Affinage

SEMA3A

Semaphorin-3A · UniProt Q14563

Length
771 aa
Mass
88.9 kDa
Annotated
2026-06-10
100 papers in source corpus 43 papers cited in narrative 44 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SEMA3A is a secreted class 3 semaphorin that functions as a bifunctional guidance cue—repelling axons and sympathetic/sensory neurons while attracting dendrites—through a tripartite receptor complex in which it binds neuropilin-1 (Nrp1) as an obligate co-receptor coupled to PlexinA1/A4, an assembly resolved by cryo-EM as a symmetric 2:2:2 complex whose membrane-proximal Plexin regions are poised to drive intracellular dimerization (PMID:34039996, PMID:11830568, PMID:23991118). Repulsive signaling proceeds through PlexinA1-associated FARP2, whose Sema3A-triggered dissociation activates Rac GEF activity and recruits Rnd1 to downregulate R-Ras while sequestering PIPKIgamma661 from talin to suppress adhesion (PMID:16286926), with downstream Rac1-PAK engagement (PMID:10508610), PTEN-dependent suppression of PI3K and activation of GSK-3 (PMID:16495486), and CRMP1 phosphorylation that remodels Filamin-A/F-actin architecture to collapse the growth cone (PMID:25358863); ERM proteins and the adhesion molecules L1CAM and CHL1 act as accessory components that drive receptor internalization and transduce the collapse response (PMID:10985345, PMID:18651636, PMID:17995939). In dendrites the same ligand instead drives growth through a distinct integrin/FAK-dependent pathway, establishing that opposing axon-versus-dendrite responses use separable effectors (PMID:19454481). Developmental responsiveness is tuned by ADAM10/17-mediated Nrp1 cleavage (PMID:24898499), and SEMA3A binds glycosaminoglycans through a C-terminal basic region required for chemorepulsion (PMID:27028639). Beyond neurodevelopment, SEMA3A patterns cardiac sympathetic innervation to control rhythm (PMID:17417650), regulates bone mass through sensory innervation and estrogen-driven autocrine osteocyte sGC-cGMP signaling (PMID:23644455, PMID:30661929), competes with VEGF for Nrp1 to exert anti-angiogenic activity (PMID:24809797, PMID:16684957), promotes M2 macrophage polarization to resolve inflammation (PMID:28540528, PMID:36598593), and acts as a direct Kv4.3 channel inhibitor whose disruption by missense mutations underlies Brugada syndrome (PMID:24963029). Loss-of-function SEMA3A mutations impairing secretion or signaling cause a Kallmann syndrome-like phenotype with defective GnRH neuron migration (PMID:22927827).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2000 High

    Established that SEMA3A does not act through Nrp1 alone but requires transmembrane adhesion molecules within the receptor complex, identifying L1CAM as a transducing component.

    Evidence Reciprocal Co-IP of L1 and Nrp1, L1-KO neuron coculture repulsion assay, and soluble L1Fc rescue

    PMID:10985345

    Open questions at the time
    • Did not resolve how L1 couples to intracellular Plexin signaling
    • Did not address dendrite responses
  2. 2002 High

    Demonstrated in vivo that Nrp1-mediated SEMA3A signaling patterns the sympathetic nervous system, extending its guidance role beyond central axons.

    Evidence Targeted disruption of Nrp1 and Sema3A in mice with in vitro sympathetic neuron migration assays using receptor-null neurons

    PMID:11830568

    Open questions at the time
    • Did not define the intracellular effectors in sympathetic neurons
    • Plexin partner not specified
  3. 2005 High

    Identified the proximal intracellular switch translating ligand binding into cytoskeletal change: FARP2 dissociation from PlexinA1 activates Rac GEF activity and downregulates R-Ras and PIPKIgamma.

    Evidence Co-IP, direct binding, Rac GEF activity assay, and neuron repulsion assay

    PMID:16286926

    Open questions at the time
    • Did not connect to terminal actin remodeling machinery
    • In vivo requirement not tested
  4. 2006 Medium

    Showed that SEMA3A growth cone collapse requires PTEN-dependent suppression of PI3K and GSK-3 activation, linking the receptor to a lipid-phosphatase signaling node.

    Evidence Live PTEN localization imaging, phosphatase-dead PTEN mutant, and pharmacological PI3K/GSK-3 manipulation in sensory neuron collapse assay

    PMID:16495486

    Open questions at the time
    • Single lab
    • Mechanism of PTEN membrane recruitment unresolved
    • Connection to FARP2/Rac arm not integrated
  5. 2007 High

    Extended SEMA3A function to organ physiology, showing it sets a cardiac sympathetic innervation gradient required for normal rhythm.

    Evidence Sema3A knockout and cardiac-specific overexpression mice with electrophysiology and innervation quantification

    PMID:17417650

    Open questions at the time
    • Did not distinguish direct channel effects from innervation effects on rhythm
  6. 2009 High

    Resolved how the same ligand produces opposite responses, showing dendrite growth uses an integrin/FAK pathway distinct from the axonal collapse machinery.

    Evidence Conditional beta1-integrin and FAK knockout in hippocampal neurons with FAK phosphorylation and parallel dendrite-growth versus collapse assays

    PMID:19454481 PMID:20159040

    Open questions at the time
    • Receptor-level basis of pathway divergence unknown
    • Site-specific FAK phosphorylation findings from a single lab
  7. 2009 Medium

    Defined the membrane events of receptor downregulation, showing ERM proteins control internalization of Nrp1 and L1CAM during collapse.

    Evidence ERM loss-of-function, receptor internalization assay, and live imaging in neocortical neurons

    PMID:18651636

    Open questions at the time
    • Single lab
    • Temporal relationship to FARP2/PTEN signaling not established
  8. 2013 High

    Demonstrated that neuronal rather than osteoblastic SEMA3A governs bone mass via sensory innervation, revealing an indirect skeletal role.

    Evidence Cell-type-specific conditional knockouts and nerve ablation epistasis in mice

    PMID:23644455

    Open questions at the time
    • Did not identify the osteocyte-intrinsic signaling later defined
    • Receptor on bone cells not specified here
  9. 2013 High

    Showed SEMA3A retains immunoregulatory signaling activity even when Nrp1 is lost, using PlexinA1/A4 to retain tumor-associated macrophages and trigger VEGFR1 phosphorylation.

    Evidence Macrophage-specific Nrp1 deletion, VEGFR1 phosphorylation assay, and in vivo tumor models

    PMID:24332039

    Open questions at the time
    • Mechanism of Nrp1-independent Plexin engagement not structurally defined
  10. 2014 High

    Connected the intracellular signaling to terminal actin reorganization through CRMP1 phosphorylation remodeling Filamin-A and weakening F-actin gelation.

    Evidence Co-IP, Y2H, mutagenesis repulsion assays, atomic force microscopy, and F-actin gelation assay

    PMID:25358863

    Open questions at the time
    • Kinase responsible for CRMP1 Ser522 phosphorylation in this context not identified
  11. 2014 Medium

    Defined which Plexins are obligatory, showing PlexinA1 and PlexinA4 (with Nrp1) transduce SEMA3A while PlexinA2 is redundant only at high expression.

    Evidence siRNA silencing and overexpression rescue in endothelial and glioblastoma cells

    PMID:25335892

    Open questions at the time
    • Single lab
    • Cell-type generality to neurons not directly tested
  12. 2014 High

    Established developmental tuning of responsiveness, showing ADAM10/17 cleavage of Nrp1 desensitizes sensory axons to SEMA3A.

    Evidence ADAM10/17 genetic ablation, cleavage-susceptibility Nrp1 mutant, and DRG axon guidance assay

    PMID:24898499

    Open questions at the time
    • Regulation of ADAM activity timing not addressed
  13. 2014 High

    Revealed a non-guidance molecular function, identifying SEMA3A as a direct Kv4.3 channel inhibitor whose disruption causes Brugada syndrome.

    Evidence Patch clamp in HEK293, Co-IP, binding-domain mutagenesis, iPSC-cardiomyocyte electrophysiology, and patient missense variants

    PMID:24963029

    Open questions at the time
    • Relationship between channel inhibition and Nrp1/Plexin signaling unresolved
  14. 2016 High

    Showed SEMA3A function depends on glycosaminoglycan binding through its C-terminal basic region, an interaction separable from direct Nrp1 binding.

    Evidence NMR, SPR, ITC, and competition binding with peptoid inhibitor SICHI

    PMID:27028639

    Open questions at the time
    • Specific GAG species and in vivo relevance not fully resolved
  15. 2017 High

    Identified PTPδ-Fyn as a kinase arm specifically driving SEMA3A-induced dendritic arborization, reinforcing pathway divergence between dendrite growth and axon collapse.

    Evidence Ptpδ knockout mice, Fyn/Src phosphorylation assays, double-heterozygous genetic interaction, and cross-species C. elegans assays

    PMID:28637841

    Open questions at the time
    • How PTPδ couples to the Nrp1/Plexin complex not defined
  16. 2019 High

    Defined a cell-autonomous skeletal mechanism, showing estrogen-induced osteocyte SEMA3A acts via Nrp1 and sGC-cGMP to maintain osteocyte survival.

    Evidence Osteocyte-specific Sema3A and Nrp1 knockouts with pharmacological sGC-cGMP rescue and ovariectomy model

    PMID:30661929

    Open questions at the time
    • Reconciliation with the earlier neuronal-source model of bone regulation not addressed
  17. 2021 High

    Provided the structural basis of receptor activation, resolving the symmetric 2:2:2 Sema3A/PlexinA4/Nrp1 assembly and a novel Nrp1 a2b1b2-Sema interface.

    Evidence Cryo-EM of the near-intact extracellular complex at 3.7 Å

    PMID:34039996

    Open questions at the time
    • Intracellular conformational changes upon activation not visualized
    • Accessory components L1/CHL1 not included in the structure

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SEMA3A's distinct molecular activities—Nrp1/Plexin guidance signaling, VEGF-competitive anti-angiogenesis, Kv4.3 channel inhibition, and GAG binding—are integrated within a single cell, and how downstream effector arms are selected to produce repulsion versus attraction, remains unresolved.
  • No unified model linking channel inhibition to canonical receptor signaling
  • Mechanism selecting FARP2/PTEN/CRMP collapse arm versus integrin/FAK/PTPδ growth arm undefined
  • Structural state of the activated intracellular Plexin dimer not resolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 3 GO:0060089 molecular transducer activity 2 GO:0098772 molecular function regulator activity 1
Localization
GO:0005576 extracellular region 2
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-168256 Immune System 3 R-HSA-162582 Signal Transduction 2
Partners
CHL1FARP2KCND3L1CAMNRP1PLXNA1PLXNA3PLXNA4
Complex memberships
Sema3A/PlexinA4/Neuropilin-1 holoreceptor complex

Evidence

Reading pass · 44 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2021 Cryo-EM structure of the Sema3A/PlexinA4/Neuropilin-1 extracellular complex at 3.7 Å resolution reveals a symmetric 2:2:2 assembly in which each subunit makes multiple interactions with others. The two PlexinA4 molecules do not interact directly but their membrane-proximal regions are poised to promote intracellular active dimer formation. A previously unknown interface between the a2b1b2 module of Nrp1 and the Sema domain of Sema3A was identified, placing the a2b1b2 module at the top of the complex far from the membrane. Cryo-EM structure determination of near-intact extracellular complex Nature communications High 34039996
2005 FARP2, a FERM domain-containing guanine nucleotide exchange factor (GEF), associates directly with plexin-A1 in the presence of neuropilin-1. Upon Sema3A binding to neuropilin-1, FARP2 dissociates from plexin-A1, activating FARP2's Rac GEF activity and recruiting Rnd1 to plexin-A1, which downregulates R-Ras. Simultaneously, the FERM domain of FARP2 sequesters PIPKIgamma661 from talin, inhibiting its kinase activity. These activities are required for Sema3A-mediated axon repulsion and suppression of neuronal adhesion. Co-immunoprecipitation, direct binding assays, Rac GEF activity assays, neuron culture repulsion assays Nature neuroscience High 16286926
2000 L1 CAM forms a stable complex with neuropilin-1 (NP-1) through direct association of their extracellular domains, making L1 a component of the Sema3A receptor complex. L1-deficient cortical axons fail to respond to Sema3A repulsion in coculture assays. Addition of soluble L1Fc chimeric molecules converts wild-type axon repulsion by Sema3A into attraction, demonstrating L1 functions within the Sema3A transducing pathway in the growth cone. Coculture repulsion assay, co-immunoprecipitation of L1 and NP-1, soluble L1Fc rescue experiment Neuron High 10985345
2006 PTEN is required for Sema3A-mediated growth cone collapse in sensory neurons. Sema3A suppresses PI3K signaling concomitant with GSK-3 activation in a PTEN-phosphatase-activity-dependent manner. Following Sema3A exposure, PTEN rapidly accumulates at the growth cone membrane, providing a mechanism by which PTEN couples Sema3A signaling to growth cone collapse. Live imaging of PTEN localization, pharmacological PI3K/GSK-3 manipulation, PTEN phosphatase mutant analysis in sensory neuron collapse assay Journal of cell science Medium 16495486
1999 Sema3A-induced growth cone collapse is mediated through Rac1 amino acids 17-32. Cell-permeable peptides spanning this region bind Rac1-interacting molecules PAK, WASP, 3BP-1, and p85beta-PI3K and inhibit Sema3A-induced growth cone collapse. A PAK CRIB-motif peptide also inhibits collapse in a Rac1-binding-dependent manner, implicating downstream Rac1-PAK signaling in the collapse response. Cell-permeable peptide competition assays, direct binding assays, growth cone collapse assay Current biology Medium 10508610
2014 CRMP1 interacts with both the actin-binding domain and the last immunoglobulin-like repeat of Filamin-A. This interaction participates in Sema3A-induced axon repulsion in neurons; alanine mutations in the interacting residues of Filamin-A or CRMP1 suppress Sema3A repulsion. A phosphomimetic CRMP1(Ser522Asp) mutant enhances Sema3A response and, by atomic force microscopy, causes Filamin-A to adopt a condensed form and weakens F-actin gelation crosslinked by Filamin-A. Co-immunoprecipitation, yeast two-hybrid, alanine mutagenesis in neuron repulsion assay, atomic force microscopy, F-actin gelation assay Nature communications High 25358863
2014 ADAM10 and ADAM17 metalloprotease-mediated cleavage of neuropilin-1 (Nrp1) promotes developmental downregulation of Sema3A responsiveness in murine sensory axons. Genetic ablation of ADAM10 and ADAM17 disrupts Nrp1 downregulation in sensory axons and correlates with gain of repulsive response to Sema3A. Overexpression of Nrp1 with high susceptibility to cleavage reverses axonal desensitization, and ADAM knockouts show guidance errors consistent with enhanced Sema3A response. Genetic knockout of ADAM10/17, Nrp1 overexpression with cleavage-susceptibility mutant, DRG axon guidance assay Nature communications High 24898499
2014 Sema3A signaling for axon repulsion requires the plexin-A1 and plexin-A4 receptors (in combination with neuropilin-1) but not plexin-A2. Silencing plexin-A2 in endothelial and glioblastoma cells does not affect Sema3A signaling. Overexpression of plexin-A2 can rescue Sema3A signaling in plexin-A1- or plexin-A4-silenced cells, indicating functional redundancy at high expression levels. siRNA silencing of specific plexins in endothelial and glioblastoma cells, functional migration/signaling assays Journal of cell science Medium 25335892
2010 A Sema3A(K108N) loss-of-function allele identified by forward genetic screen phenocopies Sema3A-null mice. The K108N mutation does not impair Sema3A expression, secretion, or binding to neuropilin-1 (Npn-1), but the protein fails to repel or collapse DRG axons in vitro. In silico modeling and mutagenesis predict that K108N disrupts interaction with the Npn-1/PlexA holoreceptor complex, interfering with signaling at the growth cone. Forward genetic screen in mice, in vitro DRG collapse/repulsion assay, binding assay to Npn-1, in silico structural modeling and mutagenesis The Journal of neuroscience Medium 20410128
2013 Hypoxia-induced Sema3A acts as a chemoattractant for tumor-associated macrophages (TAMs) by triggering VEGFR1 phosphorylation through the Nrp1/PlexinA1/PlexinA4 holoreceptor complex. In hypoxic conditions where Nrp1 is downregulated, Sema3A continues to regulate TAMs in an Nrp1-independent manner by eliciting PlexinA1/PlexinA4-mediated stop signals that retain TAMs inside the hypoxic niche. Gene deletion of Nrp1 in macrophages favors TAM entrapment in normoxic tumor regions. VEGFR1 phosphorylation assay, macrophage-specific Nrp1 gene deletion, in vivo tumor models Cancer cell High 24332039
2013 Neuron-derived (not osteoblast-derived) Sema3A regulates bone mass by modulating sensory nerve innervation of trabecular bone. Neuron-specific Sema3A knockout mice (Sema3asynapsin-/- and Sema3anestin-/-) have reduced trabecular sensory innervation and low bone mass, while osteoblast-specific knockouts (Sema3acol1-/- and Sema3aosx-/-) have normal bone mass. Ablating sensory nerves decreased bone mass in wild-type mice but not in Sema3anestin-/- mice, supporting an essential role of sensory innervation in bone homeostasis mediated by neuronal Sema3A. Cell-type-specific conditional knockout mice, sensory/sympathetic nerve density quantification, nerve ablation experiments, cell-based osteoblast differentiation assays Nature High 23644455
2019 Estrogen induces osteocyte expression of Sema3A, which acts on its own receptor (including Nrp1) on osteocytes in an autocrine/paracrine manner to promote osteocyte survival and maintain bone homeostasis via soluble guanylate cyclase-cGMP signaling. Osteocyte-specific deficiency of either Sema3A or Nrp1 recapitulates severe osteoporosis with fewer osteocytes. Conditional osteocyte-specific knockout of Sema3A and Nrp1, pharmacological sGC-cGMP agonist rescue, ovariectomy model Cell metabolism High 30661929
2007 Sema3A expressed in Purkinje fibers establishes a cardiac sympathetic innervation gradient from epicardium to endocardium. Sema3A-null mice lack this gradient and exhibit sinus bradycardia due to sympathetic dysfunction. Cardiac-specific Sema3A overexpression reduces sympathetic innervation and causes sudden death and ventricular tachycardia due to catecholamine supersensitivity and prolonged action potential duration. Sema3A knockout and cardiac-specific transgenic overexpression in mice, electrophysiological measurements, innervation density quantification Nature medicine High 17417650
2002 Neuropilin-1-mediated Sema3A signaling is required for proper patterning of the sympathetic nervous system. Neuropilin-1 and Sema3A mutant mice show displacement of sympathetic neurons and abnormal sympathetic trunk morphogenesis. Sema3A suppresses migration of sympathetic neurons from wild-type but not neuropilin-1 mutant embryos in vitro, and promotes their aggregation into compact cell masses and neurite fasciculation. Targeted gene disruption of neuropilin-1 and Sema3A, in vitro sympathetic neuron migration assay with receptor mutants Development High 11830568
2017 PTPδ mediates Sema3A-induced cortical basal dendritic arborization through activation of Fyn kinase by dephosphorylating its C-terminal Tyr527. In Ptpδ-/- brains, Fyn and Src are hyperphosphorylated at Tyr527. Sema3A stimulation induces Tyr527 dephosphorylation in wild-type but not Ptpδ-/- dendrites. Double heterozygous Ptpδ+/-; Sema3a+/- mice show reduced basal dendrite arborization, demonstrating genetic interaction. PTP-3 (C. elegans LAR homolog) participates in Sema2A-regulated axon guidance, supporting cross-species conservation. Ptpδ knockout mice, phosphorylation assays of Fyn/Src, double-heterozygous genetic interaction test, Sema3A stimulation of cultured neurons, C. elegans genetic assays The Journal of neuroscience High 28637841
2013 SEMA3A expressed locally by Purkinje cells regulates cerebellar basket cell axon branching through Neuropilin-1 (NRP1). SEMA3A-induced axon branching depends on local recruitment of soluble guanylyl cyclase (sGC) to the plasma membrane of basket cells, regulated by the Src kinase FYN. In fyn-/- mice, basket axon terminal branching is reduced specifically in the Purkinje cell layer. Sema3A and Nrp1 knockout mice, sGC localization assay, fyn knockout mice, basket axon branching quantification Current biology High 23602477
2009 The stimulation of dendrite growth by Sema3A requires integrin engagement and focal adhesion kinase (FAK). Sema3A promotes hippocampal dendrite extension via a pathway requiring FAK phosphorylation; this effect depends on integrin engagement. Conditional inactivation of beta1 integrin or FAK blocks Sema3A-stimulated dendrite growth but not collapse of axonal growth cones, demonstrating that distinct pathways mediate the opposing responses to Sema3A in axons versus dendrites. Conditional knockout of beta1 integrin and FAK in hippocampal neurons, FAK phosphorylation assay, dendrite growth and growth cone collapse assays Journal of cell science High 19454481
2010 FAK functions downstream of Sema3A in hippocampal neurons. Sema3A elicits divergent effects on FAK tyrosine phosphorylation: it increases phosphorylation of Tyr397, the kinase domain, and Tyr925, while decreasing phosphorylation of Tyr407 and Tyr861. FAK conditional ablation abolishes Sema3A-induced axon remodeling. FAKY925 phosphorylation decreases FAK-Paxillin interaction and promotes adhesion contact disassembly via alpha-actinin tyrosine phosphorylation. FAK conditional knockout in hippocampal neurons, site-specific FAK phosphorylation analysis, co-immunoprecipitation of FAK-Paxillin, adhesion contact assay Molecular and cellular neurosciences Medium 20159040
2014 SEMA3A is a naturally occurring inhibitor of Kv4.3 (Ito) potassium channels. SEMA3A selectively reduces Kv4.3 peak current density without altering cell surface expression when co-expressed in HEK293 cells. Co-immunoprecipitation and disruption of a putative toxin-binding domain on Kv4.3 revealed direct binding between SEMA3A and Kv4.3. SEMA3A also reduces Ito current in human iPSC-derived cardiomyocytes. Rare SEMA3A missense mutations in Brugada syndrome patients disrupt Kv4.3 inhibition, causing Kv4.3 gain-of-function. Whole-cell patch clamp in HEK293 cells, co-immunoprecipitation, mutational analysis of SEMA3A and Kv4.3 binding domain, iPSC-cardiomyocyte electrophysiology Circulation research High 24963029
2018 A rationally designed NRP1-independent SEMA3A point mutant binds PLXNA4 with nanomolar affinity (unlike wild-type SEMA3A which requires NRP1 co-receptor). This mutant shows greater biochemical and biological activity in cultured endothelial cells and normalizes tumor vasculature, inhibits tumor growth, and curbs metastasis in mouse pancreatic cancer models when parenterally administered. Rational protein engineering and mutagenesis, in vitro endothelial cell assays, in vivo mouse pancreatic cancer xenograft model, retinal neovascularization model Science translational medicine High 29794061
2006 Sema3A inhibits axonal regeneration after spinal cord injury in adult rats. A selective Sema3A inhibitor (SM-216289) administered to the spinal cord lesion site enhanced axon regeneration/preservation, promoted Schwann cell-mediated myelination, decreased apoptotic cell number, and enhanced angiogenesis, resulting in improved functional recovery. Spinal cord transection model in adult rats, pharmacological inhibition with SM-216289, histological and functional assessments Nature medicine Medium 17099709
2000 Sema3A inhibits branching morphogenesis of fetal mouse lung via neuropilin-1 (NP-1) as receptor or receptor component. Exogenous Sema3A reduces terminal bud number in fetal lung explants in a dose-dependent manner without affecting DNA synthesis. A soluble NP-1 ectodomain neutralizes the inhibitory effect, and fetal lungs from neuropilin-1 null mice are resistant to Sema3A treatment. Fetal lung explant culture, exogenous Sema3A treatment, soluble NP-1 neutralization, neuropilin-1 null mouse lung culture Mechanisms of development Medium 11025205
2007 Sema3A expressed in the distal hindgut mesenchyme regulates entry of sacral enteric neural crest-derived cells (ENPs) into the hindgut via neuropilin-1 expressed on migrating ENPs. In Sema3A-null fetal mice, sacral ENPs and extrinsic axons enter the distal hindgut prematurely. ENPs did not express neuropilin-2, and no change in ENP colonization timetable was detected in neuropilin-2-null mice. Co-culture assays of gut explants with COS cell clusters expressing Sema3A, Sema3A null mouse analysis, neuropilin-1 receptor expression analysis on ENPs Developmental biology Medium 17362911
2016 Sema3A interacts with its C-terminal basic region with glycosaminoglycans (GAGs) including heparin and chondroitin sulfate A, and this interaction is biologically relevant to Sema3A signaling. C-terminus-derived basic peptides bind GAGs with low-micromolar affinity. The peptoid inhibitor SICHI blocks Sema3A chemorepulsion by competing with Sema3A C-terminus peptides for GAG binding rather than by blocking direct Sema3A-Nrp1 protein-protein interaction. NMR, surface plasmon resonance, isothermal titration calorimetry, fluorescence spectroscopy, competition binding assays Biophysical journal High 27028639
2004 Sema3A and VEGF164 both signal through neuropilin-1 (Nrp1) but regulate distinct compartments of facial nerve neurons: Sema3A controls axon guidance of facial nerve neurons but is not required for somatic migration, whereas VEGF164 is essential for somatic migration but not axon guidance. These observations demonstrate that structurally distinct ligands sharing a receptor can pattern different compartments of the same cell. Genetically engineered mouse mutants (Sema3A knockout, VEGF164 mutant), analysis of facial nerve axon vs. soma behavior in vivo Genes & development High 15545635
2009 ERM proteins (ezrin, radixin, moesin) are required for Sema3A-mediated growth cone collapse and guidance in neocortical neurons. Active ERMs concentrate asymmetrically in growth cones and are rapidly and transiently inactivated by Sema3A. The FERM domain of active ERMs regulates internalization of the Sema3A receptor Npn1 and its co-receptor L1CAM, while the ERM C-terminal domain binds and caps F-actin. Live imaging of ERM localization, ERM loss-of-function experiments, receptor internalization assay, growth cone collapse and guidance assay The Journal of comparative neurology Medium 18651636
2007 CHL1, a transmembrane cell adhesion molecule, recruits ezrin (an ERM family F-actin binding protein) to the plasma membrane via a membrane-proximal RGGKYSV motif in its cytoplasmic domain. This CHL1/ERM interaction is required for Sema3A-induced growth cone collapse and CHL1-dependent neurite outgrowth and branching in cortical neurons. Cytofluorescence recruitment assay, CHL1 cytoplasmic domain mutagenesis, growth cone collapse assay, neurite outgrowth assay Journal of neurochemistry Medium 17995939
2013 Sema3A maintains corneal avascularity by inhibiting VEGF-induced angioblast migration. Sema3A is expressed at higher levels than VEGF in the lens adjacent to the presumptive cornea. Blockade of Sema3A signaling (lens removal or synthetic inhibitor injection) causes ectopic angioblast migration and corneal vascularization. Exogenous Sema3A protein inhibits VEGF-induced vascularization. Loss of Sema/Nrp1 signaling in Nrp1(Sema-) mutant mice results in ectopic angioblasts and corneal vascularization. Lens removal surgery, synthetic Sema3A inhibitor injection, exogenous Sema3A bead implantation, Nrp1(Sema-) mutant mouse analysis Developmental biology High 24809797
2019 Sema3a-Nrp1 signaling mediates the fiber-type specificity of Twist2+ (Tw2+) muscle progenitor cells. Nrp1 is expressed by Tw2+ progenitors but not Pax7+ satellite cells, and Sema3a is expressed by type I and IIa myofibers but not IIb myofibers. Sema3a-Nrp1 signaling repels Tw2+ cells from type I/IIa fibers, directing their fusion specifically with IIb fibers. Sema3a transgenic overexpression confirms this mechanism in vivo. Stripe migration assay, chimeric cell-cell fusion assay, Sema3a transgenic mouse model, RNA sequencing and immunofluorescence Developmental cell High 31474563
2013 In statoacoustic ganglion (SAG) neurons, Sema3a expressed in the dorsal otocyst acts as a repellent through a receptor complex involving Nrp1 and either PlexinA1 or PlexinA3. PlexinA1/PlexinA3 double mutant mice and Sema3a mutant mice show similar defects in SAG afferent projections (abnormal dorsal extension beyond normal vestibular target areas), establishing the ligand-receptor complex responsible. Sema3a null mouse, plexinA1/plexinA3 double knockout mouse, afferent projection analysis in inner ear PLoS one Medium 23991118
2009 Sema3A acts as a chemoattractive signal for hippocampal apical dendrites (while repelling axons). In dissociated hippocampal neurons, Sema3A promotes dendrite extension through FAK phosphorylation requiring integrin engagement. This is distinguishable from axonal growth cone collapse induced by the same molecule. Hippocampal neuron culture, dendrite growth assay, FAK phosphorylation assay, conditional integrin/FAK knockout Journal of cell science Medium 19454481
2009 Sema3A increases its own expression in satellite cells in response to HGF treatment during early myogenic differentiation. FGF2 similarly upregulates Sema3A expression, while TGF-β2 and TGF-β3 potently suppress basal Sema3A expression and cancel the upregulatory effects of HGF and FGF2. Neutralizing antibody to c-met does not abolish HGF-induced Sema3A upregulation, suggesting an alternative receptor mediates this effect. Primary satellite cell cultures, RT-PCR and immunochemistry for Sema3A, growth factor dose-response assays, c-met neutralizing antibody American journal of physiology. Cell physiology Medium 19515904
2006 In multiple myeloma endothelial cells (MMECs), loss of SEMA3A autocrine signaling tilts the VEGF165/SEMA3A balance toward VEGF165. Exogenous VEGF165 induces SEMA3A expression in normal endothelial cells but not in MMECs. Exogenous SEMA3A counteracts VEGF165 activity in MMECs as efficiently as anti-VEGFR-2 antibody, with both VEGF165 and SEMA3A competing for NRP1, VEGFR-2, and plexin-A1 receptors. Endothelial cell angiogenesis assays, VEGF165/SEMA3A expression analysis, exogenous SEMA3A treatment, anti-VEGFR-2 comparison Blood Medium 16684957
2017 SEMA3A inhibits phosphorylation of VEGFR2 and its downstream effectors Src and FAK in oral cancer cells, providing a mechanistic basis for its anti-angiogenic activity. Overexpression of SEMA3A in tongue squamous cell carcinoma cells significantly inhibited endothelial tube formation and reduced angiogenesis in CAM assay and mouse xenograft. Western blot for VEGFR2/Src/FAK phosphorylation, endothelial tube formation assay, CAM assay, tumor xenograft model BMC pharmacology & toxicology Medium 28683823
2024 Sema3A secreted by sensory neurons prevents overstretching of F-actin induced by mechanical overload through ROCK2 pathway, maintaining mitochondrial fusion dynamics. In vitro mechanical loads upregulate Sema3A in neurons but not in periodontal ligament cells. Exogenous Sema3A restores osteogenic differentiation of hPDLCs suppressed by mechanical overload. In vitro mechanical loading of neurons and hPDLCs, Sema3A exogenous treatment, ROCK2 pathway inhibitor, F-actin and mitochondrial dynamics assays International journal of oral science Medium 38238300
2019 Sema3A inhibits axonal regeneration of retinal ganglion cells via ROCK2. Sema3A promotes phosphorylation of myosin light chain 2 (MLC2), a specific downstream effector of ROCK2. The ROCK2 inhibitor Y-27632 attenuates the inhibitory effect of Sema3A on optic nerve regeneration in vivo. Optic nerve crush model, intravitreal injection of Sema3A and Y-27632, MLC2 phosphorylation assay, axon regeneration markers (GAP43, Sprr1A), F-VEPs Brain research Medium 31733191
2017 Sema3A promotes M2 macrophage polarization and inhibits M1 polarization. In vitro, recombinant Sema3A induces apoptosis of classical M1 macrophages and promotes their polarization toward resolution-phase M2 macrophages with enhanced efferocytotic ability. Sema3A heterozygote mice post-MI show increased leukocyte infiltration and impaired cardiac function compared to wild-type. In vitro recombinant Sema3A treatment of bone marrow-derived macrophages, Sema3A heterozygote mouse MI model, flow cytometry for macrophage polarization markers Basic research in cardiology Medium 28540528
2024 In PDAC cells, SEMA3A promotes cell migration and anoikis resistance through the canonical SEMA3A-NRP1 axis, associated with increased focal adhesion kinase (FAK) signaling. SEMA3A also functions as a chemoattractant for macrophages and skews their polarization toward an M2-like immunosuppressive phenotype. Macrophage depletion in SEMA3A-high tumors results in greater CD8+ T cell infiltration. Gain/loss of function in PDAC cell lines and organoids, FAK signaling assays, macrophage migration and polarization assays, macrophage depletion in vivo Gut Medium 38670629
2020 Nestin selectively facilitates phosphorylation of doublecortin (DCX) by cdk5/p35 kinase by acting as a scaffold that bridges DCX and activated cdk5/p35, but does not affect phosphorylation of other cdk5 substrates. This nestin-DCX complex mediates Sema3A sensitivity of developing cortical neuron growth cones; Dcx KO neurons phenocopy the effects of nestin loss on growth cone morphology and Sema3A responsiveness. Nestin KO and DCX KO cortical neuron cultures, cdk5 substrate phosphorylation assays, co-immunoprecipitation of nestin-DCX, growth cone collapse assay The Journal of neuroscience Medium 32273484
2019 Sema3A drives macrophage polarization toward M2 phenotype in periodontitis via activation of PI3K/AKT/mTOR signaling pathways. In vitro, Sema3A promotes LPS/IFNγ-induced M1 macrophages to convert to M2 macrophages; inhibition of PI3K signaling reduces this anti-inflammatory activity and boosts inflammatory cytokine expression. RAW264.7 macrophage polarization assay, PI3K pathway inhibitor experiments, ELISA for cytokines, in vivo mouse periodontitis model Inflammation Medium 36598593
2018 CHD7 is enriched at the Sema3a promoter in neural crest cells; loss of CHD7 function inhibits Sema3A expression, placing Sema3A downstream of CHD7 in an epigenetic regulatory loop relevant to CHARGE syndrome pathogenesis. Human SEMA3A rescues CHD7 loss of function in a Xenopus CHARGE model. A pathogenic SEMA3A variant (R66W) reduces protein secretion, while the likely-benign I668V variant does not affect protein secretion or processing. ChIP enrichment at Sema3a promoter, Xenopus CHD7 loss-of-function rescue assay, SEMA3A variant expression and secretion analysis in transfected cells Human molecular genetics Medium 29432577
2012 Nrp1(sema/sema) mutant mice lacking a functional semaphorin-binding domain in neuropilin-1 display a Kallmann syndrome-like phenotype with abnormal olfactory system development and defective embryonic GnRH cell migration to the basal forebrain. Human SEMA3A mutations (missense and frameshift) cause either impaired secretion of the protein (R66W, D538fsX31, V435I) or reduced signaling activity of the secreted protein (N153S, I400V, T688A, R733H) in GnRH cell line assays. Nrp1(sema/sema) mutant mouse histological analysis, SEMA3A variant transfection in COS-7 cells (secretion assay), GN11 GnRH cell signaling assay PLoS genetics High 22927827
2001 Adult rat brain oligodendrocytes express neuropilin-1 (the major Sema3A receptor component) and CRMP2 and CRMP5. Sema3A causes a dramatic reduction in oligodendrocyte process extension, which is reversed by Sema3A removal or blocked by anti-neuropilin-1, anti-CRMP5, or anti-CRMP2 antibodies, demonstrating that a Sema3A signaling pathway involving neuropilin-1, CRMP2, and CRMP5 modulates oligodendrocyte process extension in the adult brain. Adult rat oligodendrocyte cultures, Sema3A-conditioned medium treatment, function-blocking antibodies, process extension quantification The Journal of neuroscience Medium 11549731
2019 Disrupting Sema3A/Plexin-A1 inhibitory signaling in oligodendrocytes using a novel peptidic Plexin-A1 antagonist counteracts Sema3A inhibitory effects on oligodendrocyte migration and differentiation in vitro, and shows myelin-protective effects in the cuprizone demyelination/remyelination mouse model. In vitro oligodendrocyte migration and differentiation assay with Plexin-A1 antagonist peptide, cuprizone mouse model with DTI-MRI and histology, EAE model EMBO molecular medicine Medium 31566924

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 Impeding macrophage entry into hypoxic tumor areas by Sema3A/Nrp1 signaling blockade inhibits angiogenesis and restores antitumor immunity. Cancer cell 522 24332039
2000 Analysis of the L1-deficient mouse phenotype reveals cross-talk between Sema3A and L1 signaling pathways in axonal guidance. Neuron 347 10985345
2013 Sema3A regulates bone-mass accrual through sensory innervations. Nature 335 23644455
2006 A selective Sema3A inhibitor enhances regenerative responses and functional recovery of the injured spinal cord. Nature medicine 314 17099709
2005 FARP2 triggers signals for Sema3A-mediated axonal repulsion. Nature neuroscience 186 16286926
2007 Sema3a maintains normal heart rhythm through sympathetic innervation patterning. Nature medicine 179 17417650
2007 The CRMP family of proteins and their role in Sema3A signaling. Advances in experimental medicine and biology 173 17607942
2012 SEMA3A, a gene involved in axonal pathfinding, is mutated in patients with Kallmann syndrome. PLoS genetics 156 22927827
2004 Vascular endothelial growth factor controls neuronal migration and cooperates with Sema3A to pattern distinct compartments of the facial nerve. Genes & development 151 15545635
2002 Requirement of neuropilin 1-mediated Sema3A signals in patterning of the sympathetic nervous system. Development (Cambridge, England) 137 11830568
2019 Autoregulation of Osteocyte Sema3A Orchestrates Estrogen Action and Counteracts Bone Aging. Cell metabolism 129 30661929
2023 Evodiamine impairs HIF1A histone lactylation to inhibit Sema3A-mediated angiogenesis and PD-L1 by inducing ferroptosis in prostate cancer. European journal of pharmacology 128 37611839
2006 PTEN couples Sema3A signalling to growth cone collapse. Journal of cell science 119 16495486
1999 Sema3A-induced growth-cone collapse is mediated by Rac1 amino acids 17-32. Current biology : CB 117 10508610
2008 A recessive skeletal dysplasia, SEMD aggrecan type, results from a missense mutation affecting the C-type lectin domain of aggrecan. American journal of human genetics 107 19110214
2001 Isolation and expression pattern of human Unc-33-like phosphoprotein 6/collapsin response mediator protein 5 (Ulip6/CRMP5): coexistence with Ulip2/CRMP2 in Sema3a- sensitive oligodendrocytes. The Journal of neuroscience : the official journal of the Society for Neuroscience 107 11549731
2012 SEMA3A deletion in a family with Kallmann syndrome validates the role of semaphorin 3A in human puberty and olfactory system development. Human reproduction (Oxford, England) 101 22416012
2011 miR-124 acts through CoREST to control onset of Sema3A sensitivity in navigating retinal growth cones. Nature neuroscience 100 22138647
2009 Psoralen-ultraviolet A therapy alters epidermal Sema3A and NGF levels and modulates epidermal innervation in atopic dermatitis. Journal of dermatological science 95 19443185
2003 Evidence that Sema3A and Sema3F regulate the migration of GABAergic neurons in the developing neocortex. The Journal of comparative neurology 90 12454988
2009 Possible implication of satellite cells in regenerative motoneuritogenesis: HGF upregulates neural chemorepellent Sema3A during myogenic differentiation. American journal of physiology. Cell physiology 86 19515904
2005 MMP13 mutation causes spondyloepimetaphyseal dysplasia, Missouri type (SEMD(MO). The Journal of clinical investigation 84 16167086
2000 Repulsive axon guidance molecule Sema3A inhibits branching morphogenesis of fetal mouse lung. Mechanisms of development 82 11025205
2003 Transient downregulation of Sema3A mRNA in a rat model for temporal lobe epilepsy. A novel molecular event potentially contributing to mossy fiber sprouting. Experimental neurology 76 12821384
2017 Sema3A promotes the resolution of cardiac inflammation after myocardial infarction. Basic research in cardiology 73 28540528
2006 Loss of inhibitory semaphorin 3A (SEMA3A) autocrine loops in bone marrow endothelial cells of patients with multiple myeloma. Blood 72 16684957
2019 miR-15b-5p ameliorated high glucose-induced podocyte injury through repressing apoptosis, oxidative stress, and inflammatory responses by targeting Sema3A. Journal of cellular physiology 58 31025335
2014 Mutation screening of SEMA3A and SEMA7A in patients with congenital hypogonadotropic hypogonadism. Pediatric research 57 24522099
2018 Gpr97 Exacerbates AKI by Mediating Sema3A Signaling. Journal of the American Society of Nephrology : JASN 53 29531097
2016 Guidance Molecule SEMA3A Restricts Tumor Growth by Differentially Regulating the Proliferation of Tumor-Associated Macrophages. Cancer research 52 27197153
2007 Effects of different regions of the developing gut on the migration of enteric neural crest-derived cells: a role for Sema3A, but not Sema3F. Developmental biology 51 17362911
2007 CHL1 promotes Sema3A-induced growth cone collapse and neurite elaboration through a motif required for recruitment of ERM proteins to the plasma membrane. Journal of neurochemistry 50 17995939
2018 A rationally designed NRP1-independent superagonist SEMA3A mutant is an effective anticancer agent. Science translational medicine 49 29794061
2009 The stimulation of dendrite growth by Sema3A requires integrin engagement and focal adhesion kinase. Journal of cell science 47 19454481
2009 Increased proximal bifurcation of CA1 pyramidal apical dendrites in sema3A mutant mice. The Journal of comparative neurology 47 19655386
2014 Characterization of SEMA3A-encoded semaphorin as a naturally occurring Kv4.3 protein inhibitor and its contribution to Brugada syndrome. Circulation research 46 24963029
2000 SEMA3A regulates developing sensory projections in the chicken spinal cord. Journal of neurobiology 46 11077427
2021 Architecture of the Sema3A/PlexinA4/Neuropilin tripartite complex. Nature communications 45 34039996
2017 MicroRNA-192-5p Promote the Proliferation and Metastasis of Hepatocellular Carcinoma Cell by Targeting SEMA3A. Applied immunohistochemistry & molecular morphology : AIMM 44 26580097
2017 Diabetes Perturbs Bone Microarchitecture and Bone Strength through Regulation of Sema3A/IGF-1/β-Catenin in Rats. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 43 28135705
2016 Wedelolactone Enhances Osteoblastogenesis but Inhibits Osteoclastogenesis through Sema3A/NRP1/PlexinA1 Pathway. Frontiers in pharmacology 43 27803667
2014 Amino- and carboxyl-terminal domains of Filamin-A interact with CRMP1 to mediate Sema3A signalling. Nature communications 41 25358863
2014 The role of the plexin-A2 receptor in Sema3A and Sema3B signal transduction. Journal of cell science 39 25335892
2014 ADAM metalloproteases promote a developmental switch in responsiveness to the axonal repellant Sema3A. Nature communications 38 24898499
2013 SEMA3A signaling controls layer-specific interneuron branching in the cerebellum. Current biology : CB 38 23602477
2010 A forward genetic screen in mice identifies Sema3A(K108N), which binds to neuropilin-1 but cannot signal. The Journal of neuroscience : the official journal of the Society for Neuroscience 34 20410128
2018 Long non-coding RNA GAS5 reduces cardiomyocyte apoptosis induced by MI through sema3a. International journal of biological macromolecules 33 30099044
2023 miR-196b-5p Regulates Osteoblast and Osteoclast Differentiation and Bone Homeostasis by Targeting SEMA3A. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 32 37221130
2010 Expression by midbrain dopamine neurons of Sema3A and 3F receptors is associated with chemorepulsion in vitro but a mild in vivo phenotype. Molecular and cellular neurosciences 32 20298787
2017 Adenovirus-mediated delivery of Sema3A alleviates rheumatoid arthritis in a serum-transfer induced mouse model. Oncotarget 31 29029510
2017 Inflammatory milieu cultivated Sema3A signaling promotes chondrocyte apoptosis in knee osteoarthritis. Journal of cellular biochemistry 31 29111592
2015 Differential expression of sema3A and sema7A in a murine model of multiple sclerosis: Implications for a therapeutic design. Clinical immunology (Orlando, Fla.) 31 26686462
2011 Growth factor regulation of neural chemorepellent Sema3A expression in satellite cell cultures. American journal of physiology. Cell physiology 31 21865583
2009 Neuropilin-2 acts as a modulator of Sema3A-dependent glioma cell migration. Cell adhesion & migration 31 19855168
2019 Wnt/β-catenin signaling, which is activated in odontomas, reduces Sema3A expression to regulate odontogenic epithelial cell proliferation and tooth germ development. Scientific reports 30 30862786
2019 Disruption of Sema3A/Plexin-A1 inhibitory signalling in oligodendrocytes as a therapeutic strategy to promote remyelination. EMBO molecular medicine 29 31566924
2008 ERM proteins regulate growth cone responses to Sema3A. The Journal of comparative neurology 29 18651636
2017 Protein Tyrosine Phosphatase δ Mediates the Sema3A-Induced Cortical Basal Dendritic Arborization through the Activation of Fyn Tyrosine Kinase. The Journal of neuroscience : the official journal of the Society for Neuroscience 27 28637841
2024 Sema3A secreted by sensory nerve induces bone formation under mechanical loads. International journal of oral science 26 38238300
2017 Anti-SEMA3A Antibody: A Novel Therapeutic Agent to Suppress Glioblastoma Tumor Growth. Cancer research and treatment 26 29129044
2017 Decreased expression of Sema3A, an immune modulator, in blood sample of multiple sclerosis patients. Gene 25 28188869
2013 Overexpression of Sema3a in myocardial infarction border zone decreases vulnerability of ventricular tachycardia post-myocardial infarction in rats. Journal of cellular and molecular medicine 25 23711091
2018 ALS-related human cortical and motor neurons survival is differentially affected by Sema3A. Cell death & disease 24 29449528
2018 Aberrant Expression of miR-362 Promotes Lung Cancer Metastasis through Downregulation of Sema3A. Journal of immunology research 24 30155491
2021 Glucocorticoids suppressed osteoblast differentiation by decreasing Sema3A expression via the PIK3/Akt pathway. Experimental cell research 23 33838126
2018 Sema3a plays a role in the pathogenesis of CHARGE syndrome. Human molecular genetics 23 29432577
2017 SEMA3A partially reverses VEGF effects through binding to neuropilin-1. Stem cell research 23 28636974
2014 Sema3A maintains corneal avascularity during development by inhibiting Vegf induced angioblast migration. Developmental biology 23 24809797
2017 Sema3A drastically suppresses tumor growth in oral cancer Xenograft model of mice. BMC pharmacology & toxicology 22 28683823
2010 Focal adhesion kinase functions downstream of Sema3A signaling during axonal remodeling. Molecular and cellular neurosciences 22 20159040
2023 Sema3A Drives Alternative Macrophage Activation in the Resolution of Periodontitis via PI3K/AKT/mTOR Signaling. Inflammation 21 36598593
2020 miR-30b Promotes spinal cord sensory function recovery via the Sema3A/NRP-1/PlexinA1/RhoA/ROCK Pathway. Journal of cellular and molecular medicine 21 32977360
2018 Bu Shen Yi Sui capsule promotes remyelination correlating with Sema3A/NRP-1, LIF/LIFR and Nkx6.2 in mice with experimental autoimmune encephalomyelitis. Journal of ethnopharmacology 21 29428242
2014 CRMP1 Interacted with Spy1 During the Collapse of Growth Cones Induced by Sema3A and Acted on Regeneration After Sciatic Nerve Crush. Molecular neurobiology 21 25526860
2024 Axon guidance cue SEMA3A promotes the aggressive phenotype of basal-like PDAC. Gut 20 38670629
2019 Sema3a-Nrp1 Signaling Mediates Fast-Twitch Myofiber Specificity of Tw2+ Cells. Developmental cell 20 31474563
2019 Sema3A inhibits axonal regeneration of retinal ganglion cells via ROCK2. Brain research 19 31733191
2016 Cationic Peptides and Peptidomimetics Bind Glycosaminoglycans as Potential Sema3A Pathway Inhibitors. Biophysical journal 19 27028639
2000 Ectopic adenoviral vector-directed expression of Sema3A in organotypic spinal cord explants inhibits growth of primary sensory afferents. Developmental biology 19 10753505
2021 Cortical expression of IL1-β, Bcl-2, Caspase-3 and 9, SEMA-3a, NT-3 and P-glycoprotein as biological markers of intrinsic severity in drug-resistant temporal lobe epilepsy. Brain research 18 33516813
2020 SEMA3A and IGSF10 Are Novel Contributors to Combined Pituitary Hormone Deficiency (CPHD). Frontiers in endocrinology 18 32612575
2021 Knockdown of RMST Impedes Neuronal Apoptosis and Oxidative Stress in OGD/R-Induced Ischemic Stroke Via Depending on the miR-377/SEMA3A Signal Network. Neurochemical research 17 33409855
2020 Nestin Selectively Facilitates the Phosphorylation of the Lissencephaly-Linked Protein Doublecortin (DCX) by cdk5/p35 to Regulate Growth Cone Morphology and Sema3a Sensitivity in Developing Neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience 17 32273484
2020 MiR-203-3p inhibits the oxidative stress, inflammatory responses and apoptosis of mice podocytes induced by high glucose through regulating Sema3A expression. Open life sciences 17 33817280
2019 Semaphorin 3A (SEMA3A), protocadherin 9 (PCdh9), and S100 calcium binding protein A3 (S100A3) as potential biomarkers of carcinogenesis and chemoresistance of different neoplasms, including ovarian cancer - review of literature. Ginekologia polska 17 31059116
2010 Intrathecally administered Sema3A protein attenuates neuropathic pain behavior in rats with chronic constriction injury of the sciatic nerve. Neuroscience research 17 20888378
2007 Modulating Sema3A signal with a L1 mimetic peptide is not sufficient to promote motor recovery and axon regeneration after spinal cord injury. Molecular and cellular neurosciences 17 17997325
2003 Sema3A and neuropilin-1 expression and distribution in rat white adipose tissue. Journal of neurocytology 17 14724377
2023 Sema3A inactivates the ERK/JNK signalling pathways to alleviate inflammation and oxidative stress in lipopolysaccharide-stimulated rat endothelial cells and lung tissues. Autoimmunity 16 37128697
2019 Sema3a as a Novel Therapeutic Option for High Glucose-Suppressed Osteogenic Differentiation in Diabetic Osteopathy. Frontiers in endocrinology 16 31481931
2018 Sema3a inhibits the differentiation of Raw264.7 cells to osteoclasts under 2Gy radiation by reducing inflammation. PloS one 16 29975739
2018 The Neuropilin-1 Ligand, Sema3A, Acts as a Tumor Suppressor in the Pathogenesis of Acute Leukemia. Anatomical record (Hoboken, N.J. : 2007) 16 30378769
2013 Specific immobilization of biotinylated fusion proteins NGF and Sema3A utilizing a photo-cross-linkable diazirine compound for controlling neurite extension. Bioconjugate chemistry 16 23909702
2024 PIEZO1 Promotes Odontoblast-Mediated Reactionary Dentinogenesis via SEMA3A. Journal of dental research 15 38910430
2020 Sema3A and HIF1α co-overexpressed iPSC-MSCs/HA scaffold facilitates the repair of calvarial defect in a mouse model. Journal of cellular physiology 15 32012286
2013 Deletion of Sema3a or plexinA1/plexinA3 causes defects in sensory afferent projections of statoacoustic ganglion neurons. PloS one 15 23991118
2010 Sema-3A indirectly disrupts the regeneration process of goldfish optic nerve after controlled injury. Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie 15 20449604
2007 Role of the neuropilin ligands VEGF164 and SEMA3A in neuronal and vascular patterning in the mouse. Novartis Foundation symposium 15 18300426
2021 Long non-coding RNA Gm11974 aggravates oxygen-glucose deprivation-induced injury via miR-122-5p/SEMA3A axis in ischaemic stroke. Metabolic brain disease 14 34338972
2021 Sema3A accelerates bone formation during distraction osteogenesis in mice. Connective tissue research 13 34486459

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