Affinage

HSPB7

Heat shock protein beta-7 · UniProt Q9UBY9

Length
170 aa
Mass
18.6 kDa
Annotated
2026-06-10
40 papers in source corpus 23 papers cited in narrative 23 extracted findings
Cross-family judge faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HSPB7 is a muscle-enriched small heat shock protein that maintains sarcomeric and intercalated-disc proteostasis in the heart and skeletal muscle, where its loss is developmentally and clinically catastrophic (PMID:29078393, PMID:28827800). Its central biochemical activity is selective recognition of filamin C (FLNC): HSPB7 binds dimerized FLNC and, via its α-crystallin domain engaging FLNC Ig-like domain 24, forms a crystallographically defined heterodimer that out-competes the FLNC homodimer interface and is tuned by FLNC phosphorylation (T2677 favoring homodimer, Y2683 favoring the HSPB7 heterodimer), thereby antagonizing FLNC actin cross-linking and enhancing its mobility (PMID:40312381, PMID:41702738). This proteostatic role extends to autophagy: HSPB7 facilitates autophagic processing of damaged FLNC and titin, and its loss in zebrafish and human iPSC-cardiomyocytes drives FLNC aggregation and cardiomyopathy when autophagy is blocked (PMID:29331499). Consistent with a chaperone-distinct activity, HSPB7 is the most potent polyQ aggregation suppressor of the HSPB family through a macroautophagy-dependent (ATG5-dependent), Hsp70- and proteasome-independent mechanism encoded by its N-terminal domain, which is necessary and sufficient and can transfer this activity onto HSPB1 (PMID:20843828, PMID:31097540). In cardiomyocytes HSPB7 ablation disrupts intercalated discs with connexin 43 loss and desmoplakin/N-cadherin mislocalization, producing arrhythmia and heart failure, while embryonic loss yields lethal abnormal actin bundles cross-linking Z lines (PMID:29078393, PMID:28827800). HSPB7 constitutively localizes to SC35 nuclear speckles via its N-terminus and lacks classical refolding activity (PMID:19464326), and it contains a kinetically privileged reactive cysteine (C117) that senses reactive electrophilic species (PMID:29397684). Whether HSPB7 is a bona fide direct actin-binding protein is contested, with reconstitution studies reporting both repression of actin polymerization and failure to detect specific complexes (PMID:29078393, PMID:35977674). Beyond muscle, HSPB7 is transcriptionally regulated (by GATA4, MEF2A/AP-1, p53, MECOM, and HDAC1) and modulates osteogenic/adipogenic differentiation and tumor cell metabolism in several contexts (PMID:23850773, PMID:27632998, PMID:37170285, PMID:37732539).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1999 Medium

    Established the first molecular partner of HSPB7, linking it to the actin cytoskeletal scaffold by mapping a filamin-binding region.

    Evidence Yeast two-hybrid and co-IP with domain mapping (residues 56-119) against alpha-filamin C-terminal tail

    PMID:10593960

    Open questions at the time
    • Filamin isoform specificity (FLNA vs FLNC) not resolved here
    • No functional consequence of the interaction defined
    • Structural basis not determined
  2. 2004 Medium

    Showed HSPB7 responds to cardiac/skeletal stress by stably redistributing to myofibrillar Z/I regions, indicating a sarcomeric site of action.

    Evidence Subcellular fractionation, immunohistochemistry, and chaotrope-resistant extraction in ischemic muscle

    PMID:15480735

    Open questions at the time
    • Molecular target at the Z/I band not identified
    • Mechanism of translocation unknown
  3. 2009 Medium

    Revealed HSPB7 has a non-canonical, non-refolding role by localizing constitutively to SC35 nuclear speckles, separating it from classical chaperone sHSPs.

    Evidence Confocal imaging of GFP constructs with N-terminal domain mapping and luciferase refolding assay (negative)

    PMID:19464326

    Open questions at the time
    • Functional role at SC35 speckles undefined
    • No splicing or RNA-processing partner identified
  4. 2010 High

    Defined a distinctive disposal mechanism: HSPB7 suppresses polyQ aggregation through macroautophagy rather than refolding or proteasomal routes.

    Evidence Cell-based polyQ assays, ATG5-/- cells, Drosophila eye model, inhibitor and refolding assays

    PMID:20843828

    Open questions at the time
    • How HSPB7 routes substrates to autophagy is not molecularly defined
    • No direct autophagy-machinery partner identified
  5. 2011 Medium

    Connected HSPB7 to cytoskeletal stress signaling by showing it blocks RhoA/ROCK-driven F-actin stress fiber formation in atrial myocytes.

    Evidence HL-1 tachypacing model, calcium transient measurement, F-actin staining, ROCK inhibition, overexpression

    PMID:21731611

    Open questions at the time
    • Direct versus indirect effect on actin not resolved
    • Mechanistic link to RhoA pathway not biochemically defined
  6. 2013 Medium

    Placed HSPB7 in a GATA4-controlled developmental program required for left-right axis and heart tube morphogenesis.

    Evidence Zebrafish morpholino knockdown with gata4 genetic epistasis and confocal imaging

    PMID:23850773

    Open questions at the time
    • Morpholino specificity not corroborated by mutant
    • Molecular effector downstream of HSPB7 in Kupffer's vesicle unknown
  7. 2016 High

    Demonstrated in vivo that HSPB7 binds dimerized FLNC and is required to prevent FLNC aggregation and myopathy in skeletal muscle.

    Evidence Skeletal-muscle conditional KO mouse, co-IP, immunofluorescence

    PMID:26929074

    Open questions at the time
    • Structural basis of FLNC-dimer selectivity not defined here
    • Mechanism linking FLNC binding to aggregation prevention unresolved
  8. 2016 Medium

    Identified the transcriptional logic controlling HSPB7 in muscle, with MEF2A activating and AP-1 repressing, tying expression to muscle mass.

    Evidence ChIP-seq, siRNA knockdown, dexamethasone treatment, in vivo muscle manipulation

    PMID:27632998

    Open questions at the time
    • Direct promoter elements for each factor not fully mapped
    • Link between expression level and chaperone function not addressed
  9. 2017 High

    Showed HSPB7 is indispensable for cardiac development and regulates thin-filament length, with abnormal actin bundles—not filament elongation—causing lethality.

    Evidence Global and cardiac KO mice, in vitro actin polymerization/binding assays, HSPB7/Lmod2 double-KO rescue, immunofluorescence

    PMID:29078393

    Open questions at the time
    • Direct actin binding later disputed
    • How HSPB7 limits actin bundling mechanistically unresolved
  10. 2017 High

    Established a postnatal cardiac requirement: inducible HSPB7 loss disrupts intercalated discs and causes arrhythmia and heart failure independent of sarcomere contractile organization.

    Evidence Cardiac-specific inducible KO mouse, ECG, immunofluorescence, Western blot

    PMID:28827800

    Open questions at the time
    • Mechanism connecting HSPB7 loss to connexin 43/desmoplakin disruption not defined
    • Whether FLNC aggregation is cause or consequence unresolved
  11. 2018 High

    Defined a proteostasis mechanism in the heart: HSPB7 binds FLNC and titin and channels damaged FLNC into autophagy to sustain sarcomeric homeostasis.

    Evidence Co-IP, zebrafish mutants, HSPB7-mutant human iPSC-cardiomyocytes, autophagy inhibition and flux assays

    PMID:29331499

    Open questions at the time
    • Direct autophagy-receptor partner not identified
    • How titin binding contributes mechanistically unclear
  12. 2018 High

    Revealed a redox-sensing function: a single conserved cysteine (C117) makes HSPB7 a kinetically privileged sensor of reactive electrophilic species.

    Evidence In vitro RES adduction kinetics, C117 mutagenesis, circular dichroism, cell-based sensing, cancer-relevant mutant

    PMID:29397684

    Open questions at the time
    • Downstream signaling consequence of C117 adduction not defined
    • Physiological RES targets in muscle unknown
  13. 2019 High

    Localized the anti-aggregation activity to the flexible N-terminal domain, showing it is necessary, sufficient, and transferable to HSPB1.

    Evidence In vitro aggregation assays, NTD domain-swap chimeras, phospho-mimic mutants, microscopy

    PMID:31097540

    Open questions at the time
    • Structural basis of NTD-polyQ recognition not determined
    • Connection of NTD activity to autophagy routing unresolved
  14. 2021 Medium

    Characterized HSPB7 oligomeric behavior, showing redox- and motif-dependent large-oligomer formation and disulfide-mediated heterodimers with HspB6/HspB8.

    Evidence Recombinant protein SEC, crosslinking, cysteine modification, domain deletion, co-IP

    PMID:34360542

    Open questions at the time
    • Functional role of large oligomers unknown
    • Physiological relevance of HspB6/HspB8 heterodimers untested in vivo
  15. 2022 Medium

    Challenged the actin-binding model with a controlled negative study finding no specific, saturable G/F-actin complex.

    Evidence Blot overlay, co-sedimentation, native gels, crosslinking, heat-aggregation assay with positive controls

    PMID:35977674

    Open questions at the time
    • Discrepancy with cellular actin-regulation data unresolved
    • Whether actin effects are indirect not established
  16. 2023 Medium

    Extended HSPB7 regulation and function to cancer, with transcriptional control by MECOM/HDAC1 and suppression of glycolysis and tumor growth.

    Evidence Co-IP, ChIP, metabolic assays, cell functional assays, xenograft (multiple tumor types)

    PMID:35652621 PMID:37732539

    Open questions at the time
    • Mechanism linking HSPB7 to glycolytic enzyme levels undefined
    • Relationship to muscle chaperone role unclear
  17. 2025 High

    Provided the structural and biophysical basis of HSPB7-FLNC heterodimerization, defining phospho-regulation and the consequences for FLNC cross-linking and mobility.

    Evidence X-ray crystallography, quantitative binding with phospho-mimetic FLNC, FRAP, ancestral sequence reconstruction; plus SEC/native-gel mapping of α-crystallin domain to FLNC Ig24

    PMID:40312381 PMID:41702738

    Open questions at the time
    • In vivo demonstration of phospho-switch in stressed myocardium pending
    • Quantitative balance of homo- vs heterodimer in cells not measured
  18. 2025 Medium

    Linked FLNC disease mutations directly to disrupted HSPB7 binding, providing a mechanistic basis for FLNC-associated myopathy via lost chaperone engagement.

    Evidence SEC, native gels, crosslinking, AlphaFold3 modeling of FLNC domain 22-24 disease mutants

    PMID:40564978

    Open questions at the time
    • Functional rescue in patient cells not shown
    • Whether lost binding alone drives pathology not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how HSPB7's distinct activities—FLNC heterodimerization, autophagic substrate routing, nuclear-speckle residence, and electrophile sensing—are integrated and whether a single biochemical mechanism underlies its non-canonical, non-refolding chaperone role.
  • No unifying biochemical mechanism linking the four activities
  • Direct autophagy-receptor partner unidentified
  • Function at SC35 speckles still undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 3 GO:0008092 cytoskeletal protein binding 2 GO:0044183 protein folding chaperone 2 GO:0140299 molecular sensor activity 1
Localization
GO:0005856 cytoskeleton 2 GO:0005654 nucleoplasm 1 GO:0005730 nucleolus 1 GO:0005829 cytosol 1
Pathway
R-HSA-1266738 Developmental Biology 2 R-HSA-392499 Metabolism of proteins 2 R-HSA-9612973 Autophagy 2 R-HSA-8953897 Cellular responses to stimuli 1
Partners
FLNAFLNCHSPB6HSPB8MECOMTTN
Complex memberships
HSPB7-FLNC heterodimerHSPB7-HSPB6 heterodimerHSPB7-HSPB8 heterodimer

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 HSPB7 (cvHsp) interacts with alpha-filamin (actin-binding protein 280), with amino acid residues 56-119 of HSPB7 identified as important for this specific interaction with the C-terminal tail of alpha-filamin, as demonstrated by yeast two-hybrid and immunoprecipitation experiments. Yeast two-hybrid and co-immunoprecipitation The Journal of biological chemistry Medium 10593960
2004 Under ischemic conditions, HSPB7 (cvHsp) translocates from cytosol to the Z-/I-area of myofibrils in heart and skeletal muscle, with myofibrillar binding resisting extraction with 1 M NaSCN or 1 M urea, indicating tight association with myofibrillar components. Subcellular fractionation, immunohistochemistry, extraction assays Histochemistry and cell biology Medium 15480735
2009 HSPB7 constitutively localizes to SC35 splicing speckles in cells, driven by its N-terminus; unlike HSPB1 and HSPB5, HSPB7 does not support refolding of heat-unfolded substrates (negative result for classical chaperone activity), suggesting a non-chaperone role at SC35 speckles. Confocal microscopy (GFP-tagged constructs), luciferase refolding assay Biochimica et biophysica acta Medium 19464326
2010 HSPB7 is the most potent polyQ aggregation suppressor within the HSPB family; it prevents polyQ aggregation and toxicity by a mechanism that requires active macroautophagy (ATG5-dependent), is independent of Hsp70 machinery and proteasomal activity, and does not involve refolding of heat-denatured substrates. Cell-based polyQ aggregation assay, ATG5-/- knockout cells, Drosophila eye degeneration model, luciferase refolding assay, inhibitor studies Human molecular genetics High 20843828
2011 HSPB7 overexpression protects tachypaced atrial myocytes against calcium transient reduction and tachycardia remodeling by directly preventing F-actin stress fiber formation downstream of RhoA GTPase activation, independently of HSPB1. HL-1 atrial myocyte tachypacing model, calcium transient measurements, F-actin staining, ROCK inhibitor (Y27632), overexpression studies PloS one Medium 21731611
2013 HSPB7 expression in zebrafish is regulated by the transcription factor Gata4; depletion of Hspb7 disrupts Kupffer's vesicle morphology, impairs left-right axis establishment, and causes heart tube formation defects, with the yolk syncytial layer identified as a key site of action; genetic interaction with gata4 was confirmed. Zebrafish morpholino knockdown, genetic epistasis (gata4 interaction), confocal microscopy Developmental biology Medium 23850773
2014 HSPB7 expression is induced by p53 in a dose-dependent manner in renal cell carcinoma cells, placing HSPB7 in the p53 pathway; ectopic HSPB7 expression suppresses cancer cell growth. Dose-response transfection of p53, qPCR, cell growth assay International journal of oncology Low 24585183
2016 HSPB7 interacts specifically with dimerized filamin C (FLNC) in skeletal muscle; skeletal-muscle-specific ablation of HSPB7 causes progressive myopathy with FLNC aggregation and mislocalization, sarcomere disarray, muscle fibrosis, and abnormal upregulation/mislocalization of γ- and δ-sarcoglycan (but not dystrophin). Conditional knockout mouse model, co-immunoprecipitation, immunofluorescence Journal of cell science High 26929074
2016 MEF2A and AP-1 (Fra-2/c-Jun) transcription factors antagonistically regulate Hspb7 gene expression in skeletal muscle: MEF2A is required for dexamethasone-induced Hspb7 upregulation, while AP-1 suppresses it; Hspb7 levels affect muscle mass in vivo. ChIP-seq, siRNA knockdown, dexamethasone treatment, qPCR, in vivo muscle manipulation Journal of cell science Medium 27632998
2017 HSPB7 is indispensable for cardiac development; global or cardiac-specific HSPB7 KO results in embryonic lethality before E12.5; HSPB7 binds monomeric actin and represses actin polymerization, regulating thin filament length; KO hearts show longer actin/thin filaments, abnormal actin bundles cross-linking Z lines, upregulation of Lmod2, and mislocalization of Tmod1; genetic rescue showed abnormal actin bundles (not elongated filaments) caused lethality. Global and cardiac-specific KO mouse models, biochemical binding assays, in vitro actin polymerization assay, genetic rescue (HSPB7/Lmod2 double KO), immunofluorescence Proceedings of the National Academy of Sciences of the United States of America High 29078393
2017 Cardiac-specific inducible HSPB7 KO causes rapid heart failure and arrhythmia; loss of HSPB7 leads to structural disruption of intercalated discs, downregulation of connexin 43, mislocalization of desmoplakin and N-cadherin, and upregulation/aggregation of filamin C in cardiomyocytes, without disrupting sarcomere contractile protein organization. Cardiac-specific inducible KO mouse, ECG, immunofluorescence, Western blot PLoS genetics High 28827800
2018 Zebrafish Hspb7 is a kinetically privileged sensor for reactive electrophilic species (RES); a single conserved cysteine (C117 in zebrafish, conserved in human ortholog) reacts rapidly with native carbonyl-based RES at substoichiometric concentrations; RES adduction causes structural changes (increase in β-sheet content) detected by circular dichroism; a cancer-relevant missense mutation reduces this RES-sensing property. In vitro RES adduction kinetics, site-directed mutagenesis (C117), circular dichroism, cell-based RES sensing assay ACS chemical biology High 29397684
2018 Hspb7 binds FilaminC and Titin as interacting partners in cardiac cells; loss of Hspb7 in zebrafish causes focal cardiac fibrosis and sarcomeric abnormalities; HSPB7 loss stimulates autophagic pathways and Hspb5 expression; inhibiting autophagy in HSPB7 mutant human cardiomyocytes causes FilaminC aggregation and developmental cardiomyopathy, establishing that HSPB7 facilitates autophagic processing of damaged FilaminC to maintain sarcomeric homeostasis. Co-immunoprecipitation (FilaminC, Titin), zebrafish hspb7 mutants, human iPSC-derived cardiomyocytes with HSPB7 mutation, autophagy inhibition, autophagy flux assays Developmental biology High 29331499
2019 The flexible N-terminal domain (NTD) of HSPB7 is both necessary and sufficient for association with and inhibition of polyQ aggregation; transplanting the HSPB7 NTD onto HSPB1 (which cannot suppress polyQ aggregation) confers anti-polyQ activity and reduces oligomer size; de-oligomerization of HSPB1 alone does not suffice to gain polyQ suppression activity. In vitro aggregation assay, domain-swap chimeric constructs (NTD transplant), immunoblotting, fluorescence microscopy, phospho-mimicking HSPB1 mutants The Journal of biological chemistry High 31097540
2020 HSPB7 knockdown promotes osteogenic differentiation of human adipose-derived stem cells (hASCs), while overexpression suppresses it; the mechanism involves regulation of the ERK signaling pathway, as inhibition of ERK with U0126 or ERK1/2 siRNA blocks the pro-osteogenic effect of HSPB7 knockdown. Lentiviral knockdown/overexpression, ERK inhibitor (U0126), ERK siRNA, ALP assay, Alizarin Red staining, in vivo ectopic bone formation Stem cell research & therapy Medium 33097082
2021 Recombinant human HspB7 forms two oligomeric forms (dimers ~36 kDa and large oligomers >600 kDa); mild oxidation promotes large oligomer formation; modification of Cys126 by iodoacetamide prevents large oligomer formation; deletion of the first 13 residues or the polySer motif (residues 17-29) also prevents large oligomer formation; HspB7 can form heterodimers with HspB6 and HspB8 through a disulfide-mediated interface. Recombinant protein purification, size-exclusion chromatography, hydrophobic chromatography, chemical crosslinking, cysteine modification, domain deletion, co-immunoprecipitation International journal of molecular sciences Medium 34360542
2022 HSPB7 is not a genuine actin-binding protein: blot overlay shows HspB7 can bind G- and F-actin at the C-terminal large core domain of actin, but ultracentrifugation pelleting is nonspecific (no saturation), HspB7 cannot retard or prevent heat-induced F-actin aggregation, and native gel electrophoresis and chemical crosslinking fail to detect G-actin/HspB7 complexes, unlike confirmed actin binders DNase I and cofilin-2. Blot overlay, ultracentrifugation co-sedimentation, native gel electrophoresis, chemical crosslinking, heat-induced aggregation assay Biochimie Medium 35977674
2022 HDAC1 represses HSPB7 expression in oral squamous cell carcinoma cells through histone deacetylation of the HSPB7 promoter; sodium butyrate (NaB) inhibits HDAC1 and thereby upregulates HSPB7, suppressing cancer cell proliferation and invasion. ChIP assay (HDAC1 at HSPB7 promoter), Western blot, cell functional assays, in vivo xenograft Neoplasma Medium 35652621
2023 HSPB7 interacts with the transcription factor MECOM (which acts as a transcriptional regulator of HSPB7) and inhibits glycolysis in lung adenocarcinoma cells, reducing glucose consumption, lactic acid production, and levels of glycolytic enzymes LDHA, HK2, and PKM2. Co-immunoprecipitation, ChIP assay (MECOM at HSPB7 promoter), metabolic assays (glucose/lactate), Western blot, cell functional assays Oncology reports Medium 37732539
2023 HSPB7 silencing in bone marrow mesenchymal stromal cells (BMSCs) promotes adipogenesis while reducing osteogenic differentiation; overexpression enhances osteogenesis; both N-terminal and C-terminal domains are required for full osteoblastic potency; mechanistically, Activin A is identified as a downstream target mediating HSPB7 knockdown-induced osteogenic inhibition. Lentiviral knockdown/overexpression, domain deletion constructs, ALP/calcium/Alizarin Red/Oil Red O assays, Activin A antibody/SB431542 inhibition Stem cell research & therapy Medium 37170285
2025 HSPB7 and FLNC form a strong heterodimer whose structure was solved by X-ray crystallography; the HSPB7-FLNC heterodimer out-competes the FLNC homodimer interface; phosphorylation of FLNC at T2677 (cardiac stress-associated) favors FLNC homodimerization, while phosphorylation at Y2683 shifts equilibrium toward the HSPB7-FLNC heterodimer; HSPB7-FLNC heterodimerization is proposed to abrogate FLNC actin cross-linking and enhance FLNC diffusive mobility; this interaction arose evolutionarily around the time primitive hearts evolved in chordates. X-ray crystallography, quantitative binding assays, phospho-mimetic mutagenesis, FRAP (diffusive mobility), evolutionary ancestral sequence reconstruction Nature communications High 40312381
2025 Among the five sHSPs tested (HspB1, phospho-mimicking HspB1 3D, HspB5, HspB6, HspB7, HspB8), only HspB7 forms complexes with the FLNC C-terminal fragment (Ig-like domains 19-24); the interaction is mediated by HspB7's α-crystallin domain binding to Ig-like domain 24 of FLNC; this binding induces dissociation of FLNC dimers. Size-exclusion chromatography, native gel electrophoresis, chemical crosslinking, immunochemistry Biochemistry. Biokhimiia Medium 41702738
2025 Disease-causing mutations in FLNC domains 22-24 (EN/D in domain 22; ΔPGL and W2710X in domain 24) differentially reduce or abolish interaction with HspB7: WT~EN/D interact with HspB7 > ΔPGL; Wmut (W2710X) cannot interact with HspB7 or its α-crystallin domain; structural modeling indicates ΔPGL and Wmut expose a hydrophobic groove in domain 24 that reduces HspB7 binding. Size-exclusion chromatography, native gel electrophoresis, chemical crosslinking, AlphaFold 3 modeling, recombinant mutant proteins International journal of molecular sciences Medium 40564978

Source papers

Stage 0 corpus · 40 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Comparison of the small heat shock proteins alphaB-crystallin, MKBP, HSP25, HSP20, and cvHSP in heart and skeletal muscle. Histochemistry and cell biology 135 15480735
2010 HSPB7 is the most potent polyQ aggregation suppressor within the HSPB family of molecular chaperones. Human molecular genetics 123 20843828
2006 Proteome analysis of the dystrophin-deficient MDX diaphragm reveals a drastic increase in the heat shock protein cvHSP. Proteomics 111 16835851
2010 Common variants in HSPB7 and FRMD4B associated with advanced heart failure. Circulation. Cardiovascular genetics 107 20124441
2010 Genetic association study identifies HSPB7 as a risk gene for idiopathic dilated cardiomyopathy. PLoS genetics 100 20975947
1999 Identification and characterization of cvHsp. A novel human small stress protein selectively expressed in cardiovascular and insulin-sensitive tissues. The Journal of biological chemistry 99 10593960
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
2011 HSPB1, HSPB6, HSPB7 and HSPB8 protect against RhoA GTPase-induced remodeling in tachypaced atrial myocytes. PloS one 73 21731611
2003 Expression of small heat shock proteins HspB2, HspB8, Hsp20 and cvHsp in different tissues of the perinatal developing pig. European journal of cell biology 73 14629120
2009 HSPB7 is a SC35 speckle resident small heat shock protein. Biochimica et biophysica acta 65 19464326
2009 Cardiac signaling genes exhibit unexpected sequence diversity in sporadic cardiomyopathy, revealing HSPB7 polymorphisms associated with disease. The Journal of clinical investigation 58 20038796
2017 HSPB7 is indispensable for heart development by modulating actin filament assembly. Proceedings of the National Academy of Sciences of the United States of America 53 29078393
2016 HSPB7 interacts with dimerized FLNC and its absence results in progressive myopathy in skeletal muscles. Journal of cell science 53 26929074
2018 Hspb7 is a cardioprotective chaperone facilitating sarcomeric proteostasis. Developmental biology 38 29331499
2014 Downregulation of the tumor suppressor HSPB7, involved in the p53 pathway, in renal cell carcinoma by hypermethylation. International journal of oncology 27 24585183
2013 Small heat shock proteins Hspb7 and Hspb12 regulate early steps of cardiac morphogenesis. Developmental biology 27 23850773
2020 Deletion of metal transporter Zip14 (Slc39a14) produces skeletal muscle wasting, endotoxemia, Mef2c activation and induction of miR-675 and Hspb7. Scientific reports 25 32132660
2018 Cardiovascular Small Heat Shock Protein HSPB7 Is a Kinetically Privileged Reactive Electrophilic Species (RES) Sensor. ACS chemical biology 25 29397684
2018 SRARP and HSPB7 are epigenetically regulated gene pairs that function as tumor suppressors and predict clinical outcome in malignancies. Molecular oncology 23 29577611
2020 HSPB7 regulates osteogenic differentiation of human adipose derived stem cells via ERK signaling pathway. Stem cell research & therapy 22 33097082
2017 HSPB7 prevents cardiac conduction system defect through maintaining intercalated disc integrity. PLoS genetics 21 28827800
2019 The N terminus of the small heat shock protein HSPB7 drives its polyQ aggregation-suppressing activity. The Journal of biological chemistry 17 31097540
2016 Regulation of Hspb7 by MEF2 and AP-1: implications for Hspb7 in muscle atrophy. Journal of cell science 15 27632998
2021 Quaternary Structure and Hetero-Oligomerization of Recombinant Human Small Heat Shock Protein HspB7 (cvHsp). International journal of molecular sciences 11 34360542
2019 A Missense Mutation of the HSPB7 Gene Associated with Heat Tolerance in Chinese Indicine Cattle. Animals : an open access journal from MDPI 11 31416175
2021 Cardio-Vascular Heat Shock Protein (cvHsp, HspB7), an Unusual Representative of Small Heat Shock Protein Family. Biochemistry. Biokhimiia 10 33827396
2016 Association between polymorphisms of the HSPB7 gene and Cheyne-Stokes respiration with central sleep apnea in patients with dilated cardiomyopathy and congestive heart failure. International journal of cardiology 7 27441470
2010 Molecular characterization of rat cvHsp/HspB7 in vitro and its dynamic molecular architecture. Molecular medicine reports 7 21461572
2023 Heat shock protein B7 (HSPB7) inhibits lung adenocarcinoma progression by inhibiting glycolysis. Oncology reports 6 37732539
2025 Filamin C dimerisation is regulated by HSPB7. Nature communications 5 40312381
2023 HSPB7 oppositely regulates human mesenchymal stromal cell-derived osteogenesis and adipogenesis. Stem cell research & therapy 4 37170285
2022 Sodium butyrate inhibits oral squamous cell carcinoma proliferation and invasion by regulating the HDAC1/HSPB7 axis. Neoplasma 3 35652621
2018 HSPB7 gene polymorphism associated with anthropometric parameters of obesity and fat intake in a Central European population. Central European journal of public health 3 30660137
2014 Refined purification of large amounts of rat cvHsp/HspB7 and partial biological characterization in vitro. Protein and peptide letters 3 24555434
2022 Is the small heat shock protein HSPB7 (cvHsp) a genuine actin-binding protein? Biochimie 2 35977674
2025 Circular RNA circSCMH1 regulates glycolysis to inhibit gastric cancer metastasis via miR-296-3p/HSPB7-GLUT3 axis. Translational oncology 1 41401631
2026 C-Terminal Fragment of Filamin C Containing Immunoglobulin-Like Domains 19-24 Selectively Interacts with the Small Heat Shock Protein HspB7. Biochemistry. Biokhimiia 0 41702738
2026 HSPB7 Deficiency Drives Aortic Aneurysm Progression in Marfan Syndrome Through Vascular Smooth Muscle Cell Phenotypic Switching. Clinical and experimental pharmacology & physiology 0 42203489
2025 Effect of Mutations in the C-Terminal 22-24 Domains of Filamin C Associated with Cardio- and Myopathies on Its Interaction with Small Heat Shock Protein HspB7. International journal of molecular sciences 0 40564978
2019 Correction to: HSPB7 gene polymorphism associated with anthropometric parameters of obesity and fat intake in a Central European population. Central European journal of public health 0 30927404

Missed literature

Know a paper Affinage missed for HSPB7? Flag it for the maintainers and the community.

No submissions yet.