Affinage

S100A13

Protein S100-A13 · UniProt Q99584

Length
98 aa
Mass
11.5 kDa
Annotated
2026-06-10
38 papers in source corpus 27 papers cited in narrative 26 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

S100A13 is a homodimeric EF-hand Ca2+-binding protein that functions as a core cargo/chaperone component of the non-classical (ER/Golgi-independent) secretion machinery for signal peptide-less proteins, exporting them across the plasma membrane in response to cellular stress (PMID:11410600, PMID:12746488, PMID:20467443). Each dimer binds four Ca2+ with positive cooperativity, and Ca2+ binding drives conformational changes; unusually among S100 proteins, S100A13 does not expose a hydrophobic surface upon Ca2+ binding, and all of its alpha-helices are amphiphilic, a feature linked to its release-mediating activity (PMID:10722710, PMID:17374362, PMID:18259052). It additionally binds Cu2+ independently of Ca2+, with the two ions acting synergistically to potentiate cargo engagement: Ca2+ and Cu2+ together markedly enhance the S100A13–FGF-1 interaction and promote FGF-1 homodimerization required for export (PMID:16766622, PMID:18164517). Mechanistically, S100A13 nucleates a multiprotein release complex—forming a binary complex with the C2A domain of p40 synaptotagmin-1 that templates FGF-1 dimerization, and engaging cargo through its basic C-terminal peptide; deletion of residues 88–98 yields a dominant-negative that selectively blocks cargo release while permitting S100A13's own export (PMID:16519964, PMID:20467443, PMID:19284995). The same module exports IL-1α (Cu2+-dependently, via a heterotetrameric IL-1α–S100A13 intermediate) and prothymosin-α, whose caspase-3 cleavage removes the S100A13-interaction domain and aborts release during apoptosis (PMID:12746488, PMID:20467443, PMID:21270123). Stress-induced export is completed by SNARE-dependent membrane tethering, requiring a Ca2+-dependent S100A13–synaptotagmin-1 hetero-oligomer and syntaxin-1 (PMID:32856232), and S100A13 acts specifically at this final release step rather than in intracellular trafficking (PMID:20863990). The anti-allergic drug amlexanox antagonizes the pathway by binding the FGF-1-interaction site on S100A13 (PMID:20178375). Through IL-1α surface presentation, S100A13 elevates NF-κB activity and induces the senescence-associated secretory phenotype, accelerating cellular senescence (PMID:30670674), and it also engages the C2 domain of RAGE (PMID:24982031). Digenic mutations in S100A13 (with S100A3) cause familial pulmonary fibrosis, with patient fibroblasts showing aberrant calcium homeostasis and mitochondrial dysregulation that are rescued by wild-type or recombinant extracellular S100A13 (PMID:31073086, PMID:38099297).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1998 Medium

    Established S100A13 as a physical component of the FGF-1 non-classical release machinery, answering whether any dedicated factor accompanies signal-peptide-less FGF-1 export.

    Evidence Purification of a brain-derived FGF-1/p40 synaptotagmin-1 complex plus amlexanox inhibition of stress-induced release in cells

    PMID:9712836

    Open questions at the time
    • Did not define which S100A13 region contacts cargo
    • Functional necessity of S100A13 not yet tested by loss-of-function
  2. 2000 High

    Defined the biophysical and structural baseline—homodimer, cooperative four-Ca2+ binding, and an atypical absence of Ca2+-induced hydrophobic exposure—distinguishing S100A13 from canonical S100 proteins.

    Evidence Flow dialysis, fluorescence, circular dichroism, and immunofluorescence in multiple cell types

    PMID:10722710

    Open questions at the time
    • How the unusual surface chemistry relates to cargo export untested at this stage
    • Cu2+ binding not yet examined
  3. 2001 High

    Showed S100A13 is functionally required for FGF-1 release and mapped the requirement to its basic C-terminal domain, advancing from correlation to causal mechanism.

    Evidence Wild-type overexpression, C-terminal-deletion dominant-negative, and Cys-free FGF-1 rescue in NIH 3T3 cells

    PMID:11410600

    Open questions at the time
    • Did not resolve the molecular interface or stoichiometry of the cargo complex
    • Membrane translocation step not addressed
  4. 2003 High

    Generalized S100A13 cargo function beyond FGF-1 to IL-1α and revealed copper-dependence of cargo engagement.

    Evidence Co-immunoprecipitation, dominant-negative mutant, and Cu2+ chelation in U937 and NIH 3T3 cells

    PMID:12746488

    Open questions at the time
    • Structural basis of the Cu2+-dependent IL-1α interaction not defined here
    • Cu2+ binding site on S100A13 unmapped
  5. 2006 High

    Quantified independent Ca2+ and Cu2+ binding and connected Cu2+ to FGF-1 dimerization, explaining the metal requirement of the release pathway.

    Evidence ITC, multidimensional NMR, terbium binding, thermal denaturation, and H/D exchange

    PMID:16766622 PMID:18164517

    Open questions at the time
    • Did not establish whether metal effects operate identically for non-FGF-1 cargoes
  6. 2007 High

    Resolved the crystal structure and the lipid-binding behavior, linking amphiphilic helices and apo-form phosphatidylserine binding to a model of membrane translocation.

    Evidence X-ray crystallography at 2.0 Å and biophysical lipid-vesicle binding assays (ITC, ANS, CD)

    PMID:17374362 PMID:17991455 PMID:18259052

    Open questions at the time
    • Membrane translocation role of lipid binding inferred, not directly demonstrated in cells
  7. 2009 Medium

    Defined the S100A13–synaptotagmin-1 C2A binary complex as the template for FGF-1 dimerization and showed cargo is exported in a folded state.

    Evidence NMR titration/NOESY structure of the binary complex and DHFR folding-locked chimera export assays

    PMID:19233122 PMID:19284995

    Open questions at the time
    • Functional consequence of the binary complex inferred from structure
    • Mechanism by which a folded protein crosses the bilayer unresolved
  8. 2010 High

    Pinpointed amlexanox to the FGF-1-binding site and demonstrated, by RNAi, that S100A13 acts at the terminal release step rather than intracellular trafficking; extended the cargo repertoire to prothymosin-α with caspase-3-gated control.

    Evidence NMR solution structure with ITC/fluorescence, lentiviral shRNA in HUVECs, and co-release/dominant-negative/caspase assays in glioma cells

    PMID:20178375 PMID:20467443 PMID:20863990

    Open questions at the time
    • Membrane-crossing step still mechanistically undefined
    • How cargo selectivity is achieved across FGF-1/IL-1α/ProTα not unified
  9. 2011 Medium

    Provided structural evidence for an IL-1α–S100A13 heterotetramer as the secretion intermediate.

    Evidence Structural characterization of the IL-1α–S100A13 complex

    PMID:21270123

    Open questions at the time
    • Method detail limited
    • In vivo relevance of the tetramer not tested
  10. 2014 Medium

    Identified a moderate-affinity S100A13–RAGE C2 interaction and mapped its interface, raising a potential receptor-engagement role distinct from cargo export.

    Evidence NMR solution structure and ITC

    PMID:24982031

    Open questions at the time
    • Functional/cellular consequence of RAGE binding not demonstrated
  11. 2019 Medium

    Connected S100A13-driven IL-1α surface presentation to NF-κB/SASP activation and senescence, giving the secretion pathway a physiological output.

    Evidence Overexpression/knockdown with surface IL-1α, NF-κB reporter, SASP readouts and Cu2+ chelation across multiple senescence models

    PMID:30670674

    Open questions at the time
    • Single lab
    • Direct contribution of senescence pathway to organismal phenotypes untested
  12. 2020 High

    Established SNARE dependence of the export step, showing syntaxin-1 and a Ca2+-dependent synaptotagmin-1–S100A13 hetero-oligomer are required for membrane tethering and release.

    Evidence Pull-down, SPR, PLA, intracellular antibody blockade, BoNT/C1, and siRNA in neural cells

    PMID:32856232

    Open questions at the time
    • Whether identical SNARE machinery operates for FGF-1 and IL-1α in non-neural cells not shown
  13. 2019 Medium

    Linked S100A13 loss-of-function to familial pulmonary fibrosis with calcium/mitochondrial dysfunction, and later demonstrated rescue by wild-type and extracellular recombinant protein, establishing disease causality and reversibility.

    Evidence Patient genetics and fibroblast assays; transfection rescue and extracellular protein treatment with calcium/mitochondrial/inflammatory readouts

    PMID:31073086 PMID:38099297

    Open questions at the time
    • Digenic with S100A3, so S100A13-specific contribution entangled
    • Mechanism linking secretion function to mitochondrial/calcium phenotypes unclear
  14. 2021 Medium

    Placed S100A13 under transcriptional control of TEAD4 and SP1 and connected its expression to cancer cell invasion and chemoresistance.

    Evidence Luciferase promoter assays, RNAi/overexpression, cisplatin sensitivity, invasion and xenograft assays across OSCC, thyroid, lung and osteosarcoma models

    PMID:18061437 PMID:27008379 PMID:34358353 PMID:41787040

    Open questions at the time
    • Whether cancer phenotypes depend on the secretion function or another activity unresolved
    • SP1 axis (osteosarcoma) is single-method, Low confidence

Open questions

Synthesis pass · forward-looking unresolved questions
  • The physical mechanism by which the S100A13 complex translocates folded cargo across an intact plasma membrane—and how a single module selects among FGF-1, IL-1α, and prothymosin-α—remains unresolved.
  • No reconstituted membrane-translocation system
  • Cargo-selection determinants not defined
  • Unified model linking secretion, senescence, fibrosis and cancer phenotypes absent

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140313 molecular sequestering activity 4 GO:0060090 molecular adaptor activity 3 GO:0140299 molecular sensor activity 2 GO:0008289 lipid binding 1
Localization
GO:0005576 extracellular region 2 GO:0005829 cytosol 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-9609507 Protein localization 5 R-HSA-168256 Immune System 2 R-HSA-8953897 Cellular responses to stimuli 1
Partners
AGERFGF1IL1APTMAS100A3STX1ASYT1
Complex memberships
IL-1α–S100A13 heterotetramerS100A13–FGF-1–p40 synaptotagmin-1 release complexS100A13–prothymosin-α complex

Evidence

Reading pass · 26 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 S100A13 was identified as a component of a brain-derived multiprotein complex containing FGF-1 and p40 synaptotagmin-1 (Syn-1), and amlexanox (which binds S100A13) repressed heat shock-induced release of FGF-1 and p40 Syn-1 in a concentration-dependent manner, implicating S100A13 in regulation of the FGF-1 non-classical release pathway. Purification of brain-derived complex, co-purification/association assay, pharmacological inhibition with amlexanox in cell-based stress release assay The Journal of biological chemistry Medium 9712836
2001 S100A13 participates directly in heat shock-induced FGF-1 release: co-expression of S100A13 with FGF-1 represses constitutive S100A13 release and enables stress-induced co-release; a deletion mutant of S100A13 lacking its basic residue-rich C-terminal domain acts as a dominant-negative inhibitor of FGF-1 release; S100A13 expression also enables release of a normally non-releasable Cys-free FGF-1 mutant. Overexpression and dominant-negative deletion mutant studies in NIH 3T3 cells, conditioned medium analysis, ammonium sulfate solubility assay The Journal of biological chemistry High 11410600
2003 S100A13 mediates the copper-dependent, stress-induced non-classical release of IL-1α: IL-1α associates intracellularly with S100A13 in a Cu2+-dependent manner; a dominant-negative S100A13 mutant (lacking its novel sequence) represses IL-1α export; wild-type S100A13 overexpression eliminates the requirement for stress-induced transcription for IL-1α release. Co-immunoprecipitation, dominant-negative S100A13 mutant expression, conditioned medium western blot in U937 and NIH 3T3 cells, Cu2+ chelation experiments Journal of cell science High 12746488
1999 S100A13 (and S100A12) directly bind the anti-allergic drugs amlexanox, cromolyn, and tranilast, as demonstrated by affinity chromatography; this binding is calcium-sensitive and distinct from calmodulin interactions. Drug-coupled affinity chromatography, reversed-phase HPLC, cDNA sequencing of isolated proteins, binding confirmed with recombinant protein The Biochemical journal Medium 10051426
2000 Human recombinant S100A13 is a homodimer that binds four Ca2+ per dimer in two sets of sites with positive cooperativity (high- and low-affinity); Ca2+ binding causes conformational changes detectable by fluorescence and CD; S100A13 uniquely does not expose hydrophobic patches upon Ca2+ binding (unlike most S100 proteins); in human smooth muscle cells, S100A13 localizes to the perinuclear area, distinct from S100A2 (nuclear) and S100A1 (stress fibers). Flow dialysis, fluorescence spectrophotometry, circular dichroism, immunofluorescence with specific antisera in multiple cell types The Journal of biological chemistry High 10722710
2002 S100A13 undergoes Ca2+-dependent translocation in endothelial cells via the classical Golgi-ER pathway in response to angiotensin II stimulation, a pathway distinct from S100A6 (which uses actin stress fibers). Live cell imaging/translocation assays in endothelial cells, pharmacological disruption of Golgi-ER and actin pathways Journal of cell science Medium 12118070
2006 S100A13 binds Cu2+ and Ca2+ independently with similar micromolar affinity (two atoms per subunit); Ca2+ stabilizes S100A13 while Cu2+ destabilizes it; S100A13 can bind both ions simultaneously; Cu2+ binding is important for FGF-1 homodimer formation and subsequent non-classical secretion. Isothermal titration calorimetry, multidimensional NMR spectroscopy, terbium binding, thermal denaturation by far-UV CD, limited trypsin digestion, hydrogen-deuterium exchange Biophysical journal High 16766622
2006 FGF-1 and S100A13 are co-released from astrocytes upon serum-deprivation stress via a non-vesicular (Brefeldin A-insensitive) pathway; S100A13 is the major protein co-immunoprecipitated with FGF-1; the interaction requires the C-terminal 11 amino acid peptide of S100A13 and is Ca2+-sensitive; a Δ88–98 S100A13 mutant selectively blocks FGF-1 release but not S100A13 release itself; amlexanox blocks both; Ca2+ chelation (BAPTA-AM) abolishes both releases. Immunocytochemistry, immunoblot of conditioned medium, immunoprecipitation, GST/Strep-tag pull-down with deletion mutants, pharmacological inhibition (amlexanox, BAPTA-AM, Brefeldin A), Ca2+ imaging Neurochemistry international High 16519964
2007 ApoS100A13 (calcium-free form) preferentially binds phosphatidylserine lipid vesicles; Ca2+-bound S100A13 binds weakly; apoS100A13 undergoes subtle conformational change exposing hydrophobic surfaces upon lipid binding; these lipid interactions are proposed to facilitate membrane translocation during non-classical FGF-1 secretion. Isothermal titration calorimetry, steady-state fluorescence, equilibrium thermal unfolding, ANS binding, limited trypsin digestion, far-UV CD with phosphatidylserine SUVs Biochimica et biophysica acta Medium 17991455
2007 Ca2+ and Cu2+ synergistically enhance the S100A13–FGF-1 interaction: Ca2+ alone increases binding affinity (EC50 ~10 µM); Cu2+ alone has no effect but markedly potentiates Ca2+-enhanced binding (EC50 ~50 nM); amlexanox abolishes the Cu2+-induced potentiation; this synergistic interaction is proposed as the initial step in non-classical FGF-1 release. Quartz crystal microbalance (real-time binding assay) with Strep-tagII-S100A13 and GST-FGF1, pharmacological inhibition with amlexanox Neurochemistry international Medium 18164517
2007 Crystal structure of Ca2+-bound human S100A13 at 2.0 Å resolution reveals a homodimer with four EF-hand motifs; all alpha-helices are amphiphilic (unique among S100 family members), a feature proposed to relate to its ability to mediate FGF-1 and IL-1α release. X-ray crystallography at 2.0 Å resolution Biochemical and biophysical research communications High 17374362 18259052
2010 The molecular interface between amlexanox and S100A13 was determined: amlexanox binds specifically to the FGF-1-binding site on S100A13, preventing formation of the FGF-1-S100A13 release complex and acting as an antagonist of non-classical FGF-1 secretion. 3D solution structure by multidimensional NMR spectroscopy, ITC, fluorescence spectrophotometry Biochemistry High 20178375
2010 S100A13 is required for non-classical release of prothymosin-α (ProTα): S100A13 and ProTα are co-released upon ischemic/serum-deprivation stress; the Ca2+-dependent interaction requires the C-terminal peptide sequences of both proteins; a Δ88–98 S100A13 mutant blocks ProTα release but not S100A13 release; caspase-3 cleavage of ProTα removes its S100A13-interaction domain, preventing extracellular release during apoptosis. Immunoprecipitation, Co-release assay in C6 glioma cells, dominant-negative S100A13 mutant, caspase-3 cleavage analysis Cell death and differentiation High 20467443
2011 The IL-1α–S100A13 tetrameric complex structure was determined: IL-1α and S100A13 form a heterotetrameric complex that is a key intermediate in the non-classical (ER/Golgi-independent) pathway for IL-1α secretion. Structural determination of the IL-1α–S100A13 complex (NMR/biophysical methods implied), complex characterization The Journal of biological chemistry Medium 21270123
2009 S100A13 forms a binary complex with the C2A domain of synaptotagmin-1 (Syt1); the S100A13–C2A complex acts as a template for FGF-1 dimerization and multiprotein complex formation in the non-classical FGF-1 release pathway. 1H-15N HSQC NMR titration, 3D-filtered NOESY NMR, binary complex structure determination Biochemical and biophysical research communications Medium 19284995
2009 S100A13 and FGF-1 can be exported in fully folded conformation: DHFR-fusion chimeras of both proteins were released despite treatment with aminopterin (which locks DHFR in folded state), demonstrating that folded tertiary structure does not prevent non-classical export. DHFR chimera expression in cells, aminopterin treatment, conditioned medium analysis Biochemical and biophysical research communications Medium 19233122
2014 S100A13 interacts with the C2 domain of RAGE with moderate affinity (Kd ~1.3 µM); the solution structure of the S100A13–RAGE C2 complex was solved by NMR, defining the interface regions on S100A13. NMR solution structure determination, isothermal titration calorimetry Biochimica et biophysica acta Medium 24982031
2019 S100A13 promotes the non-classical secretion of IL-1α to the cell surface, thereby elevating NF-κB activity and inducing SASP gene expression; S100A13 knockdown reduces surface IL-1α, NF-κB activity, and SASP production; S100A13 overexpression accelerates oncogene Ras-induced senescence, drug-induced senescence, and replicative senescence; Cu2+ elevation during senescence enhances this pathway; S100A13 modulates senescence mediators p38, γ-H2AX, and mTORC1. S100A13 overexpression and knockdown in cell lines, surface IL-1α measurement, NF-κB reporter assay, SASP gene expression, Cu2+ chelation, multiple senescence models Aging Medium 30670674
2010 S100A13 knockdown by RNAi in HUVECs blocked FGF-1 release from serum-deprived cells but did not affect FGF-1 intracellular transport (cytoplasm to membrane), demonstrating S100A13 is specifically required for the final release step, not intracellular trafficking. Lentiviral shRNA knockdown, immunofluorescence, western blot of conditioned medium in HUVECs Journal of the Formosan Medical Association Medium 20863990
2020 The stress-induced non-classical release of S100A13 and ProTα requires SNARE protein-mediated membrane tethering: p40 synaptotagmin-1 (Syt1) forms a Ca2+-dependent hetero-oligomeric complex with S100A13 (confirmed by pull-down and SPR); antibody-mediated intracellular blockade of Syt1 inhibits ProTα and S100A13 release; botulinum neurotoxin/C1 (cleaving syntaxin-1) and anti-syntaxin-1 antibody/siRNA block release of Syt1, S100A13 and ProTα. Pull-down assay, surface plasmon resonance, immunoprecipitation of conditioned medium, in situ proximity ligation assay, intracellular antibody delivery, BoNT/C1 treatment, siRNA knockdown, immunocytochemistry Cellular and molecular neurobiology High 32856232
2007 S100A13 knockdown by RNAi (50–80% depletion) in highly invasive lung cancer cell lines reduced their in vitro invasive potential by 50–80%, without affecting proliferation; conversely, S100A13 overexpression in less invasive lines did not increase invasion, indicating S100A13 is required for but insufficient alone to induce invasion. RNAi knockdown, in vitro Matrigel invasion assay, transient overexpression, proliferation assay European journal of cancer Medium 18061437
2016 S100A13 knockdown in thyroid cancer cells inhibited proliferation and invasion; HMGA1 was identified as a downstream effector of S100A13 in this context; S100A13 and HMGA1 expression are positively correlated in thyroid cancer tissue; overexpression of S100A13 increased tumor growth in xenograft models. Lentiviral S100A13 knockdown, siRNA-mediated HMGA1 knockdown, MTT, colony formation, Transwell invasion assays, nude mouse xenograft, tissue microarray Journal of translational medicine Medium 27008379
2019 Digenic inheritance of mutations in S100A3 and S100A13 causes familial pulmonary fibrosis; patient-derived fibroblasts with reduced S100A13 expression show aberrant intracellular calcium homeostasis, mitochondrial dysregulation, and altered ECM component expression. Molecular genetic analysis (sequencing), patient-derived fibroblast analysis, calcium homeostasis assays, mitochondrial function assays The European respiratory journal Medium 31073086
2023 Reintroduction of wild-type S100A13 (and S100A3) into patient-derived fibroblasts (or control cells transfected with mutant constructs) restores receptor-mediated calcium signaling, reverses increased mitochondrial mass and hyperpolarization, and reduces inflammatory mediator secretion; extracellular recombinant S100A13 protein is sufficient to normalize these responses. Transfection of WT vs. mutant constructs, extracellular recombinant protein treatment, calcium signaling assays, mitochondrial mass/membrane potential measurements, inflammatory mediator quantification Frontiers in cell and developmental biology Medium 38099297
2021 TEAD4 directly binds the promoter of S100A13 transcript ENST00000440685 and activates its transcription; S100A13 knockdown increases cisplatin sensitivity in OSCC cells, while overexpression decreases it; S100A13 knockdown partially abrogates TEAD4-mediated cisplatin resistance. Luciferase reporter assay (TEAD4 binding to S100A13 promoter), RNAi knockdown, overexpression, cisplatin sensitivity assays, colony formation, apoptosis analysis Journal of oral pathology & medicine Medium 34358353
2026 SP1 transcription factor directly binds the S100A13 promoter and activates its transcription, as demonstrated by luciferase reporter assay; S100A13 promotes osteosarcoma cell migration and invasion in functional assays. Luciferase reporter assay, wound-healing assay, Transwell invasion assay Discover oncology Low 41787040

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1998 S100A13 is involved in the regulation of fibroblast growth factor-1 and p40 synaptotagmin-1 release in vitro. The Journal of biological chemistry 103 9712836
2003 S100A13 mediates the copper-dependent stress-induced release of IL-1alpha from both human U937 and murine NIH 3T3 cells. Journal of cell science 81 12746488
1999 Three distinct anti-allergic drugs, amlexanox, cromolyn and tranilast, bind to S100A12 and S100A13 of the S100 protein family. The Biochemical journal 76 10051426
2001 S100A13 participates in the release of fibroblast growth factor 1 in response to heat shock in vitro. The Journal of biological chemistry 73 11410600
1996 Characterization of the human and mouse cDNAs coding for S100A13, a new member of the S100 protein family. Biochemical and biophysical research communications 61 8878558
2010 S100A13 is a new angiogenic marker in human melanoma. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 59 20208480
2000 S100A13. Biochemical characterization and subcellular localization in different cell lines. The Journal of biological chemistry 48 10722710
2006 S100A13, a new marker of angiogenesis in human astrocytic gliomas. Journal of neuro-oncology 46 16773219
2010 Stress-induced non-vesicular release of prothymosin-α initiated by an interaction with S100A13, and its blockade by caspase-3 cleavage. Cell death and differentiation 41 20467443
2007 Identification of a novel, functional role for S100A13 in invasive lung cancer cell lines. European journal of cancer (Oxford, England : 1990) 41 18061437
2006 Copper binding affinity of S100A13, a key component of the FGF-1 nonclassical copper-dependent release complex. Biophysical journal 41 16766622
2005 FGF-1 and S100A13 possibly contribute to angiogenesis in endometriosis. Journal of reproductive immunology 41 16165218
2002 S100A13 and S100A6 exhibit distinct translocation pathways in endothelial cells. Journal of cell science 39 12118070
2014 Proteomics analysis of melanoma metastases: association between S100A13 expression and chemotherapy resistance. British journal of cancer 38 24722184
2016 The association between S100A13 and HMGA1 in the modulation of thyroid cancer proliferation and invasion. Journal of translational medicine 35 27008379
2011 The IL1alpha-S100A13 heterotetrameric complex structure: a component in the non-classical pathway for interleukin 1alpha secretion. The Journal of biological chemistry 31 21270123
2019 S100A13 promotes senescence-associated secretory phenotype and cellular senescence via modulation of non-classical secretion of IL-1α. Aging 26 30670674
2010 Molecular level interactions of S100A13 with amlexanox: inhibitor for formation of the multiprotein complex in the nonclassical pathway of acidic fibroblast growth factor. Biochemistry 23 20178375
2006 Evidence for serum-deprivation-induced co-release of FGF-1 and S100A13 from astrocytes. Neurochemistry international 23 16519964
2005 Endoglin (cd105) and S100A13 as markers of active angiogenesis in endometriosis. Reproductive biology 21 15821778
2014 Interaction of S100A13 with C2 domain of receptor for advanced glycation end products (RAGE). Biochimica et biophysica acta 20 24982031
2019 An atypical pulmonary fibrosis is associated with co-inheritance of mutations in the calcium binding protein genes S100A3 and S100A13. The European respiratory journal 15 31073086
2007 S100A13-lipid interactions-role in the non-classical release of the acidic fibroblast growth factor. Biochimica et biophysica acta 15 17991455
2007 Synergistic Ca2+ and Cu2+ requirements of the FGF1-S100A13 interaction measured by quartz crystal microbalance: an initial step in amlexanox-reversible non-classical release of FGF1. Neurochemistry international 12 18164517
2009 Protein folding does not prevent the nonclassical export of FGF1 and S100A13. Biochemical and biophysical research communications 11 19233122
2008 Structure of calcium-bound human S100A13 at pH 7.5 at 1.8 A resolution. Acta crystallographica. Section F, Structural biology and crystallization communications 11 18259052
2021 Systematic screening identifies a TEAD4-S100A13 axis modulating cisplatin sensitivity of oral squamous cell carcinoma cells. Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology 9 34358353
2020 Genome-wide analysis of DNA methylation identifies S100A13 as an epigenetic biomarker in individuals with chronic (≥ 30 years) type 2 diabetes without diabetic retinopathy. Clinical epigenetics 9 32493412
2007 Crystal structure study on human S100A13 at 2.0 A resolution. Biochemical and biophysical research communications 9 17374362
2010 Effect of human S100A13 gene silencing on FGF-1 transportation in human endothelial cells. Journal of the Formosan Medical Association = Taiwan yi zhi 7 20863990
2009 S100A13-C2A binary complex structure-a key component in the acidic fibroblast growth factor for the non-classical pathway. Biochemical and biophysical research communications 6 19284995
2023 Wild-type S100A3 and S100A13 restore calcium homeostasis and mitigate mitochondrial dysregulation in pulmonary fibrosis patient-derived cells. Frontiers in cell and developmental biology 3 38099297
2020 Involvement of SNARE Protein Interaction for Non-classical Release of DAMPs/Alarmins Proteins, Prothymosin Alpha and S100A13. Cellular and molecular neurobiology 2 32856232
2008 [Overexpressing exogenous S100A13 gene and its effect on proliferation of human thyroid cancer cell line TT]. Ai zheng = Aizheng = Chinese journal of cancer 2 18710615
2006 Crystallization and preliminary X-ray analysis of human S100A13. Acta crystallographica. Section F, Structural biology and crystallization communications 2 17077500
2026 S100A13 transcriptionally activated by SP1 facilitates osteosarcoma metastasis. Discover oncology 1 41787040
2025 S100A13-driven interaction between pancreatic adenocarcinoma cells and cancer-associated fibroblasts promotes tumor progression through calcium signaling. Cell communication and signaling : CCS 1 39871271
2026 Integrative single-cell and machine-learning analysis identifies ac4C-related S100A13 as a causal risk gene in cholangiocarcinoma. BMC cancer 0 41578226

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