasome inhibition. Co-expression in H9c2 cells, HSPB1 overexpression/knockdown, proteasome inhibitor treatment, ubiquitin conjugate detection by immunoblot Journal of molecular and cellular cardiology High 20863832
2015 Co-expression of HSPB1, HSPB4, or HSPB5 itself most effectively prevents aggregation of three HSPB5 mutants (R120G, 450ΔA, 464ΔCT) by competitive incorporation into hetero-oligomers, negating dominant-negative effects; Hsp70 co-expression did not reduce aggregation, indicating the mechanism is oligomer-based rather than general chaperone activity. Systematic co-expression of all HSPB family members with HSPB5 mutants, aggregation scoring in cells PloS one Medium 25961584
2009 HSF1 regulates p53 protein stability through alphaB-crystallin: hsf1−/− and alphaBcry−/− cells accumulate p53 due to reduced alphaB-crystallin levels. Immunoprecipitated p53R175H from wild-type MEFs pulls down both alphaB-crystallin and Fbx4 ubiquitin ligase, and ectopic Fbx4 increases p53R175H degradation in a mechanism requiring alphaB-crystallin. Co-immunoprecipitation of p53 with alphaB-crystallin and Fbx4, knockout MEF cell lines, ectopic Fbx4 expression, p53 stability assays Journal of cellular biochemistry Medium 19343786
2011 CRYAB associates with both E-cadherin and β-catenin at the cadherin/catenin adherens junction; the alpha-crystallin core domain mediates these interactions. CRYAB overexpression inhibits E-cadherin cytoplasmic internalization and maintains β-catenin at the membrane, reducing downstream cyclin-D1 and c-myc expression. Co-immunoprecipitation of endogenous E-cadherin and β-catenin with ectopic and recombinant CRYAB; domain mapping; NPC xenograft tumor suppression assay Oncogene Medium 22158051
2019 CRYAB physically interacts with β-catenin and protects it from ubiquitination and proteasomal degradation, thereby stabilizing β-catenin and promoting canonical Wnt signaling to enhance osteogenic differentiation of human BMSCs. Co-immunoprecipitation, in vitro ubiquitination assay, luciferase reporter for Wnt activity, CRYAB overexpression/knockdown in BMSCs, in vivo bone formation assay Cell proliferation Medium 31638302
2024 CRYAB interacts with ferritin heavy chain 1 (FTH1) and maintains FTH1 protein stability via the proteasome mechanism in a lactylation-dependent manner; CRYAB knockdown boosts FTH1 degradation, increases cellular iron and ROS, promoting ferroptosis and reducing osteogenic differentiation of BMSCs. IP-MS to identify CRYAB-interacting proteins, co-immunoprecipitation of CRYAB and FTH1, qRT-PCR, Western blot, ferroptosis assays (Fe/ROS levels, cell viability) Aging Medium 38787373
2016 CRYAB interacts with STAT3 and upon sinomenine treatment undergoes nuclear translocation in astrocytes, where it inhibits STAT3 activation and DNA-binding activity, suppressing neuroinflammation downstream of DRD2. Co-immunoprecipitation of CRYAB with STAT3, electrophoretic mobility shift assay (EMSA) for STAT3 DNA binding, immunofluorescence for nuclear translocation, siRNA knockdown of DRD2 and CRYAB in primary astrocytes Journal of neuroinflammation Medium 27724964
2019 CRYAB suppresses IKKβ-mediated canonical NF-κB signaling by inhibiting IKK complex formation in intestinal epithelial cells. CRYAB overexpression suppresses pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-8); CRYAB deletion markedly enhances inflammatory responses; TAT-CRYAB fusion protein protects intestinal barrier integrity in colitis models. Lentiviral overexpression and CRISPR/Cas9 knockout, Western blot for IKK complex, cytokine measurement, in vivo DSS/TNBS colitis with TAT-CRYAB treatment Mucosal immunology Medium 31481750
2013 αB-crystallin (HspB5) enhances TNF-α-induced NF-κB signaling in endothelial cells, increasing expression of adhesion molecules ICAM-1, VCAM-1, and E-selectin; αB-crystallin-deficient endothelial cells display elevated IκB and incomplete IκB degradation upon TNF-α stimulation, resulting in reduced leukocyte rolling in vivo. Ectopic expression in endothelial cells, endothelial cells from αB-crystallin-deficient mice, IκB level measurement, in vivo leukocyte rolling assay Angiogenesis Medium 23929007
2015 Phosphorylation negatively regulates exosomal secretion of cryAB: nonphosphorylated cryAB is preferentially packaged into exosomes, whereas a triple phosphomimetic (3-SD) mutant forms large cytosolic inclusions and shows decreased colocalization with MVE/exosome markers CD63 and Rab27. O-GlcNAcylation of cryAB is required for its exosomal packaging. YFP-tagged phosphomimetic construct transfection, colocalization with CD63/Rab27 by confocal microscopy, exosome isolation and immunoblot Biochimica et biophysica acta Medium 26620801
2015 Drosophila CryAB accumulates at Z-bands and around myonuclei, contains a conserved actin-binding domain, and physically interacts with the actin crosslinker Cheerio (filamin) as shown by mass spectrometry and co-immunoprecipitation. CryAB attenuation causes myonuclear clustering and altered sarcomeric actin/Cheerio patterns. Expression of CryAB(R120G) in Drosophila muscle disrupts myofibrillar integrity, produces Z-band breaks, reduces muscle performance, and causes cardiac arrhythmia. Mass spectrometry, co-immunoprecipitation, muscle-specific RNAi knockdown, transgenic expression of R120G mutant, confocal imaging of sarcomere structure, muscle performance and cardiac phenotype assays Development (Cambridge, England) High 25715399
2023 NUAK kinase phosphorylates Drosophila CryAB at two previously unidentified serine residues conserved in human CryAB sequence. NUAK and CryAB interact physically (yeast 2-hybrid). Loss of NUAK catalytic function causes CryAB aggregation in muscle tissue; a phospho-mimetic NUAK promotes CryAB phosphorylation; mutation of these serines abolishes phosphorylation. CRISPR kinase-dead mutation, yeast 2-hybrid, phospho-mimetic NUAK construct, phosphosite mutagenesis, in vivo muscle phenotype assay Genetics Medium 37713608
2007 CryAB protects mechanical (contractile/diastolic) properties of the heart while HSPB2 protects cardiac energetic balance. In genetically modified mice expressing only CryAB (DKO/mCryAB-Tg), ischemia/reperfusion caused impaired ATP/PCr recovery and massive energy wasting upon inotropic stimulation, whereas CryAB-alone hearts showed protection against diastolic dysfunction. Genetic mouse models (DKO, mCryAB transgenic, DKO/mCryAB-Tg), isolated heart ischemia/reperfusion, 31P NMR spectroscopy of cardiac energetics, contractile performance measurement FASEB journal High 17846079
2018 CRYAB translocates from cytoplasm to nucleus under heat stress and co-localizes with aggregated F-actin, reducing F-actin aggregation. CRYAB overexpression significantly reduces caspase-3-mediated apoptosis in cardiomyocytes exposed to heat stress. Stable CRYAB-overexpressing H9C2 cell lines, immunofluorescence for CRYAB localization and F-actin, cleaved-caspase 3 Western blot, flow cytometry for apoptosis Cell stress & chaperones Medium 30246229
2017 αB-crystallin (HspB5) inhibits intracellular aggregation of α-synuclein when overexpressed in Neuro-2a cells, demonstrated using bicistronic constructs that uncouple sHsp expression from fluorescent tagging to avoid oligomeric structure artifacts. Bicistronic expression plasmids in Neuro-2a cells, quantification of α-syn inclusion-containing cells by fluorescence microscopy Cell stress & chaperones Medium 28337642
2019 Oxysterol VP1-001 stereoselectively binds to the cryAB dimer (demonstrated by differential scanning fluorimetry and microscale thermophoresis); its enantiomer ent-VP1-001 does not bind and has no therapeutic effect on lens opacity, establishing that stereoselective binding to cryAB dimers is required for reversal of lens opacity in R120G mutant and aged mice. In silico docking, differential scanning fluorimetry (DSF), microscale thermophoresis (MST), topical treatment of cataract mouse models, transmission electron microscopy Investigative ophthalmology & visual science High 31369034
2024 CRYAB mutation p.E105K reduces interaction with cytochrome c and voltage-dependent anion channel (VDAC) as shown by co-immunoprecipitation, impairs OXPHOS assembly and activity, promotes apoptosis, and causes retinal ganglion cell degeneration. Cryab-deficient mice display elevated apoptosis and mitochondrial dysfunctions, establishing CRYAB as a mitochondrial chaperone with antiapoptotic activity in RGCs. Co-immunoprecipitation of p.E105K mutant and WT CRYAB with cytochrome c and VDAC, OXPHOS complex activity assays, apoptosis assays, Cryab-knockin and knockout mice with retinal phenotyping JCI insight Medium 39561005
2007 BRG1 (SWI/SNF ATPase) activates the CRYAB promoter through a 30 bp response element at the edge of a positioned nucleosome; HMGA1 proteins bind an AT-rich sequence within this element both in vitro and in vivo, and HMGA1 target sequences and HMGA1 proteins are required for maximal BRG1-mediated CRYAB promoter activation. Promoter deletion analysis, chromatin immunoprecipitation (ChIP) for HMGA1 binding in vivo, in vitro binding assay, luciferase reporter assay DNA and cell biology Medium 17723105
2016 KLF4 transcription factor directly binds the CRYAB promoter and upregulates CRYAB expression in osteosarcoma cells, promoting cell proliferation and migration via CRYAB. Chromatin immunoprecipitation (ChIP) of KLF4 at CRYAB promoter, luciferase reporter assay, KLF4 overexpression/knockdown with CRYAB expression measurement Oncotarget Medium 27105535
2023 HSPB5 interacts with SMAD4 and this interaction promotes SMAD4 canonical nuclear translocation in TGF-β1 signaling; chemical inhibitor NCI-41356 reduces HSPB5/SMAD4 interaction and blocks SMAD4 nuclear translocation, reducing pulmonary fibrosis markers in vitro and in vivo. Co-immunoprecipitation of HSPB5 with SMAD4, immunofluorescence for SMAD4 nuclear translocation, bleomycin mouse model with NCI-41356 treatment, collagen quantification Pharmaceuticals (Basel, Switzerland) Medium 37259327
2016 Phosphorylation of HspB5 at S45 and S59 (but not S19) is essential for its ability to increase dendritic complexity; non-phosphorylatable HspB5-AAA fails to protect dendrites, while phosphomimetic HspB5-AEE (S45E/S59E-like) recapitulates the wild-type effect both in vitro and in vivo (in utero electroporation). Overexpression of phospho-mutant and phosphomimetic HspB5 constructs in cultured hippocampal neurons and in vivo via in utero electroporation, Sholl analysis of dendritic morphology Cellular and molecular life sciences : CMLS Medium 27085702
2011 In vitro, HspB5 forms hetero-oligomeric complexes with HspB1 and HspB4; subunit exchange kinetics are faster between HspB5 and HspB1 than between HspB5 and HspB4; the resulting hetero-complexes have distinct structural organization, stability, and chaperone-like activities compared to homo-oligomers. Biochemical reconstitution, small-angle X-ray scattering (SAXS), subunit exchange kinetics assay, chaperone activity assays Biochimie Medium 22210387
2019 HSPB5 and HSPB1 interact with lipid membranes differently; the alpha-crystallin domain of HSPB5 is embedded within liposomes as identified by proteinase K protection followed by mass spectrometry, suggesting the alpha-crystallin domain mediates membrane interaction relevant to non-classical secretion. Liposome binding assay, proteinase K protection experiment, mass spectrometry of protected membrane-embedded domains Cell stress & chaperones Medium 31338686
2020 The 343delT HSPB5 mutant protein is extremely insoluble and does not accumulate to detectable levels in iPSC-derived skeletal myotubes and cardiomyocytes; co-expression of wild-type HSPB5 rescues 343delT solubility both in vitro and in cells through direct interaction, supporting a loss-of-function model for the recessive myopathy. iPSC-derived patient cells (homozygous and gene-corrected heterozygous), BHK21 cells lacking HSPB5, in vitro refolding assay, co-immunoprecipitation of WT and 343delT The Journal of biological chemistry Medium 27226619
2022 CRYAB (HSPB5) is identified as a senescence-induced survival gene; chemical inhibition of CRYAB by 25-hydroxycholesterol (25HC) induces senolysis in mouse and human senescent cells in culture and in vivo in mouse skeletal muscle. Single-cell RNA sequencing to identify CRYAB as senescence-induced gene, chemical inhibitor screening, validation in multiple cell types and in vivo mouse skeletal muscle iScience Medium 35198901
2024 LBH transcription factor upregulates CRYAB expression; the LBH-CRYAB signaling axis inhibits both mitochondrial apoptosis and ferroptosis in cardiomyocytes during I/R injury, with p53 identified as a mutual downstream effector for both death pathways. Pharmacological inhibitors, ectopic expression vectors, LBH/CRYAB knockout mouse models, apoptosis and ferroptosis assays in I/R injury model iScience Medium 38660406
2020 CRYAB suppresses the IKKβ-mediated canonical NF-κB pathway (but not the IKKα noncanonical path) in hepatic ischemia/reperfusion injury. CRYAB also activates M2 macrophage polarization through Akt1/mTOR signaling, alleviating liver IRI. Western blot and immunofluorescence for IKKβ/IKKα pathway components, Akt1/mTOR pathway analysis, miR-450b-5p inhibition to restore CRYAB, in vivo hepatic IRI mouse model Cell death & disease Medium 32532961
2020 A phosphomimetic form of HspB5 (but not wild-type or non-phosphorylatable forms) increases plasma membrane trafficking, function, and stability of F508del-CFTR, with effects further enhanced by CFTR corrector/potentiator drugs. Phosphomimetic and non-phosphorylatable HspB5 mutant expression in cell lines, CFTR surface biotinylation, electrophysiology (CFTR function), co-immunoprecipitation International journal of molecular sciences Medium 32650630

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 Hsp27 (HspB1) and alphaB-crystallin (HspB5) as therapeutic targets. FEBS letters 258 17467701
2012 Small heat shock proteins HSP27 (HspB1), αB-crystallin (HspB5) and HSP22 (HspB8) as regulators of cell death. The international journal of biochemistry & cell biology 231 22521623
2001 Alpha-B crystallin gene (CRYAB) mutation causes dominant congenital posterior polar cataract in humans. American journal of human genetics 205 11577372
2019 M2 macrophages promote NSCLC metastasis by upregulating CRYAB. Cell death & disease 113 31097690
2020 Inhibition of miR-450b-5p ameliorates hepatic ischemia/reperfusion injury via targeting CRYAB. Cell death & disease 103 32532961
2016 Sinomenine activates astrocytic dopamine D2 receptors and alleviates neuroinflammatory injury via the CRYAB/STAT3 pathway after ischemic stroke in mice. Journal of neuroinflammation 86 27724964
2011 A novel CRYAB mutation resulting in multisystemic disease. Neuromuscular disorders : NMD 85 21920752
2014 Inflammatory cytokines, interleukin-1 beta and tumor necrosis factor-alpha, upregulated in glioblastoma multiforme, raise the levels of CRYAB in exosomes secreted by U373 glioma cells. Biochemical and biophysical research communications 83 25261722
2007 Aging skeletal muscle shows a drastic increase in the small heat shock proteins alphaB-crystallin/HspB5 and cvHsp/HspB7. European journal of cell biology 78 17761354
2014 HspB1, HspB5 and HspB4 in Human Cancers: Potent Oncogenic Role of Some of Their Client Proteins. Cancers 77 24514166
2019 Progression of the role of CRYAB in signaling pathways and cancers. OncoTargets and therapy 73 31239701
2010 The p.G154S mutation of the alpha-B crystallin gene (CRYAB) causes late-onset distal myopathy. Neuromuscular disorders : NMD 70 20171888
2017 The novel αB-crystallin (CRYAB) mutation p.D109G causes restrictive cardiomyopathy. Human mutation 61 28493373
2015 A conserved histidine modulates HSPB5 structure to trigger chaperone activity in response to stress-related acidosis. eLife 59 25962097
2006 Interruption of CryAB-amyloid oligomer formation by HSP22. The Journal of biological chemistry 58 17092938
2021 Salvianolic acid A relieves cognitive disorder after chronic cerebral ischemia: Involvement of Drd2/Cryab/NF-κB pathway. Pharmacological research 57 34800628
2018 Rosemary Reduces Heat Stress by Inducing CRYAB and HSP70 Expression in Broiler Chickens. Oxidative medicine and cellular longevity 55 30425783
2011 Tumor suppressor Alpha B-crystallin (CRYAB) associates with the cadherin/catenin adherens junction and impairs NPC progression-associated properties. Oncogene 55 22158051
2018 The small heat shock proteins, especially HspB4 and HspB5 are promising protectants in neurodegenerative diseases. Neurochemistry international 52 29425965
2013 Protein interactomes of three stress inducible small heat shock proteins: HspB1, HspB5 and HspB8. International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group 52 23697380
2006 Identification of a CRYAB mutation associated with autosomal dominant posterior polar cataract in a Chinese family. Investigative ophthalmology & visual science 52 16877416
2016 A novel dominant D109A CRYAB mutation in a family with myofibrillar myopathy affects αB-crystallin structure. BBA clinical 48 27904835
2010 Selective degradation of aggregate-prone CryAB mutants by HSPB1 is mediated by ubiquitin-proteasome pathways. Journal of molecular and cellular cardiology 47 20863832
2017 The small heat shock proteins αB-crystallin (HSPB5) and Hsp27 (HSPB1) inhibit the intracellular aggregation of α-synuclein. Cell stress & chaperones 46 28337642
2015 Drosophila small heat shock protein CryAB ensures structural integrity of developing muscles, and proper muscle and heart performance. Development (Cambridge, England) 45 25715399
2019 Small heat shock protein CRYAB inhibits intestinal mucosal inflammatory responses and protects barrier integrity through suppressing IKKβ activity. Mucosal immunology 44 31481750
2020 MiRNA-671-5p Promotes prostate cancer development and metastasis by targeting NFIA/CRYAB axis. Cell death & disease 43 33144585
2010 Infantile onset myofibrillar myopathy due to recessive CRYAB mutations. Neuromuscular disorders : NMD 40 21130652
2018 BYD Ameliorates Oxidative Stress-Induced Myocardial Apoptosis in Heart Failure Post-Acute Myocardial Infarction via the P38 MAPK-CRYAB Signaling Pathway. Frontiers in physiology 39 29867551
2009 Identification of a novel CRYAB mutation associated with autosomal recessive juvenile cataract in a Saudi family. Molecular vision 39 19461931
2022 Senolysis induced by 25-hydroxycholesterol targets CRYAB in multiple cell types. iScience 38 35198901
2007 CRYAB and HSPB2 deficiency alters cardiac metabolism and paradoxically confers protection against myocardial ischemia in aging mice. American journal of physiology. Heart and circulatory physiology 38 17873008
2021 Presence and activation of pro-inflammatory macrophages are associated with CRYAB expression in vitro and after peripheral nerve injury. Journal of neuroinflammation 37 33761953
2009 A novel mutation in CRYAB associated with autosomal dominant congenital nuclear cataract in a Chinese family. Molecular vision 36 19597569
2015 Phosphorylation negatively regulates exosome mediated secretion of cryAB in glioma cells. Biochimica et biophysica acta 34 26620801
2018 CRYAB protects cardiomyocytes against heat stress by preventing caspase-mediated apoptosis and reducing F-actin aggregation. Cell stress & chaperones 32 30246229
2015 Missense Mutations in CRYAB Are Liable for Recessive Congenital Cataracts. PloS one 32 26402864
2007 Unmasking different mechanical and energetic roles for the small heat shock proteins CryAB and HSPB2 using genetically modified mouse hearts. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 31 17846079
2024 CRYAB suppresses ferroptosis and promotes osteogenic differentiation of human bone marrow stem cells via binding and stabilizing FTH1. Aging 30 38787373
2009 Heat shock factor 1 deficiency via its downstream target gene alphaB-crystallin (Hspb5) impairs p53 degradation. Journal of cellular biochemistry 30 19343786
2021 Novel Secreted Protein of Mycoplasma bovis MbovP280 Induces Macrophage Apoptosis Through CRYAB. Frontiers in immunology 29 33659004
2020 Qishen Granule alleviates endoplasmic reticulum stress-induced myocardial apoptosis through IRE-1-CRYAB pathway in myocardial ischemia. Journal of ethnopharmacology 29 31945401
2019 CRYAB promotes osteogenic differentiation of human bone marrow stem cells via stabilizing β-catenin and promoting the Wnt signalling. Cell proliferation 29 31638302
2005 Differential expression of alphaB-crystallin and Hsp27-1 in anaplastic thyroid carcinomas because of tumor-specific alphaB-crystallin gene (CRYAB) silencing. Cell stress & chaperones 29 16184762
2020 CRYAB inhibits migration and invasion of bladder cancer cells through the PI3K/AKT and ERK pathways. Japanese journal of clinical oncology 28 31829429
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
2017 Upregulation and phosphorylation of HspB1/Hsp25 and HspB5/αB-crystallin after transient middle cerebral artery occlusion in rats. Cell stress & chaperones 27 28425051
2016 Krüppel-like factor 4 promotes human osteosarcoma growth and metastasis via regulating CRYAB expression. Oncotarget 27 27105535
2019 Mechanism of Action of VP1-001 in cryAB(R120G)-Associated and Age-Related Cataracts. Investigative ophthalmology & visual science 26 31369034
2011 Cardioprotective effect of nicorandil, a mitochondrial ATP-sensitive potassium channel opener, prolongs survival in HSPB5 R120G transgenic mice. PloS one 26 21541347
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
2013 Analysis of the dominant effects mediated by wild type or R120G mutant of αB-crystallin (HspB5) towards Hsp27 (HspB1). PloS one 24 23950959
2019 The small heat shock proteins, HSPB1 and HSPB5, interact differently with lipid membranes. Cell stress & chaperones 23 31338686
1990 Human alpha B-crystallin (CRYA2) gene mapped to chromosome 11q12-q23. Human genetics 23 2370055
2023 Salvianolic acid A improve mitochondrial respiration and cardiac function via inhibiting apoptosis pathway through CRYAB in diabetic cardiomyopathy. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 21 36773525
2013 αB-crystallin/HspB5 regulates endothelial-leukocyte interactions by enhancing NF-κB-induced up-regulation of adhesion molecules ICAM-1, VCAM-1 and E-selectin. Angiogenesis 21 23929007
2020 Mog1 knockout causes cardiac hypertrophy and heart failure by downregulating tbx5-cryab-hspb2 signalling in zebrafish. Acta physiologica (Oxford, England) 20 33032360
2010 Later retinal degeneration following childhood surgical aphakia in a family with recessive CRYAB mutation (p.R56W). Ophthalmic genetics 20 20141356
2016 HspB5/αB-crystallin increases dendritic complexity and protects the dendritic arbor during heat shock in cultured rat hippocampal neurons. Cellular and molecular life sciences : CMLS 19 27085702
2007 HMGA1 mediates the activation of the CRYAB promoter by BRG1. DNA and cell biology 19 17723105
2009 Changes in retinal alphaB-crystallin (cryab) RNA transcript levels during periods of altered ocular growth in chickens. Experimental eye research 18 19878675
2020 A novel dominant mutation in CRYAB gene leading to a severe phenotype with childhood onset. Molecular genetics & genomic medicine 16 32420686
2022 In high-grade ovarian carcinoma, platinum-sensitive tumor recurrence and acquired-resistance derive from quiescent residual cancer cells that overexpress CRYAB, CEACAM6, and SOX2. The Journal of pathology 15 35302657
2016 The Human 343delT HSPB5 Chaperone Associated with Early-onset Skeletal Myopathy Causes Defects in Protein Solubility. The Journal of biological chemistry 15 27226619
2022 CRYAB reduces cigarette smoke-induced inflammation, apoptosis, and oxidative stress by retarding PI3K/Akt and NF-κB signaling pathways in human bronchial epithelial cells. Allergologia et immunopathologia 14 36086960
2020 Chaperone-Like Activity of HSPB5: The Effects of Quaternary Structure Dynamics and Crowding. International journal of molecular sciences 14 32668633
2018 Sub-Toxic Human Amylin Fragment Concentrations Promote the Survival and Proliferation of SH-SY5Y Cells via the Release of VEGF and HspB5 from Endothelial RBE4 Cells. International journal of molecular sciences 14 30463298
2018 HSPB5 engages multiple states of a destabilized client to enhance chaperone activity in a stress-dependent manner. The Journal of biological chemistry 14 30567736
2015 Rescue of αB Crystallin (HSPB5) Mutants Associated Protein Aggregation by Co-Expression of HSPB5 Partners. PloS one 14 25961584
2011 Association of Alpha B-Crystallin (CRYAB) genotypes with breast cancer susceptibility in Taiwan. Cancer genomics & proteomics 14 21980040
2024 In-depth analysis of serum antibodies against Epstein-Barr virus lifecycle proteins, and EBNA1, ANO2, GlialCAM and CRYAB peptides in patients with multiple sclerosis. Frontiers in immunology 13 39742283
2022 Novel mycoplasma nucleomodulin MbovP475 decreased cell viability by regulating expression of CRYAB and MCF2L2. Virulence 13 36121023
2021 Identification of CRYAB+ KCNN3+ SOX9+ Astrocyte-Like and EGFR+ PDGFRA+ OLIG1+ Oligodendrocyte-Like Tumoral Cells in Diffuse IDH1-Mutant Gliomas and Implication of NOTCH1 Signalling in Their Genesis. Cancers 13 33925547
2020 HspB5 Activates a Neuroprotective Glial Cell Response in Experimental Tauopathy. Frontiers in neuroscience 13 32595446
2013 Differential expression and regulation of Cryab in mouse uterus during preimplantation period. Reproduction (Cambridge, England) 13 23579188
2013 CRYAB modulates the activation of CD4+ T cells from relapsing-remitting multiple sclerosis patients. Multiple sclerosis (Houndmills, Basingstoke, England) 13 23736536
2010 αB-crystallin (HspB5) in familial amyloidotic polyneuropathy. International journal of experimental pathology 13 20804537
2006 CRYAB promoter polymorphisms: influence on multiple sclerosis susceptibility and clinical presentation. Clinica chimica acta; international journal of clinical chemistry 13 17010329
2024 The activation of LBH-CRYAB signaling promotes cardiac protection against I/R injury by inhibiting apoptosis and ferroptosis. iScience 12 38660406
2019 αB-crystallin (CRYAB) regulates the proliferation, apoptosis, synthesis and degradation of extracellular matrix of chondrocytes in osteoarthritis. Experimental cell research 12 31226261
2019 Anti-inflammatory and Oto-Protective Effect of the Small Heat Shock Protein Alpha B-Crystallin (HspB5) in Experimental Pneumococcal Meningitis. Frontiers in neurology 12 31244750
2022 The crystallin alpha B (HSPB5)-tripartite motif containing 33 (TRIM33) axis mediates myocardial fibrosis induced by angiotensinogen II through transforming growth factor-β (TGF-β1)-Smad3/4 signaling. Bioengineered 11 35333698
2021 Analysis of amyloid-like secondary structure in the Cryab-R120G knock-in mouse model of hereditary cataracts by two-dimensional infrared spectroscopy. PloS one 11 34520490
2020 Effect of cataract-associated mutations in the N-terminal domain of αB-crystallin (HspB5). Experimental eye research 11 32533979
2016 Induction and phosphorylation of the small heat shock proteins HspB1/Hsp25 and HspB5/αB-crystallin in the rat retina upon optic nerve injury. Cell stress & chaperones 11 26475352
2022 Role of methylation-related genes CRYAB and SLC39A11 in the occurrence and development of lung adenocarcinoma. Annals of translational medicine 9 36388803
2021 Long Noncoding RNA lnc-TSSK2-8 Activates Canonical Wnt/β-Catenin Signaling Through Small Heat Shock Proteins HSPA6 and CRYAB. Frontiers in cell and developmental biology 9 34041241
2019 Adipocyte abundances of CES1, CRYAB, ENO1 and GANAB are modified in-vitro by glucose restriction and are associated with cellular remodelling during weight regain. Adipocyte 9 31037987
2019 Radiation-Stimulated Translocation of CD166 and CRYAB to the Endothelial Surface Provides Potential Vascular Targets on Irradiated Brain Arteriovenous Malformations. International journal of molecular sciences 9 31757032
2008 HspB5/alphaB-crystallin: properties and current progress in neuropathy. Current neurovascular research 9 18473830
2025 Activation mechanism of small heat shock protein HSPB5 revealed by disease-associated mutants. Proceedings of the National Academy of Sciences of the United States of America 8 40377988
2022 Effects of the CRYAB gene on stem cell-like properties of colorectal cancer and its mechanism. Journal of cancer research and therapeutics 8 36204880
2020 HspB5/αB-crystallin phosphorylation at S45 and S59 is essential for protection of the dendritic tree of rat hippocampal neurons. Journal of neurochemistry 8 33220080
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
2013 Characterization of migration parameters on peripheral and central nervous system T cells following treatment of experimental allergic encephalomyelitis with CRYAB. Journal of neuroimmunology 8 23602713
2024 Mutation of CRYAB encoding a conserved mitochondrial chaperone and antiapoptotic protein causes hereditary optic atrophy. JCI insight 7 39561005
2021 PIK3R1, SPNB2, and CRYAB as Potential Biomarkers for Patients with Diabetes and Developing Acute Myocardial Infarction. International journal of endocrinology 7 34887920
2020 Phosphorylation of the Chaperone-Like HspB5 Rescues Trafficking and Function of F508del-CFTR. International journal of molecular sciences 7 32650630
2023 HSPB5 Inhibition by NCI-41356 Reduces Experimental Lung Fibrosis by Blocking TGF-β1 Signaling. Pharmaceuticals (Basel, Switzerland) 6 37259327
2023 Identification of CryAB as a target of NUAK kinase activity in Drosophila muscle tissue. Genetics 6 37713608

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