Affinage

S100A7

Protein S100-A7 · UniProt P31151

Length
101 aa
Mass
11.5 kDa
Annotated
2026-06-10
100 papers in source corpus 37 papers cited in narrative 37 extracted findings
Cross-family judge faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

S100A7 (psoriasin) is a calcium-binding EF-hand protein that functions as a dimer with a His3Asp zinc-coordination site at the dimer interface, acting both as a secreted antimicrobial/proinflammatory effector and as an intracellular signaling modulator in epithelial homeostasis and cancer (PMID:9562557, PMID:10026247). Its atomic structure reveals a distorted N-terminal EF-hand that binds only one calcium ion strongly with no large conformational change, while two histidines and an aspartate from the dimer interface chelate zinc in a manner reminiscent of metalloproteases (PMID:9562557, PMID:10026247). The protein is the principal E. coli-killing factor secreted by keratinocytes and the vaginal epithelium, and zinc saturation abolishes this activity, establishing zinc sequestration as the core antibacterial mechanism; full activity requires the central region (aa 35–80) and the zinc-binding motif, and the oxidized intramolecular-disulfide form (S100A7ox) is the active antibacterial species, with disulfide bonds enhancing metal sequestration at the His3Asp sites (PMID:15568027, PMID:17159909, PMID:20571488, PMID:28976190). This nutritional-immunity function is exploited by Neisseria gonorrhoeae, whose outer membrane protein TdfJ binds human S100A7 and extracts its zinc via the ZnuABC transporter (PMID:31369630). Extracellularly, S100A7 signals through the receptor RAGE in a zinc-dependent manner to activate ERK, NF-κB, and p38 MAPK, driving leukocyte and macrophage chemotaxis, endothelial proliferation/angiogenesis, abnormal keratinocyte differentiation, and tumor growth and metastasis; in breast cancer models RAGE blockade or tumor-associated macrophage depletion abrogates its pro-tumorigenic effects, and downstream cPLA2/PGE2 production establishes an immunosuppressive microenvironment (PMID:18606705, PMID:25572331, PMID:22158945, PMID:27060579, PMID:35135586). Intracellularly, S100A7 engages partners that determine context-specific outcomes: it binds Jab1 (CSN5) through a defined C-terminal interface within its hydrophobic cleft to activate Akt/NF-κB pro-survival signaling in ERα-negative cells, stabilizes and reconstitutes the fatty-acid-binding activity of E-FABP in a zinc-disruptable cytosolic complex, binds the β6 integrin cytoplasmic tail to enable αvβ6-dependent carcinoma invasion, and associates with the β-catenin complex to promote its degradation (PMID:12839573, PMID:10191275, PMID:15994944, PMID:19810752, PMID:21132011, PMID:18223693). Its dual pro- versus anti-tumorigenic behavior tracks with ERα status, suppressing β-catenin/TCF4 and migration in ERα-positive cells while promoting invasion in ERα-negative cells (PMID:22016394). S100A7 transcription is driven by Src/Stat3, STAT3 (downstream of IGF-1/IGF-1R, OSM/IL-6) and PKC and repressed by a TSLP–JAK2/STAT3/Sin3a axis, while its secretion follows a biphasic TLR–NF-κB/p38–caspase-1–IL-1α program sustained by caspase-8 downregulation (PMID:18263703, PMID:20101226, PMID:31731716, PMID:27958610, PMID:27498343, PMID:33557316, PMID:31775025).

Mechanistic history

Synthesis pass · year-by-year structured walk · 25 steps
  1. 1999 High

    Defining the atomic architecture answered how S100A7 binds metals: it is an EF-hand homodimer that binds one calcium per monomer without major conformational change, and—critically—forms a His3Asp zinc site at the dimer interface whose occupancy reorganizes the adjacent EF-hand loop.

    Evidence X-ray crystallography at 1.05 Å (MAD/holmium) and paired Zn-loaded/Zn-free structures at atomic resolution

    PMID:10026247 PMID:9562557

    Open questions at the time
    • Structure alone did not establish the biological function of the zinc site
    • No bound physiological ligand or partner in these structures
  2. 2001 High

    Identification of S100A7 as a transglutaminase substrate showed a covalent post-translational route to crosslink the protein at its solvent-exposed termini, providing a regulatory handle on its function.

    Evidence In vitro transglutaminase assays with recombinant S100 proteins and identification of reactive termini

    PMID:11258932

    Open questions at the time
    • In vivo consequences of crosslinking on antimicrobial or signaling activity not established
    • Physiological context of crosslinking unclear
  3. 2004 High

    Linking the zinc site to biology, S100A7 was shown to be the principal keratinocyte-secreted E. coli-killing factor, with zinc saturation abolishing activity—establishing zinc sequestration as the antibacterial mechanism.

    Evidence In vitro bacterial killing, in vivo antibody neutralization in human skin, and zinc-saturation experiments

    PMID:15568027

    Open questions at the time
    • Spectrum of susceptible organisms beyond E. coli not defined
    • Structural requirements within the protein not yet mapped
  4. 2006 High

    Domain mapping clarified which regions confer antibacterial activity: the central region (aa 35–80) plus the zinc-binding motif are required, with proteolysis abolishing and EF-hand mutation/heat sparing activity.

    Evidence Recombinant protein mutagenesis with bacterial adhesion/survival, protease, and heat-denaturation assays

    PMID:17159909

    Open questions at the time
    • Atomic basis for how the central region engages bacteria not resolved
    • Role of redox state not yet considered
  5. 2010 High

    Extension to mucosal sites showed S100A7 is constitutively secreted and is the major E. coli-cidal factor of vaginal fluid, generalizing its antibacterial role beyond skin.

    Evidence HPLC fractionation coupled to bacterial killing in vaginal fluid plus organotypic epithelium

    PMID:20571488

    Open questions at the time
    • Regulation of constitutive secretion in this tissue not defined
    • Interaction with commensal flora not addressed
  6. 2017 High

    Redox biochemistry refined the antibacterial mechanism: the oxidized disulfide form (S100A7ox), not reduced or disulfide-null variants, is the active species, with disulfide bonds enhancing high-affinity zinc sequestration at the His3Asp sites.

    Evidence Reconstituted in vitro biochemistry, thioredoxin assays, Zn2+ affinity titrations, mutagenesis, and bacterial growth inhibition

    PMID:28976190

    Open questions at the time
    • In vivo redox state at sites of action not measured
    • Cysteine thiolates do not form an extra zinc site, leaving the disulfide's mechanistic role on metal affinity incompletely explained
  7. 2019 High

    A pathogen counter-strategy was defined: N. gonorrhoeae TdfJ binds human S100A7 and extracts its zinc via ZnuABC, showing host nutritional immunity can be hijacked as a zinc source.

    Evidence Direct recombinant binding assay, ZnuABC-deficient mutant, human-versus-murine species specificity, and bacterial growth assays

    PMID:31369630

    Open questions at the time
    • Whether other pathogens use analogous receptors not addressed
    • Structural basis of the TdfJ–S100A7 interface not solved
  8. 2003 Medium

    Establishing intracellular partnerships, S100A7 was localized to cytosol/ER and shown to redistribute to focal-adhesion-like structures on calcium elevation while binding and stabilizing E-FABP.

    Evidence Confocal immunofluorescence with calcium challenge and cross-linker co-precipitation in keratinocytes

    PMID:12839573

    Open questions at the time
    • Functional consequence of focal-adhesion localization not defined
    • Single-lab imaging without orthogonal genetic perturbation
  9. 1999 High

    The S100A7–E-FABP interaction was reconstituted with purified proteins, showing the complex restores oleic-acid binding and is disrupted by physiological zinc, linking S100A7's metal sensing to lipid-binding function.

    Evidence Overlay assay, in vitro reconstitution, oleic-acid binding, co-IP from psoriatic scale, and confocal microscopy

    PMID:10191275

    Open questions at the time
    • Downstream physiological role of the lipid-binding complex unclear
    • How zinc disruption is regulated in cells not shown
  10. 2005 High

    S100A7 was shown to drive anchorage-independent survival in ERα-negative breast cancer through a defined Jab1-binding domain activating NF-κB and Akt, identifying a pro-survival intracellular signaling node.

    Evidence Stable transfection, reciprocal IP, yeast two-hybrid, binding-domain mutagenesis, reporter assays, and xenografts

    PMID:15994944

    Open questions at the time
    • Mechanism by which Jab1 binding links to Akt/EGFR not fully resolved
    • ERα-dependence of the effect not yet explained
  11. 2009 High

    Structural and biophysical mapping localized the Jab1 interface to residues in the N-terminal hydrophobic cleft (with Met12 as a gatekeeper), connecting the dye-binding pocket to protein-protein interaction.

    Evidence Crystal structures with naphthalene dyes at 1.6 Å, fluorescence, ITC, and yeast two-hybrid mutagenesis

    PMID:19810752

    Open questions at the time
    • Co-structure with Jab1 not determined
    • Whether endogenous ligands occupy the cleft in vivo unknown
  12. 2010 High

    S100A7 was shown to bind the β6 integrin cytoplasmic tail and be required for αvβ6-dependent carcinoma invasion, defining an integrin-linked invasion mechanism.

    Evidence Proteomic pull-down, reciprocal co-IP, siRNA, Transwell/organotypic invasion, and Tat-peptide competition

    PMID:21132011

    Open questions at the time
    • Signaling downstream of the S100A7–β6 complex not delineated
    • Calcium/zinc dependence of the interaction not tested
  13. 2008 High

    Identification of RAGE as the extracellular receptor explained how S100A7 acts as a chemoattractant and why its signaling is zinc-dependent, distinguishing it from the RAGE-independent paralog S100A15.

    Evidence Chemotaxis and in vitro binding assays with zinc-dependence and an in vivo inflammation model

    PMID:18606705

    Open questions at the time
    • Stoichiometry and structure of the S100A7–RAGE complex not solved
    • Contribution of other receptors not excluded
  14. 2008 Medium

    S100A7–RAGE signaling was shown to drive breast cancer invasion and modulate EGFR-family signaling, while a reciprocal study established S100A7 as a negative regulator of β-catenin via GSK3β-independent degradation in oral SCC.

    Evidence shRNA and overexpression, phospho-Westerns, co-IP, β-catenin degradation assays, angiogenesis and xenograft/in vivo models

    PMID:18223693 PMID:18320059

    Open questions at the time
    • Molecular basis of GSK3β-independent β-catenin degradation unresolved
    • How RAGE signaling intersects with intracellular β-catenin regulation unclear
  15. 2010 Medium

    The pro- versus anti-tumorigenic switch was resolved through ERα status: in ERα-positive cells S100A7 suppresses migration and tumor growth by downregulating β-catenin/TCF4 and raising GSK3β activity, opposite to its ERα-negative role.

    Evidence Stable overexpression, GSK3β inhibitor rescue, migration/proliferation assays, and nude-mouse xenografts

    PMID:22016394

    Open questions at the time
    • Mechanistic link between ERα status and divergent β-catenin handling not defined
    • Single-lab system
  16. 2010 High

    In vivo transgenic and macrophage-depletion studies established RAGE-mediated tumor-associated macrophage recruitment as a central effector of S100A7's pro-tumorigenic activity.

    Evidence MMTV-mS100a7a15 transgenic mice, chemotaxis assays, in vivo TAM depletion, and tumor/metastasis quantification (also RAGE-deficient mice and sRAGE)

    PMID:22158945 PMID:25572331

    Open questions at the time
    • Chemokine ligands recruiting TAMs not fully enumerated
    • Whether epithelial-intrinsic vs stromal RAGE dominates not dissected
  17. 2011 Medium

    S100A7 was shown to promote angiogenesis through RAGE by increasing VEGF and driving ROS-dependent endothelial proliferation and tube formation, linking it to tumor vascularization.

    Evidence Recombinant protein treatment, sRAGE blockade, ROS measurement, antioxidant Bcl-2, plus ROS/hypoxia induction and angiogenic-factor readouts in keratinocytes

    PMID:22189627 PMID:27155199

    Open questions at the time
    • Direct vs paracrine endothelial effects not fully separated
    • Single-lab angiogenesis assays
  18. 2012 Medium

    Direct binding of S100A7 to RAGE was confirmed and shown to be required for osteosarcoma migration, invasion, and MMP activity, generalizing the RAGE axis beyond breast cancer.

    Evidence Recombinant protein pull-down, RAGE siRNA, and migration/invasion/MMP assays

    PMID:22783409

    Open questions at the time
    • Downstream signaling in osteosarcoma not mapped
    • Single-lab study
  19. 2014 Medium

    In keratinocyte biology, S100A7 was shown to strengthen the tight-junction barrier and modulate differentiation through GSK-3/MAPK and PKC pathways, defining roles in epidermal homeostasis distinct from cancer signaling.

    Evidence TER and permeability assays, GSK-3/MAPK and PKC inhibitors, siRNA/lentiviral perturbation, and differentiation-marker analysis

    PMID:24842328 PMID:27958610

    Open questions at the time
    • Whether barrier and differentiation effects require RAGE not resolved
    • Reconciliation with pro-differentiation vs abnormal-differentiation outcomes incomplete
  20. 2016 Medium

    RAGE-MyD88-NF-κB signaling by extracellular S100A7 was shown to upregulate IL-6 and shift keratinocytes toward abnormal differentiation, mechanistically connecting S100A7 to psoriasis-like epidermal phenotypes.

    Evidence Recombinant protein treatment, RAGE pathway analysis, and differentiation-marker readouts in 2D and reconstituted human epidermis

    PMID:27060579

    Open questions at the time
    • Relative contribution of IL-6 vs other RAGE outputs not quantified
    • In vivo validation in human psoriasis limited
  21. 2017 Medium

    A RAGE-p38-calpain-1 cascade was defined linking S100A7 to mature IL-1α production, and a separate TLR3-p38 injury pathway was shown to induce S100A7 driving loricrin and wound closure, placing S100A7 within inflammatory amplification loops.

    Evidence Recombinant protein, pathway inhibitors, siRNA of RAGE/p38/calpain-1, imiquimod psoriasis model, and TLR3-ligand wound-closure assays

    PMID:27535424 PMID:28060905

    Open questions at the time
    • Feedback between IL-1α/IL-17 and S100A7 only partially mapped
    • In vivo causality in human disease not established
  22. 2008 High

    Flagellin/TLR5 was identified as the principal microbial inducer of S100A7 in keratinocytes, defining the upstream sensing that triggers its antimicrobial expression.

    Evidence TLR ligand screen, ΔFliC E. coli mutant, and TLR5 siRNA with RT-PCR/protein readout

    PMID:18263703

    Open questions at the time
    • Transcription factors downstream of TLR5 not fully resolved here
    • Other inducers (e.g., cytokines) addressed in separate studies
  23. 2019 Medium

    Secretion control was resolved as biphasic: an acute TLR–NF-κB/p38–caspase-1–IL-1α phase and a chronic phase sustained by caspase-8 downregulation, explaining constitutive S100A7 release in inflammatory skin disease.

    Evidence Pathway-inhibitor and caspase-8 siRNA dissection with TLR stimulation and secretion assays

    PMID:31775025

    Open questions at the time
    • Mechanism of caspase-8 downregulation in disease not defined
    • Non-classical secretion route not structurally characterized
  24. 2016 Medium

    Transcriptional regulation was mapped to STAT3-centered control: STAT3 directly binds the S100A7 promoter and is engaged downstream of Src, OSM/IL-6, and IGF-1/IGF-1R to induce S100A7, while a TSLP–JAK2/STAT3/Sin3a complex represses it.

    Evidence Promoter/reporter and ChIP assays, pharmacological inhibitors, CRISPR IGF-1R KO, siRNA, and skin-equivalent/cancer models

    PMID:20101226 PMID:27498343 PMID:31731716 PMID:33557316

    Open questions at the time
    • How the same factor (STAT3) yields activation vs repression in different contexts unresolved
    • Cofactor switching (e.g., Sin3a) only partially defined
  25. 2022 Medium

    The immune-modulatory output of S100A7/RAGE was extended to immunosuppression: signaling induces cPLA2/PGE2 to recruit suppressive myeloid cells and exclude T cells, and to drive neutrophil/NET-mediated metastasis, identifying targetable downstream effectors.

    Evidence Transgenic and PDX models with cPLA2 inhibitor and CODEX imaging; plus neutrophil/NET assays with DNase1 and TLR2 inhibition in cervical cancer models

    PMID:35135586 PMID:39384116

    Open questions at the time
    • Whether cPLA2 and NET pathways operate in the same tumors not established
    • Relative contribution to clinical immune evasion unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the same protein integrates its three modes—zinc-sequestering antimicrobial, RAGE-engaging proinflammatory ligand, and ERα-dependent intracellular signaling switch—into a unified context-dependent regulatory logic remains unresolved.
  • No structure of S100A7 bound to RAGE, Jab1, β6, or β-catenin
  • Molecular basis of the ERα-dependent pro/anti-tumorigenic switch undefined
  • In vivo coupling between redox state, metal occupancy, and which function dominates not measured

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140313 molecular sequestering activity 4 GO:0048018 receptor ligand activity 3 GO:0098772 molecular function regulator activity 3 GO:0060089 molecular transducer activity 2 GO:0008289 lipid binding 1
Localization
GO:0005576 extracellular region 2 GO:0005829 cytosol 2 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1643685 Disease 4 R-HSA-168256 Immune System 4 R-HSA-1266738 Developmental Biology 3
Partners
CTNNB1E-FABPITGB6JAB1RAGETDFJ

Evidence

Reading pass · 37 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 Crystal structure of human psoriasin (S100A7) determined at atomic resolution (1.05 Å) by MAD phasing using holmium substitution, revealing a dimeric EF-hand protein with a distorted N-terminal EF-hand loop lacking a crucial calcium-binding residue, indicating the protein binds only one calcium ion per monomer strongly, with no large conformational change upon calcium binding. X-ray crystallography (MAD phasing, 1.05 Å resolution) Structure High 9562557
1999 Crystal structures of Ca2+-bound S100A7 in Zn2+-loaded and Zn2+-free states revealed a zinc-binding site formed by three histidine residues and one aspartate at the dimer interface, coordinating zinc similarly to collagenase metalloproteases. Loss of zinc causes reorganization of the adjacent EF-hand loop, making it resemble a calcium-loaded EF-hand. X-ray crystallography (two crystal forms, Zn2+-loaded and Zn2+-free) Biochemistry High 10026247
2004 Psoriasin (S100A7) is the principal E. coli-killing antimicrobial compound secreted by keratinocytes in vitro and in vivo. Zn2+-saturated psoriasin showed diminished antimicrobial activity, implicating zinc sequestration as the antibacterial mechanism. In vivo treatment with anti-psoriasin antibodies inhibited skin E. coli-killing activity. In vitro bacterial killing assay, in vivo antibody neutralization in human skin, zinc-saturation experiments Nature immunology High 15568027
2006 S100A7 antibacterial activity against E. coli requires the central region (amino acids 35–80) and the zinc-binding motif. Mutation of the zinc-binding motif reduced antibacterial activity, but this reduction was reversed by simultaneous removal of the amino terminus, indicating the central region alone is sufficient for full activity. Protease treatment abolished activity whereas EF-hand calcium-binding motif mutation or heat denaturation had only minor effects. Recombinant protein mutagenesis, bacterial adhesion/survival assays, heat denaturation and protease treatment experiments The Journal of investigative dermatology High 17159909
2001 S100A7 is a substrate for both type I and type II transglutaminases, which form covalent ε-(γ-glutamyl)lysine bonds at the solvent-exposed amino- and carboxyl-terminal ends of the protein, providing a mechanism to regulate S100A7 function. In vitro transglutaminase assay with recombinant S100 proteins; biochemical characterization Biochemistry High 11258932
2003 S100A7 is present in the cytosol and endoplasmic reticulum (BiP/GRP78-positive tubular structures) in keratinocytes. Upon calcium elevation, cytoplasmic S100A7 redistributes to α-actinin- and paxillin-positive peripheral focal adhesion-like structures. S100A7 co-localizes with and co-precipitates epidermal fatty acid binding protein (E-FABP) in these structures, and S100A7 expression stabilizes E-FABP protein levels. Confocal immunofluorescence microscopy, calcium challenge experiments, cross-linker co-precipitation The Journal of investigative dermatology Medium 12839573
1999 S100A7 and E-FABP form a complex in the cytosol of keratinocytes, reconstituted in vitro using purified proteins in the presence of EDTA. Complex formation is disrupted by physiological concentrations of Zn2+ (0.1 mM) but not Ca2+ or Mg2+ at physiological levels. The complex retains oleic acid-binding properties of E-FABP, whereas free S100A7 alone does not bind oleic acid. Co-immunoprecipitation confirmed the interaction in psoriatic scale extracts. Overlay assay, in vitro complex reconstitution with purified proteins, oleic acid binding assay, co-immunoprecipitation, confocal microscopy The Biochemical journal High 10191275
2005 S100A7 promotes survival under anchorage-independent growth in ERα-negative breast cancer cells (MDA-MB-231) by activating NF-κB (~3-fold) and phospho-Akt (~4-fold). These effects depend on a Jab1 (CSN5/COP9 signalosome subunit 5)-binding domain within S100A7, as confirmed by immunoprecipitation, yeast two-hybrid assay, and mutant S100A7 lacking the Jab1-binding site. Enhanced EGFR signaling was also found to correlate with increased phospho-Akt. Stable transfection, immunoprecipitation, yeast two-hybrid assay, reporter gene assay, Western blot, xenograft tumor model Cancer research High 15994944
2008 S100A7 signals as a chemoattractant through RAGE (receptor for advanced glycation end products). S100A7-RAGE binding, downstream signaling, and chemotaxis are zinc-dependent in vitro, reflecting zinc-mediated changes in S100A7 dimer structure. The highly homologous S100A15 uses a distinct Gi protein-coupled receptor rather than RAGE for chemotaxis. Antibody generation, chemotaxis assays, in vitro binding assays, zinc-dependence studies, in vivo inflammation model Journal of immunology High 18606705
2008 E. coli flagellin is the principal inducer of S100A7c (psoriasin) expression in human epidermal keratinocytes, acting through TLR5. A flagellin-deficient E. coli strain (ΔFliC) did not induce S100A7c, and siRNA knockdown of TLR5 suppressed induction by both flagellin and wild-type E. coli supernatant. TLR ligand screening, flagellin-deficient bacterial mutant, siRNA knockdown of TLR5, RT-PCR and protein measurement FASEB journal High 18263703
2008 S100A7 promotes breast cancer growth and metastasis via RAGE-dependent activation of ERK and NF-κB signaling and cell migration. In an S100A7-transgenic mouse model, RAGE neutralizing antibody or soluble RAGE inhibited tumor progression, and RAGE/S100A7 drove recruitment of MMP9-positive tumor-associated macrophages. RAGE-deficient mice, neutralizing antibody injection, soluble RAGE administration, signaling assays (ERK, NF-κB), transgenic mouse model, macrophage depletion Cancer research High 25572331
2008 S100A7 overexpression in ERα-negative breast cancer cells promotes cell invasion via RAGE-dependent signaling. S100A7 downregulation in MDA-MB-468 cells reduced EGF-directed migration and decreased phosphorylation of EGFR (Tyr1173), HER2 (Tyr1248), Src (Tyr416), and SHP2 (Tyr542), indicating S100A7 modulates EGF receptor signaling. S100A7 downregulation also reduced angiogenesis in vivo and osteoclast formation associated with decreased IL-8 expression. shRNA knockdown, phospho-Western blot, migration assays, Matrigel plug angiogenesis assay, intra-tibial bone injection in SCID mice PloS one Medium 18320059
2008 S100A7 reciprocally negatively regulates β-catenin signaling in oral squamous cell carcinoma: S100A7 associates with the β-catenin complex and promotes β-catenin degradation via a GSK3β-independent non-canonical mechanism. Conversely, β-catenin signaling negatively regulates S100A7 expression. S100A7 inhibited SCCOC cell proliferation in vitro and tumor growth/invasion in vivo. Co-immunoprecipitation, β-catenin degradation assay, tumor xenograft model, loss-of-function/gain-of-function experiments in cell lines and mouse model Oncogene Medium 18223693
2009 S100A7 crystal structures in complex with naphthalene-based dyes (2,6-ANS and 1,8-ANS) at 1.6 Å identified a hydrophobic binding cleft formed by the N-terminal helices of each monomer, with Met12 acting as a gatekeeper. Yeast two-hybrid mutagenesis showed that Leu78 (within the Met12 cleft), Gln88, and Asp56 contribute to Jab1 binding, linking the hydrophobic pocket to the Jab1 interaction interface. X-ray crystallography (1.6 Å), steady-state fluorescence, time-resolved fluorescence, isothermal titration calorimetry, yeast two-hybrid mutagenesis Biochemistry High 19810752
2009 S100A7 expression in primary cortico-hippocampal neuron cultures inhibits generation of Aβ1-42 and Aβ1-40 peptides coincident with selective promotion of ADAM-10-mediated non-amyloidogenic α-secretase activity. Expression of human S100A7 in transgenic mouse brains also promoted α-secretase activity. Adenoviral S100A7 overexpression in primary neuronal cultures, ELISA for Aβ peptides, α-secretase activity assay, S100A7 transgenic mice PloS one Medium 19159013
2010 S100A7 enhances macrophage chemotaxis via RAGE receptor activation in vitro. In vivo, mS100a7a15 induction in MMTV-mS100a7a15 transgenic mice enhanced breast tumor growth, metastasis, and recruitment of tumor-associated macrophages. In vivo TAM depletion inhibited the pro-tumorigenic effects of mS100a7a15 induction, establishing TAM recruitment as a key mechanism. Transgenic mouse model (MMTV-mS100a7a15), macrophage chemotaxis assay, in vivo macrophage depletion, tumor growth/metastasis quantification Cancer research High 22158945
2010 S100A7 expression in ERα-positive breast cancer cells (MCF7, T47D) suppresses migration, proliferation, and tumor growth in vivo by downregulating the β-catenin/TCF4 pathway, increasing GSK3β activity, and enhancing β-catenin/E-cadherin interaction. GSK3β inhibitor treatment reversed β-catenin suppression in S100A7-overexpressing ERα+ cells. This is opposite to its pro-tumorigenic role in ERα-negative cells. Stable overexpression, migration/proliferation assays, GSK3β inhibitor experiments, nude mouse xenograft model, Western blot The Journal of biological chemistry Medium 22016394
2011 Extracellular psoriasin (S100A7) increases VEGF expression in mammary epithelial cells and promotes endothelial cell proliferation, tube formation, and ROS generation through RAGE. Soluble RAGE (sRAGE) inhibited psoriasin-induced endothelial proliferation, tube formation, and ROS production. Antioxidant Bcl-2 abolished psoriasin's proliferative effect on endothelial cells. Recombinant protein treatment, sRAGE blockade, shRNA knockdown, adenoviral overexpression, ROS measurement, endothelial cell proliferation/tube formation assays Breast cancer research and treatment Medium 22189627
2010 Psoriasin (S100A7) is constitutively expressed and secreted in the vaginal epithelium and accounts for ~2.5–3% of total vaginal fluid protein. HPLC fractionation showed that psoriasin co-eluted with E. coli-killing activity of vaginal fluid, establishing it as the major E. coli-cidal factor of the female genital tract. HPLC fractionation with bacterial killing assay, organotypic vaginal epithelium model, protein quantification Mucosal immunology High 20571488
2010 Psoriasin (S100A7) expression is induced by reactive oxygen species (ROS) and hypoxia in keratinocytes. Downregulation of psoriasin by siRNA reduced ROS-induced expression of VEGF, HB-EGF, MMP-1, and thrombospondin 1. Extracellular psoriasin induced endothelial cell proliferation, migration, and tube formation comparable to VEGF, with effects suggested to be mediated by PI3K and NF-κB pathways. siRNA knockdown, ROS induction, hypoxia exposure, angiogenic factor measurement, endothelial cell functional assays The British journal of dermatology Medium 27155199
2010 S100A7 expression is induced by oncostatin-M (OSM) and IL-6 in breast tumor cells, dependent on STAT3, PI3K, and ERK1/2 signaling, as demonstrated by pharmacological blockade. siRNA knockdown of S100A7 eliminated the pro-migratory effects of OSM treatment, positioning S100A7 as a downstream effector of OSM/IL-6 in breast cancer cell migration. Cytokine stimulation, pathway inhibitors (STAT3, PI3K, ERK1/2), siRNA knockdown, migration assays Oncogene Medium 20101226
2012 S100A7 promotes migration and invasion of osteosarcoma cells through RAGE. Pull-down assay confirmed direct binding of recombinant S100A7 to RAGE. siRNA knockdown of RAGE suppressed S100A7-enhanced migration, invasion, and matrix metalloproteinase activity of osteosarcoma cells. In vitro pull-down assay with recombinant proteins, siRNA knockdown of RAGE, migration/invasion assays, MMP activity measurement Oncology letters Medium 22783409
2014 S100A7/psoriasin strengthens the tight junction (TJ) barrier of keratinocytes by selectively increasing expression of TJ proteins (claudins, occludin), enhancing transepithelial electrical resistance, and reducing paracellular permeability. This was mediated through GSK-3 and MAPK pathways, as shown by specific inhibitors. S100A7 also increased β-catenin and E-cadherin accumulation at cell-cell contacts. Western blot, RT-PCR, transepithelial electrical resistance assay, paracellular permeability assay, GSK-3 and MAPK inhibitors, immunofluorescence The British journal of dermatology Medium 24842328
2016 Extracellular S100A7 signals through RAGE to activate the MyD88-IκB/NF-κB cascade in keratinocytes, upregulating IL-6, which inhibits epidermal differentiation markers (keratin 1, keratin 10, involucrin, loricrin) and increases abnormal differentiation markers (keratin 6, keratin 16). This was confirmed in a reconstituted human epidermis model. Recombinant protein treatment, Western blot, RT-PCR, reconstituted human epidermis model, RAGE signaling pathway analysis Experimental dermatology Medium 27060579
2017 S100A7 induces mature interleukin-1α (17 kDa) expression in normal human epidermal keratinocytes via the RAGE-p38 MAPK-calpain-1 pathway; inhibitors or siRNA knockdown of each component abolished mature IL-1α induction. In imiquimod-induced psoriasis mouse model, mS100a7a15, mature IL-1α, and calpain-1 were highly co-expressed, and IL-17a neutralization attenuated mS100a7a15 expression. Recombinant protein treatment, pharmacological inhibitors, siRNA knockdown (RAGE, p38 MAPK, calpain-1), Western blot, imiquimod mouse model PloS one Medium 28060905
2017 S100A7 in squamous carcinoma cells is transcriptionally regulated by Src/Stat3 signaling. Src inhibitor (SU6656) and Stat3 inhibitor (S3I-201) reduced S100A7 protein levels. Stat3 transactivated the S100A7 5'-upstream promoter region. S100A7 overexpression decreased E-cadherin and increased Twist (EMT markers), while S100A7 knockdown had opposite effects, demonstrating S100A7 as a downstream effector of Src/Stat3 promoting EMT and invasion. Pharmacological inhibitors of Src/Stat3, luciferase promoter assay, siRNA/overexpression, Western blot, Transwell invasion assay, zebrafish metastasis model Antioxidants Medium 31731716
2017 S100A7 promotes keratinocyte differentiation via the protein kinase C pathway. siRNA-mediated knockdown of psoriasin reduced expression of involucrin, desmoglein 1, transglutaminase 1, and CD24. Lentiviral overexpression of psoriasin mimicking the psoriatic milieu caused an altered differentiation gene expression pattern resembling psoriatic epidermis. siRNA knockdown, lentiviral overexpression, PKC pathway inhibitors, Western blot, immunohistochemistry Acta dermato-venereologica Medium 27958610
2017 Biochemical analysis showed that S100A7 exists as reduced (S100A7red, free thiols) and oxidized (S100A7ox, intramolecular disulfide) forms. S100A7ox is a substrate for the mammalian thioredoxin system in the apo state, but not when Ca2+- or Zn2+-bound, and metal binding depresses the disulfide redox midpoint potential. Both redox forms coordinate 2 equivalents of Zn(II) with subnanomolar affinity; Cys thiolates do not form an additional high-affinity Zn2+ site. Only S100A7ox (not S100A7red or disulfide-null variants) exhibits antibacterial activity against select bacteria, suggesting disulfide bonds enhance metal sequestration at the His3Asp sites to confer antibacterial properties. In vitro biochemical assays, thioredoxin reduction assay, Zn2+ titration/affinity measurements, metal substitution experiments, bacterial growth inhibition assay, mutagenesis (disulfide-null variants) Biochemistry High 28976190
2010 S100A7 associates with and is required for αvβ6 integrin-dependent carcinoma cell invasion. S100A7 bound preferentially to the β6 cytoplasmic domain (requiring the unique C-terminal 11 aa) in a proteomic screen and co-precipitated with endogenous β6. siRNA knockdown of S100A7 abrogated αvβ6-mediated invasion in Transwell and organotypic assays. Membrane-permeant Tat-peptides encoding the β6 C-terminal residues blocked S100A7-β6 interaction and inhibited αvβ6-dependent invasion. Proteomic pull-down with recombinant β6 cytoplasmic domain, co-immunoprecipitation of endogenous proteins, siRNA knockdown, Transwell and organotypic invasion assays, Tat-peptide inhibition Oncogene High 21132011
2019 N. gonorrhoeae outer membrane protein TdfJ binds directly to human S100A7 and internalizes zinc from it in a ZnuABC zinc transporter-dependent manner. This interaction is restricted to the human version of S100A7 (not murine), and zinc presence in S100A7 is required to support gonococcal growth, establishing S100A7 as a zinc source exploited by gonococci to overcome host nutritional immunity. Direct binding assay (recombinant proteins), ZnuABC-deficient bacterial mutant, species-specificity test (human vs. murine S100A7), bacterial growth assays PLoS pathogens High 31369630
2019 Sustained secretion of S100A7 from keratinocytes in response to bacterial exposure is biphasic: an initial phase mediated by TLR signaling activating NFκB/p38MAPK/caspase-1/IL-1α, and a chronic sustained phase regulated by Caspase-8 downregulation. Caspase-8 downregulation is concomitantly observed in inflammatory skin diseases with constitutive S100A7 release. Mechanistic dissection with pathway inhibitors, siRNA knockdown of caspase-8, TLR ligand stimulation, S100A7 secretion assays Cell reports Medium 31775025
2016 TSLP downregulates S100A7 and β-defensin 2 expression in keratinocytes via JAK2/STAT3-dependent signaling. STAT3 directly regulated the S100A7 promoter, and the STAT3/Sin3a complex controlled S100A7 transcriptional activity. This suppression occurred even in the presence of IL-17, a strong S100A7 inducer. siRNA knockdown, pharmacological inhibitors, reporter/promoter assay, Western blot, reconstituted human skin equivalent model The Journal of investigative dermatology Medium 27498343
2017 TLR3 activation following skin injury induces S100A7 expression through p38 MAPK. S100A7 then acts on keratinocytes to induce terminal differentiation marker loricrin through activation of p38 MAPK and caspase-1, promoting skin stratification and wound closure. TLR3 ligand stimulation, p38 MAPK inhibitors, caspase-1 inhibitors, gene expression analysis, wound closure assays Science China. Life sciences Medium 27535424
2021 S100A7 overexpression downregulates TLR4 and upregulates RAGE expression in breast cancer cells. LPS treatment of breast cancer cells increased S100A7 expression, suggesting an LPS/S100A7/TLR4/RAGE signaling axis. S100A7 and TLR4 expression showed inverse correlation in human breast cancer samples. Stable overexpression, LPS treatment, Western blot, immunohistochemistry in human tumor samples Molecular oncology Low 33969603
2022 S100A7/RAGE signaling promotes expression of cPLA2, which generates prostaglandin E2 (PGE2) to create an immunosuppressive tumor microenvironment. cPLA2 inhibition suppressed S100A7-mediated tumor growth and metastasis in transgenic and PDX mouse models, reduced immunosuppressive myeloid cell recruitment, and increased infiltration of activated CD4+ and CD8+ T cells. S100A7-overexpressing cell lines and transgenic mice, cPLA2 pharmacological inhibitor (AACOCF3), PDX mouse model, CODEX multiplexed imaging, mechanistic signaling studies Journal of experimental & clinical cancer research High 35135586
2021 IGF-1/IGF-1R signaling in ER-positive breast cancer cells engages STAT3 activation and STAT3 recruitment to the S100A7 promoter, increasing S100A7 expression. Secreted S100A7 then activates RAGE signaling in vascular endothelial cells to promote angiogenesis. CRISPR IGF-1R knockout, STAT3 inhibitors, ChIP assay for STAT3 at S100A7 promoter, gene expression studies, endothelial tube formation assay Cancers Medium 33557316
2024 Cervical cancer-derived S100A7 exerts chemotactic effects on neutrophils and promotes neutrophil extracellular trap (NET) generation by elevating ROS levels (rather than autophagy) in neutrophils. NETs in turn enhanced cancer cell migration via TLR2/P38-MAPK/ERK/NFκB signaling and promoted lymphangiogenesis and lymphatic vessel permeability. DNase 1-mediated NETs digestion or TLR2 inhibition abolished NETs-induced metastatic potential. Neutrophil chemotaxis assay, ROS measurement, DNase 1 treatment, TLR2 siRNA/inhibitor, S100A7-overexpressing cell lines, footpad implantation mouse model, immunohistochemistry Cancer letters Medium 39384116

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 Antimicrobial psoriasin (S100A7) protects human skin from Escherichia coli infection. Nature immunology 507 15568027
2008 The antimicrobial protein psoriasin (S100A7) is upregulated in atopic dermatitis and after experimental skin barrier disruption. The Journal of investigative dermatology 176 18754038
1999 Psoriasin (S100A7) expression and invasive breast cancer. The American journal of pathology 150 10595935
2008 Chemotactic activity of S100A7 (Psoriasin) is mediated by the receptor for advanced glycation end products and potentiates inflammation with highly homologous but functionally distinct S100A15. Journal of immunology (Baltimore, Md. : 1950) 143 18606705
2015 RAGE mediates S100A7-induced breast cancer growth and metastasis by modulating the tumor microenvironment. Cancer research 128 25572331
1999 Zinc-binding site of an S100 protein revealed. Two crystal structures of Ca2+-bound human psoriasin (S100A7) in the Zn2+-loaded and Zn2+-free states. Biochemistry 112 10026247
2011 S100A7 enhances mammary tumorigenesis through upregulation of inflammatory pathways. Cancer research 111 22158945
2012 Vitamin D analog calcipotriol suppresses the Th17 cytokine-induced proinflammatory S100 "alarmins" psoriasin (S100A7) and koebnerisin (S100A15) in psoriasis. The Journal of investigative dermatology 107 22402441
1998 EF-hands at atomic resolution: the structure of human psoriasin (S100A7) solved by MAD phasing. Structure (London, England : 1993) 97 9562557
2006 S100A7 (Psoriasin)--mechanism of antibacterial action in wounds. The Journal of investigative dermatology 96 17159909
1998 Psoriasin (S100A7). The international journal of biochemistry & cell biology 93 9693957
1999 Psoriasin (S100A7): a putative urinary marker for the follow-up of patients with bladder squamous cell carcinomas. Electrophoresis 83 10197442
2001 S100A7, S100A10, and S100A11 are transglutaminase substrates. Biochemistry 80 11258932
2004 S100A7 and the progression of breast cancer. Breast cancer research : BCR 79 15217486
1995 Comparative expression of the psoriasin (S100A7) and S100C genes in breast carcinoma and co-localization to human chromosome 1q21-q22. International journal of cancer 78 7591220
2019 Dietary Flavonoids Luteolin and Quercetin Inhibit Migration and Invasion of Squamous Carcinoma through Reduction of Src/Stat3/S100A7 Signaling. Antioxidants (Basel, Switzerland) 74 31731716
2011 Utility of 10 immunohistochemical markers including novel markers (desmocollin-3, glypican 3, S100A2, S100A7, and Sox-2) for differential diagnosis of squamous cell carcinoma from adenocarcinoma of the Lung. Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer 70 21623236
2003 Psoriasin (S100A7) expression is altered during skin tumorigenesis. BMC dermatology 69 12600274
2010 Novel S100A7 (psoriasin)/S100A15 (koebnerisin) subfamily: highly homologous but distinct in regulation and function. Amino acids 68 20596736
2006 Psoriasin (S100A7) is significantly up-regulated in human epithelial skin tumours. Journal of cancer research and clinical oncology 67 17136347
2003 Psoriasin (S100A7) expression is associated with poor outcome in estrogen receptor-negative invasive breast cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 67 12855640
2009 S100A7, a novel Alzheimer's disease biomarker with non-amyloidogenic alpha-secretase activity acts via selective promotion of ADAM-10. PloS one 66 19159013
2005 Expression patterns of S100A7 (psoriasin) and S100A9 (calgranulin-B) in keratinocyte differentiation. Experimental dermatology 66 15740587
2005 The S100A7-c-Jun activation domain binding protein 1 pathway enhances prosurvival pathways in breast cancer. Cancer research 66 15994944
2018 The TGFβ-induced lncRNA TBILA promotes non-small cell lung cancer progression in vitro and in vivo via cis-regulating HGAL and activating S100A7/JAB1 signaling. Cancer letters 65 29908210
2011 Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation. Breast cancer research and treatment 65 22189627
2010 S100A7 (psoriasin) is induced by the proinflammatory cytokines oncostatin-M and interleukin-6 in human breast cancer. Oncogene 65 20101226
2008 Flagellin is the principal inducer of the antimicrobial peptide S100A7c (psoriasin) in human epidermal keratinocytes exposed to Escherichia coli. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 65 18263703
2009 Human hair follicle epithelium has an antimicrobial defence system that includes the inducible antimicrobial peptide psoriasin (S100A7) and RNase 7. The British journal of dermatology 62 19416233
2013 S100A7 overexpression is a predictive marker for high risk of malignant transformation in oral dysplasia. International journal of cancer 60 24122701
2018 Up-regulated lncRNA-MSX2P1 promotes the growth of IL-22-stimulated keratinocytes by inhibiting miR-6731-5p and activating S100A7. Experimental cell research 56 29339075
2015 Leukocyte-derived koebnerisin (S100A15) and psoriasin (S100A7) are systemic mediators of inflammation in psoriasis. Journal of dermatological science 55 26055798
2008 Reciprocal negative regulation between S100A7/psoriasin and beta-catenin signaling plays an important role in tumor progression of squamous cell carcinoma of oral cavity. Oncogene 55 18223693
2014 The antimicrobial protein S100A7/psoriasin enhances the expression of keratinocyte differentiation markers and strengthens the skin's tight junction barrier. The British journal of dermatology 53 24842328
2017 S100A7 promotes the migration, invasion and metastasis of human cervical cancer cells through epithelial-mesenchymal transition. Oncotarget 52 28212564
2009 Psoriasin (S100A7) up-regulation in oral squamous cell carcinoma and its relation to clinicopathologic features. Oral oncology 52 19147391
2004 S100A7 (psoriasin) expression is associated with aggressive features and alteration of Jab1 in ductal carcinoma in situ of the breast. Breast cancer research : BCR 51 15217497
2003 S100A7 (psoriasin) interacts with epidermal fatty acid binding protein and localizes in focal adhesion-like structures in cultured keratinocytes. The Journal of investigative dermatology 50 12839573
2008 Selective expression of S100A7 in lung squamous cell carcinomas and large cell carcinomas but not in adenocarcinomas and small cell carcinomas. Thorax 48 18364444
1999 Calcium-binding protein S100A7 and epidermal-type fatty acid-binding protein are associated in the cytosol of human keratinocytes. The Biochemical journal 45 10191275
2011 Expression and regulation of antimicrobial peptide psoriasin (S100A7) at the ocular surface and in the lacrimal apparatus. Investigative ophthalmology & visual science 44 21551409
2010 Psoriasin (S100A7) is a major Escherichia coli-cidal factor of the female genital tract. Mucosal immunology 44 20571488
2003 Genomic and phylogenetic analysis of the S100A7 (Psoriasin) gene duplications within the region of the S100 gene cluster on human chromosome 1q21. Journal of molecular evolution 43 12664160
2017 Overexpression of Psoriasin (S100A7) Contributes to Dysregulated Differentiation in Psoriasis. Acta dermato-venereologica 42 27958610
2013 Visfatin enhances the production of cathelicidin antimicrobial peptide, human β-defensin-2, human β-defensin-3, and S100A7 in human keratinocytes and their orthologs in murine imiquimod-induced psoriatic skin. The American journal of pathology 42 23499548
2008 Psoriasin (S100A7) is a principal antimicrobial peptide of the human tongue. Mucosal immunology 42 19079183
2017 S100A7: from mechanism to cancer therapy. Oncogene 41 28825725
2010 PsOr1, a potential target for RNA interference-based pest management. Insect molecular biology 41 20854479
2008 Detection of psoriasin/S100A7 in the sera of patients with psoriasis. The British journal of dermatology 41 19016707
2022 cPLA2 blockade attenuates S100A7-mediated breast tumorigenicity by inhibiting the immunosuppressive tumor microenvironment. Journal of experimental & clinical cancer research : CR 40 35135586
2021 Activation of the S100A7/RAGE Pathway by IGF-1 Contributes to Angiogenesis in Breast Cancer. Cancers 40 33557316
2018 OLFM4, LY6D and S100A7 as potent markers for distant metastasis in estrogen receptor-positive breast carcinoma. Cancer science 40 30137688
2013 Differential expression and in vivo secretion of the antimicrobial peptides psoriasin (S100A7), RNase 7, human beta-defensin-2 and -3 in healthy human skin. Experimental dermatology 40 23614747
2016 S100A7: A rAMPing up AMP molecule in psoriasis. Cytokine & growth factor reviews 39 26872860
2016 S100A7 (psoriasin) inhibits human epidermal differentiation by enhanced IL-6 secretion through IκB/NF-κB signalling. Experimental dermatology 38 27060579
2005 Psoriasin (S100A7) and calgranulin-B (S100A9) induction is dependent on reactive oxygen species and is downregulated by Bcl-2 and antioxidants. Cancer biology & therapy 38 16082188
2007 S100A7 (Psoriasin), highly expressed in ductal carcinoma in situ (DCIS), is regulated by IFN-gamma in mammary epithelial cells. BMC cancer 37 17986321
2008 S100A7-downregulation inhibits epidermal growth factor-induced signaling in breast cancer cells and blocks osteoclast formation. PloS one 36 18320059
2005 Expression analysis of the mouse S100A7/psoriasin gene in skin inflammation and mammary tumorigenesis. BMC cancer 35 15717926
2011 Tumor-suppressive effects of psoriasin (S100A7) are mediated through the β-catenin/T cell factor 4 protein pathway in estrogen receptor-positive breast cancer cells. The Journal of biological chemistry 34 22016394
2007 Identification and validation of S100A7 associated with lung squamous cell carcinoma metastasis to brain. Lung cancer (Amsterdam, Netherlands) 34 17418446
2018 S100A7 Regulates Ovarian Cancer Cell Metastasis and Chemoresistance Through MAPK Signaling and Is Targeted by miR-330-5p. DNA and cell biology 33 29485916
2016 Psoriasin (S100A7) promotes stress-induced angiogenesis. The British journal of dermatology 33 27155199
2016 TSLP Down-Regulates S100A7 and ß-Defensin 2 Via the JAK2/STAT3-Dependent Mechanism. The Journal of investigative dermatology 33 27498343
2012 S100A7 promotes the migration and invasion of osteosarcoma cells via the receptor for advanced glycation end products. Oncology letters 32 22783409
1999 Genomic structure, promoter characterisation and mutational analysis of the S100A7 gene: exclusion of a candidate for familial psoriasis susceptibility. Human genetics 32 10190323
2020 Alarmins HMGB1, IL-33, S100A7, and S100A12 in Psoriasis Vulgaris. Mediators of inflammation 31 32377165
2006 Estrogen receptor-beta regulates psoriasin (S100A7) in human breast cancer. Breast cancer research and treatment 31 17009105
1999 Probable interaction between S100A7 and E-FABP in the cytosol of human keratinocytes from psoriatic scales. Molecular and cellular biochemistry 31 10331666
2024 S100A7 orchestrates neutrophil chemotaxis and drives neutrophil extracellular traps (NETs) formation to facilitate lymph node metastasis in cervical cancer patients. Cancer letters 30 39384116
2019 The novel interaction between Neisseria gonorrhoeae TdfJ and human S100A7 allows gonococci to subvert host zinc restriction. PLoS pathogens 30 31369630
2010 Psoriasin (S100A7) associates with integrin β6 subunit and is required for αvβ6-dependent carcinoma cell invasion. Oncogene 29 21132011
2021 Weighted gene coexpression network and experimental analyses identify lncRNA SPRR2C as a regulator of the IL-22-stimulated HaCaT cell phenotype through the miR-330/STAT1/S100A7 axis. Cell death & disease 28 33452236
2013 Opposing functions of psoriasin (S100A7) and koebnerisin (S100A15) in epithelial carcinogenesis. Current opinion in pharmacology 28 23664757
2002 Urinary excretion of epidermal-type fatty acid-binding protein and S100A7 protein in patients with cutaneous melanoma. Melanoma research 28 12459653
2012 Psoriasin (S100A7) is a positive regulator of survival and invasion of prostate cancer cells. Urologic oncology 27 22694938
2017 Human S100A7 Induces Mature Interleukin1α Expression by RAGE-p38 MAPK-Calpain1 Pathway in Psoriasis. PloS one 26 28060905
2017 Biochemical and Functional Evaluation of the Intramolecular Disulfide Bonds in the Zinc-Chelating Antimicrobial Protein Human S100A7 (Psoriasin). Biochemistry 26 28976190
2016 S100A7 has an oncogenic role in oral squamous cell carcinoma by activating p38/MAPK and RAB2A signaling pathway. Cancer gene therapy 26 27767088
2014 The antimicrobial peptides psoriasin (S100A7) and koebnerisin (S100A15) suppress extracellular matrix production and proliferation of human fibroblasts. Skin pharmacology and physiology 26 25502330
2016 Low vitamin D-modulated calcium-regulating proteins in psoriasis vulgaris plaques: S100A7 overexpression depends on joint involvement. International journal of molecular medicine 24 27573000
2013 Differential role of psoriasin (S100A7) in estrogen receptor α positive and negative breast cancer cells occur through actin remodeling. Breast cancer research and treatment 24 23535840
2013 S100A7 enhances invasion of human breast cancer MDA-MB-468 cells through activation of nuclear factor-κB signaling. World journal of surgical oncology 24 23618129
2008 Association of psoriasin (S100A7) with clinical manifestations of systemic sclerosis: is its presence in whole saliva a potential predictor of pulmonary involvement? The Journal of rheumatology 24 18634149
2021 Lipopolysaccharide from the commensal microbiota of the breast enhances cancer growth: role of S100A7 and TLR4. Molecular oncology 22 33969603
2019 Sustained Secretion of the Antimicrobial Peptide S100A7 Is Dependent on the Downregulation of Caspase-8. Cell reports 22 31775025
2015 miR-29b defines the pro-/anti-proliferative effects of S100A7 in breast cancer. Molecular cancer 22 25622979
2006 S100A7 (Psoriasin): a story of mice and men. The Journal of investigative dermatology 22 16778811
2017 MicroRNA-26b-5p regulates cell proliferation, invasion and metastasis in human intrahepatic cholangiocarcinoma by targeting S100A7. Oncology letters 21 29387225
2009 Identification and characterization of binding sites on S100A7, a participant in cancer and inflammation pathways. Biochemistry 21 19810752
2019 Mechanical stress induced S100A7 expression in human dental pulp cells to augment osteoclast differentiation. Oral diseases 20 30614184
2015 The Characteristics and Function of S100A7 Induction in Squamous Cell Carcinoma: Heterogeneity, Promotion of Cell Proliferation and Suppression of Differentiation. PloS one 20 26053695
2012 The expression of Psoriasin (S100A7) and CD24 is linked and related to the differentiation of mammary epithelial cells. PloS one 20 23300877
2011 S100A7/psoriasin expression in the human lung: unchanged in patients with COPD, but upregulated upon positive S. aureus detection. BMC pulmonary medicine 20 21324122
2007 S100A7 (psoriasin) influences immune response genes in human breast cancer. Experimental cell research 20 17560571
2017 Molecular and cellular impact of Psoriasin (S100A7) on the healing of human wounds. Experimental and therapeutic medicine 19 28565822
2016 TLR3 activation induces S100A7 to regulate keratinocyte differentiation after skin injury. Science China. Life sciences 19 27535424
2012 Differential occurrence of S100A7 in breast cancer tissues: a proteomic-based investigation. Proteomics. Clinical applications 19 22641350
2012 Post-operative recurrent trachomatous trichiasis is associated with increased conjunctival expression of S100A7 (psoriasin). PLoS neglected tropical diseases 19 23285311
2007 The expression of interleukin-22 and S100A7, A8, A9 mRNA in patients with psoriasis vulgaris. Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban 18 18060647

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