Affinage

HSPB1

Heat shock protein beta-1 · UniProt P04792

Round 2 corrected
Length
205 aa
Mass
22.8 kDa
Annotated
2026-04-28
130 papers in source corpus 40 papers cited in narrative 40 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HSPB1 (Hsp27) is an ATP-independent small heat shock protein that functions as a molecular chaperone, anti-apoptotic factor, and cytoskeletal regulator, with its diverse activities controlled by phosphorylation-dependent oligomeric dynamics. It forms large (~24-mer) oligomers that dissociate to chaperone-active dimers upon phosphorylation at Ser15, Ser78, and Ser82 by MAPKAP kinase-2 (downstream of p38 MAPK) or protein kinase C; the N-terminal domain encodes the oligomer–dimer equilibrium determinants and is essential for substrate engagement, while the alpha-crystallin domain harbors a client-binding groove also used for autoinhibitory intramolecular contacts (PMID:1332886, PMID:10383393, PMID:25699602, PMID:31974309, PMID:22264079). Phosphorylated HSPB1 stabilizes actin filaments, promotes BMP-2-induced cell migration, co-aggregates with unfolded substrates to facilitate Hsp70-mediated disaggregation, negatively regulates ferroptosis by suppressing iron-mediated lipid ROS, sequesters cytochrome c to block Apaf-1/caspase-9-dependent apoptosis, and directs client proteins (GATA-1, MST1) to ubiquitin–proteasomal degradation (PMID:7799959, PMID:10980706, PMID:34429462, PMID:25728673, PMID:20410505, PMID:27555231). Mutations in the alpha-crystallin domain cause axonal Charcot-Marie-Tooth disease type 2F (CMT2F) and distal hereditary motor neuropathy by disrupting oligomer dynamics, impairing SQSTM1/p62-dependent autophagy, and increasing Cdk5-mediated neurofilament hyperphosphorylation that compromises axonal transport (PMID:15122254, PMID:23728742, PMID:30669930).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1992 High

    Identifying the upstream kinase for stress-induced HSPB1 phosphorylation resolved how extracellular signals control HSPB1 post-translational modification: MAPKAP kinase-2 phosphorylates Ser15, Ser78, and Ser82 downstream of p38 MAPK.

    Evidence In vitro kinase assay with co-purification and peptide mapping of phosphorylation sites

    PMID:1332886

    Open questions at the time
    • Whether other kinases independently phosphorylate HSPB1 in vivo was not addressed
    • Stoichiometry and kinetics of phosphorylation at each site in living cells remained unknown
  2. 1993 High

    Establishing HSPB1 as an ATP-independent molecular chaperone defined its core biochemical activity: preventing aggregation of thermally or chemically unfolding proteins and promoting their refolding.

    Evidence Reconstituted in vitro chaperone assays with purified HSPB1 and multiple model substrates (citrate synthase, alpha-glucosidase)

    PMID:8093612

    Open questions at the time
    • Mechanism of substrate recognition was undefined
    • Whether chaperone activity was regulated in vivo was unknown
  3. 1995 High

    Linking phosphorylation to actin stabilization revealed a non-chaperone effector function: phosphorylation-dependent oligomer dissociation is required for HSPB1 to protect microfilaments from heat- and drug-induced disruption.

    Evidence Wild-type vs. non-phosphorylatable (pm3) mutant HSPB1 stable transfection in hamster cells with cytochalasin and heat shock

    PMID:7799959

    Open questions at the time
    • Direct binding interface between HSPB1 and F-actin was not mapped
    • Whether actin stabilization and chaperone holdase activity share the same binding surface was unknown
  4. 1999 High

    Phosphomimetic dissection showed that progressive phosphorylation shifts HSPB1 from large oligomers to tetramers/dimers; this oligomeric transition inversely controls thermal chaperone activity and oxidative stress protection, establishing the oligomer–activity paradigm.

    Evidence Phosphomimetic mutagenesis (S15D/S78D/S82D), gel filtration, thermal aggregation assay, cell survival in L929 and 13.S.1.24 cells

    PMID:10383393

    Open questions at the time
    • Whether smaller species are more active toward all substrates or only some was untested
    • Structural basis of substrate binding by dimers vs. oligomers was unknown
  5. 2000 High

    Discovery that HSPB1 sequesters cytochrome c to block Apaf-1/caspase-9 assembly provided a direct molecular mechanism for its anti-apoptotic role, independent of its chaperone or actin functions.

    Evidence Cell-free caspase activation assay and co-immunoprecipitation of HSPB1 with cytochrome c

    PMID:10980706

    Open questions at the time
    • Binding stoichiometry and affinity of HSPB1–cytochrome c interaction were not determined
    • Whether phosphorylation state affects cytochrome c binding was unexplored
  6. 2000 High

    Structural analysis of the C-terminal extension revealed substrate-selective roles: it is required for chaperone activity toward some but not all clients, and it remains flexible during client interaction, contributing to accessible hydrophobic surface.

    Evidence NMR, analytical ultracentrifugation, electron microscopy, and dual-substrate chaperone assays on Hsp25 C-terminal deletion mutants

    PMID:10727931

    Open questions at the time
    • Which clients require the C-terminal extension and why was not systematically catalogued
    • Role of C-terminal extension in oligomer formation was not fully resolved
  7. 2004 High

    Identification of HSPB1 mutations as the genetic cause of CMT2F and distal hereditary motor neuropathy established the gene's essential role in axonal integrity; mutant HSPB1 disrupted neurofilament assembly and reduced neuronal viability.

    Evidence Genetic linkage and mutation screening in CMT2F/dHMN families; transfection of mutant HSPB1 in neuronal cells with neurofilament assembly assay

    PMID:15122254

    Open questions at the time
    • Whether mutations act via loss-of-function, gain-of-toxic-function, or both was unresolved
    • The precise structural consequences of mutations on oligomer dynamics were unknown
  8. 2010 High

    Demonstrating that phosphorylated HSPB1 translocates to the nucleus, binds acetylated GATA-1, and promotes its ubiquitination and proteasomal degradation revealed a novel mechanism by which HSPB1 controls transcription factor turnover during erythroid differentiation.

    Evidence siRNA knockdown, reciprocal co-IP of HSPB1 with GATA-1, nuclear fractionation, ubiquitination assay in K562 and CD34+ erythroid differentiation models

    PMID:20410505

    Open questions at the time
    • The E3 ligase recruited by HSPB1 for GATA-1 ubiquitination was not identified
    • Whether HSPB1 promotes degradation of other transcription factors via the same mechanism was untested
  9. 2012 High

    EPR spectroscopy of systematically spin-labeled HSPB1 mapped the N-terminal domain as the determinant of the oligomer–dimer equilibrium and showed that substrate binding buries N-terminal residues, structurally resolving how client engagement is coupled to oligomeric state.

    Evidence Systematic cysteine mutagenesis with EPR spectroscopy, sucrose gradient sedimentation, substrate (T4 lysozyme) binding assays

    PMID:22264079

    Open questions at the time
    • Atomic-resolution structure of HSPB1 oligomer with bound substrate was lacking
    • How the N-terminal domain distinguishes different clients was not addressed
  10. 2013 High

    CMT-causing HSPB1 mutations were shown to increase Cdk5-mediated neurofilament hyperphosphorylation and impair kinesin-dependent anterograde transport, with Cdk5 inhibition rescuing the transport defect—providing a druggable pathomechanistic axis.

    Evidence Stable transduction of WT and mutant HSPB1 in neuronal cells, axonal transport assay, Cdk5 inhibition, co-IP of neurofilament with kinesin

    PMID:23728742

    Open questions at the time
    • How HSPB1 mutations activate Cdk5 was not determined
    • Whether Cdk5 inhibition rescues axonal degeneration in vivo was untested
  11. 2015 High

    Native mass spectrometry resolved the full phosphorylation-dependent oligomeric landscape, demonstrating that triple-phosphomimetic HSPB1 exists predominantly as dimers with enhanced chaperone activity against both amorphous and fibrillar aggregation—reconciling earlier conflicting reports about phosphorylation and activity.

    Evidence Native MS of WT and progressive phosphomimetic mutants, chaperone assays against amorphous and amyloid aggregation

    PMID:25699602

    Open questions at the time
    • Whether dimers are the sole chaperone-active species in cells was not confirmed in vivo
    • Phosphorylation heterogeneity within oligomers in native tissues remained unmeasured
  12. 2015 High

    HSPB1 was established as a negative regulator of ferroptosis: PKC-mediated phosphorylation of HSPB1 suppresses iron-dependent lipid ROS accumulation, defining a new cell death modality controlled by this chaperone.

    Evidence siRNA knockdown and overexpression of HSPB1, PKC inhibition, lipid ROS and iron measurements, xenograft model

    PMID:25728673

    Open questions at the time
    • Direct molecular target through which HSPB1 controls iron metabolism was not identified
    • Whether chaperone activity or a distinct function mediates ferroptosis suppression was unclear
  13. 2016 Medium

    HSPB1 was shown to promote proteasomal degradation of MST1, the core Hippo pathway kinase, thereby activating YAP—extending its client-degradation function beyond GATA-1 to a key tumor-suppressor pathway.

    Evidence Gain/loss-of-function in prostate, breast, and lung cancer cells, co-IP, proteasome inhibition rescue, phospho-YAP immunofluorescence

    PMID:27555231

    Open questions at the time
    • Whether HSPB1 directly binds MST1 or acts through an adaptor was not resolved
    • Ubiquitin ligase identity for MST1 degradation was not determined
    • Independent replication in non-cancer contexts is lacking
  14. 2019 High

    Relaxation dispersion NMR revealed that HSPB1 monomers (generated by disulfide reduction) are highly chaperone-active but conformationally unstable, with partial unfolding in the alpha-crystallin domain dimerization interface—the same region where neuropathy mutations cluster—linking structural dynamics to both function and disease.

    Evidence Relaxation dispersion and high-pressure NMR, redox manipulation, in vitro chaperone assays

    PMID:30842409

    Open questions at the time
    • Whether monomer-driven chaperone activity is physiologically relevant given rapid dimerization tendency was unclear
    • Redox regulation of HSPB1 oligomeric state in vivo was not quantified
  15. 2019 High

    HSPB1 was found to interact with SQSTM1/p62 via its PB1 domain, and this interaction is required for p62 body formation and autophagosome biogenesis; CMT-linked mutations impair this interaction, directly connecting HSPB1-dependent autophagy to neuropathic disease.

    Evidence LC-MS/MS interactome, co-IP, domain mapping, HSPB1-KO rescue experiments, patient-derived motor neurons

    PMID:30669930

    Open questions at the time
    • Whether autophagy impairment is the primary driver of CMT2F or acts in concert with neurofilament defects was unresolved
    • Structural basis of HSPB1–p62 PB1 domain interaction was not determined
  16. 2020 High

    NMR and mutagenesis showed that the tau-binding groove on the alpha-crystallin domain is autoinhibited by HSPB1's own N-terminal region; disrupting these intramolecular contacts greatly enhances chaperone activity toward tau, establishing a mechanism for regulated substrate access.

    Evidence In vitro chaperone assays with tau, NMR, ACD–NTR interaction-disrupting mutations, domain deletions

    PMID:31974309

    Open questions at the time
    • Whether phosphorylation at the N-terminal domain releases autoinhibition in the same manner was not directly tested
    • In vivo relevance for tau pathology in neurodegenerative disease was not demonstrated
  17. 2021 High

    HSPB1 was shown to co-aggregate with unfolded substrates, reshaping aggregates into forms efficiently disaggregated by HSP70—redefining HSPB1's holdase function as an active co-aggregation and disaggregation-facilitating mechanism rather than passive aggregation prevention.

    Evidence Reconstituted in vitro co-aggregation and disaggregation assays with oligomerization-deficient mutants, substrate refolding measurement

    PMID:34429462

    Open questions at the time
    • Whether co-aggregation occurs and is functionally relevant in cells was not demonstrated
    • Structural organization of HSPB1 within co-aggregates was not resolved
  18. 2024 Medium

    Demonstration that reactive astrocytes secrete HSPB1 and that neighboring neurons take it up—reducing pathological tau inclusions—established a non-cell-autonomous chaperone mechanism relevant to neurodegeneration.

    Evidence Conditioned medium transfer, live imaging of HSPB1 uptake, immunofluorescence of human AD brain, siRNA knockdown, tau inclusion assay

    PMID:38507480

    Open questions at the time
    • Secretion mechanism (conventional vs. unconventional) is undefined
    • Quantitative contribution of extracellular HSPB1 relative to cell-autonomous pools in neuroprotection is unknown
    • Replication across independent labs is needed

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: how phosphorylation heterogeneity within native HSPB1 oligomers controls substrate selectivity in vivo; the identity of E3 ubiquitin ligases recruited by HSPB1 for client degradation; whether gain-of-toxic-function versus loss-of-chaperone-function underlies CMT2F; and the mechanistic basis by which HSPB1 modulates iron metabolism to suppress ferroptosis.
  • No high-resolution structure of a full-length HSPB1 oligomer with bound client
  • Relative contribution of autophagy impairment vs. neurofilament transport defects in CMT2F pathogenesis
  • Direct ferroptosis-relevant molecular target of HSPB1 is unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0044183 protein folding chaperone 7 GO:0008092 cytoskeletal protein binding 4 GO:0098772 molecular function regulator activity 4 GO:0140313 molecular sequestering activity 1
Localization
GO:0005829 cytosol 5 GO:0005856 cytoskeleton 4 GO:0005576 extracellular region 2 GO:0005634 nucleus 2
Pathway
R-HSA-8953897 Cellular responses to stimuli 7 R-HSA-162582 Signal Transduction 4 R-HSA-392499 Metabolism of proteins 3 R-HSA-5357801 Programmed Cell Death 3 R-HSA-168256 Immune System 1 R-HSA-9612973 Autophagy 1
Partners
G6PDGATA1MAPKAPK2MST1SIRT1SQSTM1TGFB1I1TLR3
Complex memberships
Hsp25/Hsp70/Hsp110 chaperone complex

Evidence

Reading pass · 40 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 MAPKAP kinase-2 (MK2) is the major kinase responsible for phosphorylating small mammalian heat shock proteins, phosphorylating Ser15 and Ser86 of murine Hsp25 and Ser15, Ser78, and Ser82 of human Hsp27 in response to growth factors and heat shock. In vitro kinase assay, co-purification, peptide substrate mapping FEBS letters High 1332886
1993 Murine Hsp25 and human Hsp27 function as ATP-independent molecular chaperones, preventing aggregation of unfolding proteins (citrate synthase, alpha-glucosidase) under heat shock conditions and promoting their refolding after urea denaturation. In vitro chaperone assay with purified proteins, thermal aggregation and refolding assays The Journal of biological chemistry High 8093612
1995 Phosphorylation of HSP27 by MAPKAP kinase reduces its large oligomeric size and is required for actin filament stabilization; phosphorylated HSP27 protects microfilaments from heat-induced disruption and accelerates actin recovery, while a non-phosphorylatable mutant (HSP27-pm3) fails to provide these protective effects. Stable transfection of wild-type and phosphorylation-site mutant HSP27 in Chinese hamster cells; cytochalasin D treatment; heat shock survival; immunofluorescence of actin Molecular and cellular biology High 7799959
1999 Phosphorylation of Hsp27/Hsp25 at Ser15, Ser78, Ser82 (mimicked by S15D/S78D/S82D triple mutant) causes dissociation of large oligomers to tetramers, significantly decreases chaperone activity in thermal denaturation and refolding assays, and abolishes protection against oxidative stress when overexpressed in cells. In vitro phosphorylation, phosphomimetic mutagenesis, gel filtration, thermal aggregation assay, cell survival assays in L929 and 13.S.1.24 cells The Journal of biological chemistry High 10383393
2000 Hsp27 inhibits the mitochondrial apoptotic pathway by binding cytochrome c released from mitochondria to the cytosol, thereby preventing cytochrome-c-mediated interaction of Apaf-1 with procaspase-9 and subsequent caspase activation. Cell-free caspase activation assay, co-immunoprecipitation of Hsp27 with cytochrome c, apoptosis assays Nature cell biology High 10980706
2000 The C-terminal extension of mouse Hsp25 is required for full chaperone activity toward some substrates (dithiothreitol-reduced alpha-lactalbumin) but not others (thermally aggregating citrate synthase); deletion of the C-terminal extension reduces accessible hydrophobic surface and protein stability while the extension remains flexible during client interaction. 1H NMR spectroscopy, analytical ultracentrifugation, electron microscopy, CD spectroscopy, chaperone assays with citrate synthase and alpha-lactalbumin European journal of biochemistry High 10727931
2000 Hsp25 overexpression provides radioresistance associated with upregulation of Bcl2, cell cycle delay, and reduced apoptosis; the radioresistance operates through pathways independent of cell-cycle synchronization alone. Stable transfection of Hsp25 in L929 cells, clonogenic survival assay, flow cytometry, immunoblotting Radiation research Medium 11023606
2000 Hsp25 overexpression in mouse L929 cells increases the glutathione pool by enhancing reduction of oxidized glutathione (GSSG) to GSH through elevated glutathione reductase and glutathione peroxidase activities, providing protection against ionizing radiation. Stable transfection, clonogenic radiation survival, glutathione composition analysis, enzyme activity assays Journal of cellular physiology Medium 10699971
2000 Hsp110 forms a large native complex with hsc70 and hsp25; in vitro, purified hsp25, hsp70, and hsp110 spontaneously assemble into this complex and luciferase migrates into it after heat shock; the peptide-binding domain of hsp110 is required for its interaction with hsp25. Co-immunoprecipitation, in vitro reconstitution with purified proteins, deletion mutagenesis of hsp110 FEBS letters Medium 10631312
2000 HSP25/p38 MAPK pathway is necessary for cardiomyocyte differentiation of P19 cells: antisense HSP25 expression reduced cardiomyocyte differentiation and expression of cardiac actin and desmin, while inhibition of p38/SAPK2 by SB203580 blocked differentiation at an early mesodermal stage upstream of HSP25 induction. Antisense expression in P19 cells, p38 kinase inhibitor (SB203580), RT-PCR for cardiac markers, immunofluorescence Developmental biology Medium 10656759
2001 hsp27 physically interacts with hic-5/ARA55 through the hsp27 C-terminal domain and hic-5 LIM domains; this interaction inhibits the ability of hsp27 to protect cells against heat-induced death, as a non-interacting truncation mutant of hic-5 did not inhibit hsp27 protection. Yeast two-hybrid screen, co-immunoprecipitation, deletion mapping, heat shock cell survival assay The Journal of biological chemistry Medium 11546764
2001 After sciatic nerve axotomy, p38 kinase activation is required for Hsp25 induction in spinal motor neurons, and Hsp25 forms a complex with Akt in these neurons, suggesting Hsp25 links p38 and PI-3K/Akt survival pathways. Sciatic nerve axotomy in vivo, kinase inhibition, co-immunoprecipitation of Hsp25 with Akt Brain research. Molecular brain research Medium 11589997
2001 Stress-induced dissociation of large Hsp27 oligomers is mediated by two kinase cascades: p38 MAPK-activated MAPKAP kinase-2/3 (activated by metals, hypertonic stress, anisomycin) and protein kinase C (activated by phorbol ester); both kinases converge on Hsp27 phosphorylation. Sucrose density gradient centrifugation, specific kinase inhibitors (SB203580, staurosporine, bisindolylmaleimide), immunoassay Cell stress & chaperones Medium 11525238
2002 HSP25 phosphorylation (regulated by p38 MAPK) mediates its translocation to F-actin bundles and nuclear granules in heat-stressed myoblasts; association with actin filaments stabilizes them against subsequent cytochalasin or severe heat stress; only phosphorylated HSP25 isoforms associate with the cytoskeletal fraction. Immunofluorescence, Triton X-100 fractionation, isoform analysis, kinase inhibitors, cytochalasin treatment Cell stress & chaperones Medium 12380682
2002 HSP25-induced radioresistance requires downregulation of ERK2 but not ERK1: overexpression of ERK2 (but not ERK1) in Hsp25-overexpressing cells abolished radioresistance and reversed Hsp25-induced changes in cell cycle proteins (cyclin D1, cyclin A, cdc2) and Bcl-2 levels. Transient transfection of ERK1/ERK2, clonogenic survival assay, immunoblotting, MEK inhibitor PD98059 Cell death and differentiation Medium 11965498
2004 Mutations in HSPB1 (Hsp27) cause axonal Charcot-Marie-Tooth disease (CMT2F) and distal hereditary motor neuropathy; four mutations cluster in the alpha-crystallin domain and one in the C-terminal region; mutant HSPB1-expressing neuronal cells showed reduced viability, and co-transfection of mutant HSPB1 with NEFL resulted in altered neurofilament assembly. Genetic linkage, mutation screening, neuronal cell transfection, cell viability assay, neurofilament assembly assay in cells lacking cytoplasmic intermediate filaments Nature genetics High 15122254
2005 Cadmium activates p38 MAPK signaling in mesangial cells leading to sequential phosphorylation of HSP25 (Ser15 before Ser86), reduction of HSP25 oligomeric size, association of HSP25 with microfilaments, and mesangial cell contraction; SB-203580 inhibits all these responses, and dominant-negative p38 blocks HSP25 phosphorylation. Dominant-negative p38 transfection, p38 inhibitor SB-203580, phospho-site-specific analysis, microfilament association, cell contraction assay, isolated glomeruli experiments American journal of physiology. Renal physiology Medium 15687248
2007 AKT phosphorylates HspB1 (Hsp27) in granular keratinocytes; Akt-mediated HspB1 phosphorylation promotes a transient interaction with filaggrin and intracellular redistribution of HspB1; loss of epidermal HspB1 causes hyperkeratinization and misprocessing of filaggrin. Conditional knockout of Akt in epidermis, co-immunoprecipitation of HspB1 with filaggrin, immunofluorescence, skin phenotype analysis The Journal of biological chemistry Medium 17439945
2010 In late-stage erythroid differentiation, HSP27 is phosphorylated in a p38-dependent manner, translocates to the nucleus, binds to GATA-1 transcription factor (when GATA-1 is acetylated), and promotes GATA-1 ubiquitination and proteasomal degradation; HSP27 depletion causes GATA-1 accumulation and impairs terminal erythroid maturation. siRNA knockdown of HSP27, co-immunoprecipitation of HSP27 with GATA-1, nuclear fractionation, ubiquitination assay, erythroid differentiation models (K562, CD34+ cells) Blood High 20410505
2011 BMP-2-induced cell migration requires activation of the p38/MK2/Hsp25 pathway; phosphorylated Hsp25 colocalizes with BMP receptor complexes in lamellipodia; a phosphorylation-deficient Hsp25 mutant abolishes BMP-2-induced migration; this pathway acts in parallel to the Cdc42/PAK/LIMK1 axis for actin remodeling. Chemical inhibition of p38/MK2, genetic ablation (p38α and MK2 knockout cells), phosphomutant overexpression, cell migration assay, immunofluorescence colocalization PloS one High 21297993
2012 The N-terminal domain of Hsp27 encodes the determinants of oligomer-to-dimer equilibrium dissociation; cysteine mutagenesis identifies residues shifting the equilibrium; upon dissociation, N-terminal domain residues become solvent-exposed and dynamically disordered; substrate (T4 Lysozyme) binding involves N-terminal domain regions transitioning to a buried environment in the complex. Systematic cysteine mutagenesis, EPR spectroscopy with spin-labels, sucrose gradient sedimentation, substrate binding assays Biochemistry High 22264079
2013 HSPB1 mutations causing CMT neuropathy increase Cdk5-mediated phosphorylation of neurofilaments (NFs), reduce NF binding to anterograde motor kinesin, and impair anterograde NF transport; Cdk5 inhibition rescues NF phosphorylation and kinesin binding in mutant HSPB1 cells. Stable transduction of neuronal cells with WT and mutant HSPB1, axonal transport assay, Cdk5 inhibition, co-immunoprecipitation of NF with kinesin Acta neuropathologica High 23728742
2013 Extracellular HSP27 exerts proangiogenic effects via interaction with Toll-like receptor 3 (TLR3) on endothelial cells; this interaction (detected by immunoprecipitation) leads to internalization of HSP27/TLR3 to endosomes, cytosolic Ca2+-dependent NF-κB activation, increased VEGF transcription, and VEGF receptor-2 secretion promoting cell migration. Co-immunoprecipitation, SPR analysis, live-cell internalization imaging, NF-κB reporter assay, siRNA knockdown, chick chorioallantoic membrane angiogenesis assay FASEB journal Medium 23804239
2014 MMP9 cleaves HSPB1 and generates anti-angiogenic C-terminal fragments; the C-terminal HSPB1 fragment shows greater interaction with VEGF than full-length HSPB1 and inhibits VEGF-induced endothelial cell activation; HSPB1 cleavage occurs during lung tumor progression in vivo and is absent in MMP9-null mice. In vitro MMP9 cleavage assay, cleavage site mapping, VEGF binding assay, in vivo tumor models with WT and MMP9-null mice, immunofluorescence of tumor endothelium PloS one Medium 24465581
2015 Phosphomimetic mutations at Ser15, Ser78, and Ser82 of Hsp27 progressively decrease average oligomeric size (triple mutant is predominantly a dimer); this correlates with enhanced chaperone activity against both amorphous and fibrillar protein aggregation; the data support dimers as the chaperone-active form. Native mass spectrometry, phosphomimetic mutagenesis, chaperone assays against amorphous and fibrillar aggregation Chemistry & biology High 25699602
2015 HSPB1 is a negative regulator of ferroptosis: erastin-induced ferroptosis is mediated by HSF1-dependent HSPB1 upregulation, and protein kinase C-mediated HSPB1 phosphorylation reduces iron-mediated lipid ROS production; knockdown of HSF1 or HSPB1 enhances ferroptosis while HSPB1 overexpression or heat shock pretreatment inhibits it. siRNA knockdown of HSF1 and HSPB1, HSPB1 overexpression, PKC inhibition, lipid ROS measurement, iron metabolism assay, xenograft mouse model Oncogene High 25728673
2015 HSP25 depletion in H9c2 cells increases p53 acetylation at K379 by reducing the interaction between SIRT1 and p53; HSP25 directly interacts with SIRT1 and its knockdown leads to dissociation of SIRT1 from p53, upregulation of Bax, cytochrome c release, and caspase-3/9 activation. Co-immunoprecipitation of HSP25 with SIRT1, siRNA knockdown, flow cytometry for apoptosis, immunoblotting for acetylated p53 and apoptotic markers Cell stress & chaperones Medium 26515559
2016 HSPB1 activates G6PD by enhancing its interaction with SIRT2, leading to SIRT2-mediated deacetylation and activation of G6PD; this sustains cellular NADPH and pentose phosphate production in response to oxidative stress or DNA damage. Co-immunoprecipitation of G6PD with SIRT2 in presence/absence of HSPB1, NADPH and pentose measurement, siRNA knockdown PloS one Medium 27711253
2016 Hsp27 promotes proteasomal degradation of ubiquitinated MST1 (the core Hippo kinase), thereby reducing phosphorylation/activity of LATS1 and MOB1, leading to YAP nuclear localization and activation; Hsp27 knockdown induces YAP phosphorylation and cytoplasmic retention, while overexpression has the opposite effect. Gain/loss-of-function experiments in prostate, breast, and lung cancer cells, co-immunoprecipitation, proteasome inhibition, phospho-YAP immunofluorescence Scientific reports Medium 27555231
2018 Membrane-associated androgen receptor (AR) activates HSP27, which in turn mediates AR membrane-to-nuclear signal transduction to potentiate transcriptional activity of nuclear AR; AR membrane transport depends on microtubule motor KIF5B, which physically interacts with AR in an androgen-enhanced manner. Co-immunoprecipitation and pulldown assays (AR with KIF5B and HSP27), siRNA knockdown of KIF5B, AR transcriptional reporter assay The Journal of biological chemistry Medium 29934310
2018 In intestinal mesenchymal cells, MK2-mediated Hsp27 phosphorylation is required for the production of tumorigenic effector molecules that drive epithelial proliferation, apoptosis, and angiogenesis; conditional MK2 deletion in intestinal mesenchymal cells reduces tumor growth in the Apcmin/+ model. Cell-type-specific conditional MK2 knockout mice (Apcmin/+ model), colitis-associated carcinogenesis model, tumor multiplicity and size analysis, mechanistic downstream analysis Proceedings of the National Academy of Sciences of the United States of America High 29844172
2019 The redox state of HSP27 regulates its chaperone activity: reduction of disulfide bonds promotes monomer formation which are highly active chaperones but prone to self-aggregation; relaxation dispersion and high-pressure NMR reveal that the dimerization beta-strands in the alpha-crystallin domain partially unfold in monomers; neuropathy-causing mutations cluster to this dynamic region. Relaxation dispersion NMR, high-pressure NMR, chaperone activity assays in vitro, redox manipulation Nature communications High 30842409
2019 Wild-type HSPB1 interacts with the autophagy receptor SQSTM1/p62 via p62's PB1 domain; this interaction is necessary for SQSTM1/p62 body formation and subsequent autophagosome/phagophore formation; HSPB1 mutations associated with CMT neuropathy reduce p62 body formation and impair autophagic flux. LC-MS/MS interactome of WT and mutant HSPB1 variants, co-immunoprecipitation, HSPB1 knockout cells, rescue experiments, patient-derived motor neurons Autophagy High 30669930
2020 Ivermectin directly binds a phosphorylation pocket in the 24-monomer Hsp27 complex (composed of 12 dimers) flanked by serine residues between N-terminal domains, inhibiting MAPKAP2-mediated Hsp27 phosphorylation and depolymerization, thereby blocking Hsp27-regulated survival signaling and client-oncoprotein interactions. Biochemical, structural, and computational characterization of the 24-mer complex; direct binding assay; kinase phosphorylation assay; tumor models The Journal of clinical investigation High 31845908
2020 HspB1 chaperone activity toward tau (an amyloid-forming client) requires engagement of the disordered N-terminal region (NTR); ACD binding alone is insufficient for chaperone function; the tau-binding groove on the ACD also binds short hydrophobic regions within HspB1's own NTR, and mutations disrupting these intrinsic ACD-NTR interactions greatly enhance chaperone activity toward tau. In vitro chaperone assays, NMR, mutagenesis to disrupt intrinsic ACD-NTR interactions, domain deletion analysis Proceedings of the National Academy of Sciences of the United States of America High 31974309
2021 Human HSPB1 co-aggregates with unfolded substrates (firefly luciferase, lactate dehydrogenase) to form smaller, more regularly shaped aggregates; co-aggregated HSPB1 facilitates efficient disaggregation and refolding of substrates led by HSP70; HSPB1 homo-oligomerization is not required for this activity, and HSPB1 itself is extracted during disaggregation. In vitro co-aggregation assay, reconstituted disaggregation assay with HSP70, oligomerization-deficient mutants, substrate refolding measurement Scientific reports High 34429462
2021 Bmal1 (circadian clock) regulates the redox state of HSPB1; Bmal1 knockdown decreases homooxidized HSPB1 (formed via S-thiolated modification at Cys141), and the HSPB1-C141S mutant increases cardiomyocyte apoptosis and ROS while decreasing GSH during oxidative stress. Bmal1 knockdown/overexpression in cardiomyocytes, HSPB1-C141S mutagenesis, ROS measurement, GSH/GSSG ratio, apoptosis assay, in vivo circadian rhythm disruption model Oxidative medicine and cellular longevity Medium 34239687
2023 FYN kinase phosphorylates TOPK/PBK at Y272, promoting TOPK activity that in turn phosphorylates HSPB1 at Ser15; the FYN-TOPK-HSPB1 cascade facilitates gastric cancer proliferation and metastasis. Co-IP, pulldown, 32P isotope kinase assays, phosphoproteomics, TOPK knockout mice, TOPK-Y272F mutation preventing FYN interaction Journal of experimental & clinical cancer research Medium 37016377
2024 crVDAC3 (a circular RNA) binds HSPB1 protein and inhibits its ubiquitination and degradation, leading to HSPB1 accumulation; knockdown of crVDAC3 reduces HSPB1 levels, increases ROS and labile iron pool, and induces ferroptosis; paritaprevir disrupts the crVDAC3-HSPB1 interaction to promote HSPB1 ubiquitination. RNA pull-down, mass spectrometry, RNA immunoprecipitation, co-immunoprecipitation, ferroptosis assays (C11-BODIPY, iron quantification), molecular docking, PDX model Drug resistance updates Medium 39243601
2024 Reactive astrocytes secrete HSPB1 extracellularly; both astrocytes and neurons can take up astrocyte-secreted HSPB1; uptake is accompanied by attenuation of the inflammatory response in reactive astrocytes and reduced pathological tau inclusions in neurons, establishing a non-cell-autonomous chaperone protective mechanism. Conditioned medium transfer, live imaging of HSPB1 uptake, immunofluorescence of human AD brain, siRNA knockdown in astrocytes, tau inclusion assay in neurons Science advances Medium 38507480

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Global, in vivo, and site-specific phosphorylation dynamics in signaling networks. Cell 2861 17081983
2012 Insights into RNA biology from an atlas of mammalian mRNA-binding proteins. Cell 1718 22658674
2005 A human protein-protein interaction network: a resource for annotating the proteome. Cell 1704 16169070
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2006 A probability-based approach for high-throughput protein phosphorylation analysis and site localization. Nature biotechnology 1336 16964243
2011 Systematic and quantitative assessment of the ubiquitin-modified proteome. Molecular cell 1334 21906983
2009 Defining the human deubiquitinating enzyme interaction landscape. Cell 1282 19615732
2006 Substrate and functional diversity of lysine acetylation revealed by a proteomics survey. Molecular cell 1260 16916647
2004 Large-scale characterization of HeLa cell nuclear phosphoproteins. Proceedings of the National Academy of Sciences of the United States of America 1159 15302935
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
1993 Small heat shock proteins are molecular chaperones. The Journal of biological chemistry 1035 8093612
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