Affinage

ANTXR1

Anthrax toxin receptor 1 · UniProt Q9H6X2

Length
564 aa
Mass
62.8 kDa
Annotated
2026-06-09
75 papers in source corpus 26 papers cited in narrative 26 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ANTXR1 (TEM8) is a type I transmembrane receptor with an integrin-like vWA domain that couples the extracellular matrix to the actin cytoskeleton and governs ECM homeostasis and pathological angiogenesis (PMID:22340594, PMID:23602711). Its extracellular vWA domain adopts an integrin fold and binds the C5 domain of collagen VI alpha3, the urokinase plasminogen activator (uPA), and the anthrax toxin protective antigen (PA) through a defined interface at residues 56-57 and 154-160, with Leu56 setting its lower PA affinity relative to CMG2 (PMID:14871805, PMID:20585457, PMID:30241478). Engagement of collagen drives endothelial adhesion, migration, and tube formation, requiring the vWA plus transmembrane domains, and TEM8 is essential for tumor-induced angiogenesis and xenograft growth (PMID:15777794, PMID:15993844, PMID:22340594). ANTXR1 surface availability is gated by N-glycosylation-dependent folding and ER quality control, by actin-binding proteins (alpha-smooth muscle actin, transgelin) that mask its extracellular epitope, and by post-translational control through ASB10-mediated ubiquitylation and K453 lactylation (PMID:25781883, PMID:21129411, PMID:34285210, PMID:40683418). Downstream, ANTXR1 activates a RhoC/ROCK1/SMAD5 axis driving cancer stemness and vasculogenic mimicry, and engages Wnt signaling via LRP6 and GSK3beta/beta-catenin to control self-renewal and gamma-globin repression (PMID:34285210, PMID:23832666, PMID:35942209). In vivo, ANTXR1 is required for anthrax toxin entry in kidney and spleen, acts downstream of Runx2 to set chondrocyte proliferation, and drives maladaptive cardiac collagen remodeling through TGFbeta (PMID:34871548, PMID:32244499, PMID:41039173). Loss-of-function mutations in ANTXR1 cause GAPO syndrome through defective ECM homeostasis (PMID:23602711).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2004 Medium

    Establishing that the TEM8 ectodomain recognizes a specific ECM ligand answered what this orphan tumor-endothelial marker physically binds, anchoring it to the extracellular matrix.

    Evidence Pulldown using the TEM8 extracellular domain as bait, with domain mapping to collagen alpha3(VI) C5

    PMID:14871805

    Open questions at the time
    • Binding affinity and stoichiometry not quantified
    • Functional consequence of the collagen VI interaction not yet established
  2. 2005 Medium

    Functional assays showed TEM8 is not merely a binder but an active mediator of endothelial adhesion, migration, and tube formation, defining its role in vessel morphogenesis.

    Evidence Overexpression, dominant-negative ectodomain, ribozyme knockdown, and domain-deletion constructs in endothelial and CHO cells

    PMID:15777794 PMID:15993844

    Open questions at the time
    • Did not identify the intracellular effectors linking TEM8 to the cytoskeleton
    • vWA+TM sufficiency for tubule formation tested only in CHO surrogate cells
  3. 2006 Medium

    Dissecting the anthrax intoxication pathway clarified which steps require ANTXR1 and showed the cytoplasmic tail is dispensable for toxin entry, defining the receptor's mechanistic contribution.

    Evidence ANTXR1 overexpression in RAW 264.7 macrophages with PA oligomerization, acidification inhibition, tail-deletion mutants, and apoptosis markers

    PMID:16882031

    Open questions at the time
    • Performed in overexpression macrophage model
    • Did not address physiological receptor levels
  4. 2007 Medium

    Mutagenesis of PA defined residue-level determinants distinguishing TEM8 from the related receptor CMG2, providing the basis for receptor-selective toxin targeting.

    Evidence Phage display selection and cytotoxicity assays in CHO cells expressing TEM8 or CMG2

    PMID:17251181

    Open questions at the time
    • Mapped the PA side of the interface but not yet the TEM8 side
    • Selectivity tested only in engineered CHO cells
  5. 2010 High

    The crystal structure plus structure-guided mutagenesis revealed an integrin fold and pinpointed the TEM8 PA-binding interface, explaining its lower toxin affinity relative to CMG2 and how the cytoskeleton can remodel its surface conformation.

    Evidence 1.7 A X-ray structure of the vWA domain with mutagenesis; separately, actin-binding protein overexpression with conformation-sensitive antibody readout

    PMID:20585457 PMID:21129411

    Open questions at the time
    • Structure limited to the isolated vWA domain
    • Mechanism linking intracellular actin proteins to ectodomain conformation not resolved at atomic level
  6. 2012 High

    Genetic knockout combined with antibody blockade established TEM8 as required for pathological angiogenesis and a therapeutic target across multiple tumor types.

    Evidence Tem8-/- mice, xenograft models of melanoma/breast/colon/lung, and anti-TEM8 ectodomain antibodies

    PMID:22340594

    Open questions at the time
    • Downstream signaling driving the angiogenic requirement not defined here
    • Distinction between tumor-cell-intrinsic and stromal roles incomplete
  7. 2013 High

    Human genetics tied ANTXR1 loss to GAPO syndrome and to ECM accumulation, while ligand stimulation linked the receptor to Wnt-driven cancer stemness, establishing its dual roles in ECM homeostasis and self-renewal.

    Evidence Whole-exome sequencing with NMD analysis and mouse phenotype comparison; C5A ligand stimulation, RNAi, mammosphere and in vivo metastasis assays

    PMID:23602711 PMID:23832666

    Open questions at the time
    • How loss of an ECM receptor causes excess ECM accumulation not mechanistically resolved in 2013
    • Direct biochemical link between ANTXR1 and LRP6/Wnt not yet shown
  8. 2016 Medium

    Rescue experiments defined ANTXR1 as a cell-autonomous, CTGF-dependent suppressor of collagen I and fibronectin, and showed surface delivery depends on N-glycosylation, mechanistically connecting receptor loss to ECM accumulation.

    Evidence Antxr1-/- primary fibroblasts with isoform re-expression and VEGF perturbation; N-glycosylation mutants with trafficking/ER quality control assays

    PMID:25781883 PMID:28011198

    Open questions at the time
    • The signaling intermediate between ANTXR1 and CTGF not identified
    • Relative contributions of CTGF versus VEGF arms not quantified in vivo
  9. 2020 High

    In vivo genetics and signaling profiling placed ANTXR1 in tissue-specific programs: a Runx2-driven role in chondrocyte proliferation, a RANKL-coupled role in osteoclast differentiation, and ovarian-cancer Rac1/JNK and MEK/ERK/STAT3 cascades under GATA2 transcriptional control.

    Evidence Antxr1 knockout and chondrocyte-specific transgenic mice; gain/loss-of-function in bone marrow macrophages; overexpression with pathway inhibitors and promoter binding in ovarian cancer cells

    PMID:30686531 PMID:32244499 PMID:32774719

    Open questions at the time
    • Whether the same downstream effectors operate across these tissues unknown
    • Dose sensitivity of chondrocyte phenotypes not mechanistically explained
  10. 2021 High

    Identification of the RhoC/ROCK1/SMAD5 cascade and the ASB10 E3 ligase defined both a stemness-driving downstream pathway and an upstream determinant of ANTXR1 protein abundance, and organ-resolved imaging clarified receptor utilization for anthrax toxin.

    Evidence Overexpression/knockdown with RhoC/ROCK1/pSMAD5 readouts, ubiquitylation and ASB10 co-IP in TNBC; LFn-NLS-Cre + PA in vivo imaging with TEM8/CMG2 knockout mice

    PMID:34285210 PMID:34871548

    Open questions at the time
    • How ANTXR1 activates RhoC at the membrane not defined
    • Trigger for ASB10-mediated turnover beyond ERalpha context unclear
  11. 2022 Medium

    Demonstrating a direct ANTXR1-LRP6 interaction provided the biochemical basis for ANTXR1 activation of Wnt/beta-catenin, extending its signaling role to gamma-globin repression.

    Evidence Co-IP for ANTXR1-LRP6, gain/loss-of-function and Wnt/GSK3beta pharmacological rescue in K562, CD34+, and HUDEP-2 cells

    PMID:35942209

    Open questions at the time
    • Single co-IP for the LRP6 interaction without structural mapping
    • Direct versus indirect control of SOX6 not fully separated
  12. 2024 High

    Multiple disease-model studies established ANTXR1 as a driver of maladaptive cardiac ECM remodeling and as a determinant of fibroblast senescence, reframing GAPO as a progeroid disorder and ANTXR1 as a cardiac therapeutic target.

    Evidence Antxr1 knockout and neutralizing antibodies across MI, pressure-overload, and HFpEF mouse models with TGFbeta pathway analysis; ANTXR1-deficient human fibroblasts with senescence, nuclear architecture, and actin assays; glioblastoma Src/PI3K/AKT/GSK3beta/beta-catenin profiling

    PMID:38653789 PMID:39191501 PMID:41039173

    Open questions at the time
    • How ANTXR1 loss accelerates senescence mechanistically not resolved
    • Connection between cardiac TGFbeta remodeling and the fibroblast ECM program not directly tested
  13. 2025 Medium

    Identification of K453 lactylation linked the tumor metabolic microenvironment to ANTXR1 stability and the RhoC/ROCK1/SMAD5 axis, and a CALCR interaction was reported to couple ANTXR1 to AKT signaling.

    Evidence Histone lactylation ChIP, mass-spec site mapping of K453, and gain/loss-of-function with xenografts; CALCR co-IP and knockdown with AKT readout in gastric cancer

    PMID:40195530 PMID:40683418

    Open questions at the time
    • CALCR-ANTXR1 link rests on a single co-IP with limited ANTXR1-specific follow-up
    • Enzyme depositing K453 lactylation not identified

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular events converting ANTXR1 ligand engagement into its divergent intracellular outputs (RhoC, Wnt/LRP6, MEK/ERK, AKT) and the unifying mechanism by which receptor loss produces ECM accumulation and senescence remain unresolved.
  • No structure of the full-length receptor or ligand-bound complexes beyond the vWA domain
  • Tissue-specific selection among downstream pathways unexplained
  • Direct cytoskeletal effectors of the cytoplasmic tail not identified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0001618 virus receptor activity 4 GO:0060089 molecular transducer activity 4 GO:0098631 cell adhesion mediator activity 3 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005886 plasma membrane 3 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1266738 Developmental Biology 3 R-HSA-1474244 Extracellular matrix organization 3 R-HSA-1643685 Disease 3
Partners
ASB10CALCRCOL6A3LRP6PLAU

Evidence

Reading pass · 26 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 TEM8/ANTXR1 extracellular domain binds the C5 domain of collagen alpha 3(VI); the TEM8-interacting region was mapped to the COOH-terminal C5 domain of collagen alpha 3(VI) using the extracellular domain of TEM8 as bait to identify ligands. Pulldown/ligand identification using TEM8 extracellular domain as bait Cancer research Medium 14871805
2005 TEM8 overexpression in endothelial cells enhances cell adhesion to collagen 3-fold and increases migration 3-fold; the recombinant TEM8 extracellular domain (TEM8-ED) binds preferentially to collagen and acts as a dominant-negative inhibitor of endogenous TEM8, blocking both adhesion and migration without affecting beta1 integrin activation. TEM8 protein expression is upregulated 5-fold upon initiation of tube formation in HUVEC. Overexpression in endothelial cells; dominant-negative extracellular domain inhibition; adhesion and migration assays (denudation, Boyden chamber); tube formation assay Experimental cell research Medium 15777794
2005 The vWA domain together with the transmembrane domain of TEM8 is required for tubule formation; knockdown of TEM8 via ribozyme transgene significantly reduced microvessel formation and migration in HECV endothelial cells. CHO cells expressing only the vWA+TM domains of TEM8 formed tubule-like structures, whereas other isolated domains did not. Ribozyme-mediated knockdown; domain deletion constructs transfected into CHO cells; microtubule/tube formation assay; migration assay Biochemical and biophysical research communications Medium 15993844
2007 TEM8 interacts with the M2 isoenzyme of pyruvate kinase (M2-PK); TEM8-Fc fusion protein (extracellular domain of TEM8 linked to Fc) trapped M2-PK and suppressed tumor growth and metastasis in xenograft models. Co-interaction/pulldown implied by TEM8-Fc trapping of M2-PK; in vivo xenograft tumor growth assays Journal of the National Cancer Institute Low 17925540
2007 Phage display selection identified PA domain 4 (residues 605-729) as the principal region contacting TEM8; substitutions R659S and M662R in PA enhanced specificity toward TEM8-overexpressing cells over CMG2-expressing cells, and N657Q significantly reduced toxicity on TEM8 but not CMG2 cells, demonstrating distinct residue-level determinants of PA binding to TEM8. Phage display selection; cellular cytotoxicity assays with CHO cells expressing TEM8 or CMG2 The Journal of biological chemistry Medium 17251181
2010 Crystal structure of the TEM8 extracellular vWA domain resolved at 1.7 Å reveals a typical integrin fold; structure-based mutagenesis identified residues 56, 57, and 154-160 as the PA-binding interface, with Leu56 being a key determinant of lower PA-binding affinity relative to CMG2. An L56A TEM8 variant showed increased affinity for PA. X-ray crystallography (1.7 Å); structure-based mutagenesis; PA binding affinity assays PloS one High 20585457
2010 The cell surface conformation of TEM8 is regulated by the actin cytoskeleton; overexpression of alpha-smooth muscle actin or transgelin (an actin-binding protein) converted TEM8 from an antibody-accessible (SB5-exposed) to an SB5-masked form on the cell surface, demonstrating that intracellular actin components alter TEM8 extracellular domain structure. Overexpression of actin-binding proteins; differential antibody recognition of cell surface TEM8; immunotoxin killing assays Biochimica et biophysica acta Medium 21129411
2012 Genetic disruption of Tem8 impairs growth of human tumor xenografts (melanoma, breast, colon, lung); antibodies against the TEM8 extracellular domain blocked anthrax intoxication, inhibited tumor-induced angiogenesis, and showed broad antitumor activity in vivo, establishing TEM8 as required for pathological angiogenesis. Genetic knockout (Tem8-/- mice); xenograft tumor growth assays; anti-TEM8 antibody blocking experiments Cancer cell High 22340594
2013 ANTXR1 activation by its natural ligand C5A (a collagen VI alpha3 fragment) increases cancer stem cell self-renewal (mammosphere assay) and activates Wnt signaling including upregulation of LRP6, phosphorylation of GSK3alpha/beta, and expression of Wnt target genes. RNAi silencing of ANTXR1 reduced LRP6 and ZEB1 expression, self-renewal, invasion, tumorigenicity, and metastasis. Ligand stimulation with C5A; RNAi knockdown; mammosphere assay; Western blot for Wnt pathway components; in vivo tumorigenicity/metastasis assays Cancer research Medium 23832666
2013 Loss-of-function mutations in ANTXR1 (nonsense, splicing) cause GAPO syndrome; nonsense mutations trigger nonsense-mediated mRNA decay resulting in loss of ANTXR1, and the major GAPO phenotypes (dental abnormalities, extracellular matrix accumulation) recapitulate Antxr1-mutant mouse phenotypes, establishing ANTXR1 as required for extracellular matrix homeostasis. Whole exome sequencing; identification of homozygous mutations; comparison to Antxr1-mutant mouse phenotype American journal of human genetics High 23602711
2016 In Antxr1-deficient primary fibroblasts, increased collagen type I (Col1a1) and fibronectin (Fn1) expression occurs via a cell-autonomous ANTXR1-dependent mechanism partly mediated through CTGF; VEGF signaling acts in parallel. Re-expression of the longest ANTXR1 isoform (sv1) in mutant fibroblasts decreased Ctgf, Col1a1, and Fn1 transcripts but had no effect on VEGF expression, demonstrating ANTXR1 regulation of ECM via a CTGF-dependent pathway. Primary fibroblasts from Antxr1+/+ and Antxr1-/- mice; shRNA knockdown of VEGF; rescue by ANTXR1 sv1 re-expression; VEGF neutralizing antibody; qRT-PCR/Western blot Matrix biology Medium 28011198
2016 TEM8 N-glycosylation is required for proper folding and trafficking to the cell surface; absence of N-linked glycans on either the vWA or Ig-like extracellular domains leads to misfolding and retention by ER quality control machinery, preventing surface expression. N-glycosylation mutants; cell surface trafficking assays; ER quality control assays PloS one Medium 25781883
2018 TEM8 functions as a receptor for urokinase plasminogen activator (uPA); uPA binding stimulates phosphorylation of TEM8 and augments EGFR and ERK1/2 phosphorylation. TEM8-Fc abrogated the TEM8-uPA interaction, blocked uPA-induced HepG2 cell migration in vitro, and inhibited MCF-7 xenograft growth and metastasis in vivo. Co-immunoprecipitation/pulldown; phosphorylation assays (Western blot); TEM8-Fc blocking; migration assay; xenograft mouse model Cell communication and signaling Medium 30241478
2020 ANTXR1 positively regulates RANKL-induced osteoclast differentiation and bone resorption; gain- and loss-of-function studies showed ANTXR1 affects phosphorylation of JNK, Akt, IkappaB, and PLCgamma2 and subsequently alters c-Fos and NFATc1 levels. ANTXR1 manipulation in bone marrow macrophages also modulated HUVECs tube formation via secretion of MMP-9 and VEGF-A, with no effect on osteoblast differentiation. Gain- and loss-of-function in bone marrow macrophages; osteoclast differentiation assay; phosphorylation Western blots; HUVEC tube formation assay; bone resorption assay Biochemical and biophysical research communications Medium 30686531
2020 TEM8 overexpression in ovarian cancer cells activates Rac1/Cdc42/JNK and MEK/ERK/STAT3 signaling pathways, promoting proliferation, G0/G1 transition, migration, and invasion while suppressing apoptosis. Pharmacological inhibition of RAC1 (EHop-016) or MEK (PD98059) suppressed malignant behaviors in TEM8-overexpressing cells. Transcription factor GATA2 binds the TEM8 promoter region (TATTAGTTATCTTT site) and regulates TEM8 expression. Overexpression; pathway inhibitor treatment; Western blot for phosphorylated signaling components; promoter binding assay (ChIP/luciferase implied); proliferation, apoptosis, migration, invasion assays American journal of translational research Medium 32774719
2020 Antxr1 is a direct transcriptional target of Runx2 in chondrocytes; Antxr1 deletion in mice results in shorter limbs from E16.5 due to reduced chondrocyte proliferation. Chondrocyte-specific Antxr1 transgenic overexpression also caused shortened limbs with increased BrdU uptake and apoptosis, accompanied by matrix mineralization, showing dose-sensitive roles in chondrocyte proliferation and apoptosis. Antxr1-/- mouse; chondrocyte-specific transgenic overexpression; BrdU incorporation assay; apoptosis assay; Runx2 target gene analysis; histological analysis of growth plates International journal of molecular sciences High 32244499
2021 TEM8 increases active RhoC levels and induces ROCK1-mediated phosphorylation of SMAD5, a signaling cascade essential for promoting cancer cell stemness and vasculogenic mimicry capacity in TNBC. ASB10, an ERalpha trans-activated E3 ligase, ubiquitylates TEM8 for proteasomal degradation; ASB10 deficiency in TNBC results in elevated TEM8 levels. Mechanistic dissection by overexpression/knockdown; Western blot for RhoC, ROCK1, pSMAD5; ubiquitylation assay; co-immunoprecipitation for ASB10-TEM8 interaction; vasculogenic mimicry assay Nature communications High 34285210
2021 In vivo imaging assay using LFn-NLS-Cre chimaeric protein with PA shows that TEM8 is required for anthrax toxin intoxication in the kidney and spleen, while CMG2 is dominant in liver, heart, and leukocytes; combined loss of both receptors completely abolishes intoxication, demonstrating organ-specific receptor utilization. Transgenic Cre-reporter mice; chimeric LFn-NLS-Cre protein + PA co-administration; confocal microscopy; flow cytometry; TEM8- and CMG2-deficient mice The Journal of biological chemistry High 34871548
2022 ANTXR1 interacts with LRP6 to promote nuclear entry of beta-catenin and activate Wnt/beta-catenin signaling, thereby repressing gamma-globin (HBG) expression. Overexpression of ANTXR1 decreased gamma-globin; knockdown increased it. The regulatory effect was reversed by XAV939 (Wnt inhibitor) and LiCl (GSK3beta inhibitor). ANTXR1 overexpression also increased c-Jun-mediated SOX6 transcription, which silences gamma-globin. Overexpression and knockdown in K562, CD34+ cord blood, HUDEP-2 cells; Co-IP for ANTXR1-LRP6 interaction; pharmacological modulation of Wnt pathway; ChIP/promoter analysis for SOX6 Journal of immunology research Medium 35942209
2024 ANTXR1 deficiency in human fibroblasts induces a senescent phenotype associated with defects in nuclear architecture and actin dynamics, proposing GAPO syndrome as a progeroid disorder. ANTXR1 knockdown/deficiency in human fibroblasts; senescence assays; nuclear architecture imaging; actin dynamics assays Scientific reports Medium 38653789
2024 ANTXR1 mediates collagen turnover in the heart; genetic disruption of Antxr1 or treatment with neutralizing antibodies prevented cardiac deterioration after acute myocardial infarction and improved function in pressure overload and obesity-induced heart failure models. Mechanistic studies revealed ANTXR1 antibody blockade improved post-infarct scar formation and attenuated late-stage chronic TGFbeta-mediated extracellular matrix remodeling. Antxr1 genetic knockout; neutralizing antibody treatment; multiple heart failure mouse models (MI, pressure overload, obesity-induced HFpEF); functional cardiac measurements; histological scar analysis; TGFbeta pathway assessment Nature cardiovascular research High 41039173
2025 CALCR (a G-protein-coupled receptor) physically interacts with ANTXR1 as shown by co-immunoprecipitation; CALCR knockdown decreased AKT phosphorylation, linking the CALCR-ANTXR1 complex to AKT signaling in gastric cancer. Co-immunoprecipitation; CALCR knockdown; Western blot for AKT phosphorylation; xenograft mouse model Scientific reports Low 40195530
2025 CAF-derived lactate promotes ANTXR1 transcription via histone lactylation and induces ANTXR1 lactylation at lysine 453. ANTXR1 K453 lactylation promotes protein stability and activates the RhoC/ROCK1/SMAD5 signaling pathway, driving colorectal cancer stemness and oxaliplatin resistance. Histone lactylation ChIP on ANTXR1 promoter; site-specific lactylation at K453 identified by mass spectrometry; gain/loss-of-function; Western blot for RhoC/ROCK1/SMAD5; CDX/PDX xenograft models Cancer letters Medium 40683418
2024 TEM8 overexpression in glioblastoma activates the Src/PI3K/AKT/GSK-3beta/beta-catenin pathway, leading to beta-catenin stabilization and activation of its transcriptional program; TEM8 overexpression promotes proliferation, invasion, migration, and chemo-radioresistance, while knockdown reverses these effects. Overexpression and knockdown; Western blot for Src, PI3K, AKT, GSK3beta, beta-catenin; proliferation, invasion, migration assays; DNA methylation array correlation Cancer genomics & proteomics Medium 39191501
2006 PA-induced cytotoxicity in macrophages overexpressing ANTXR1 requires direct interaction with ANTXR1, oligomerization of PA, channel formation, and endosomal acidification, but is independent of the ANTXR1 cytoplasmic tail. Overexpression of ANTXR1 extends PA-oligomer half-life and sensitizes cells to lethal toxin. PA-alone cytotoxicity proceeds via caspase-3 activation, DNA fragmentation, PARP cleavage, and Bid activation (apoptosis). ANTXR1 overexpression in RAW 264.7 macrophages; PA oligomerization assay; endosomal acidification inhibition; cytoplasmic tail deletion mutants; caspase activation assays; apoptosis markers Cellular microbiology Medium 16882031
2010 ANTXR1 is dynamically expressed in chick embryo and FGF signaling is sufficient (but not necessary) to induce ANTXR1 expression in facial mesenchyme; in vitro, ANTXR1 can link ECM components with the actin cytoskeleton to promote cell adhesion and spreading. Suppression subtractive hybridization screen; FGF gain-of-function/loss-of-function in chick embryo; cell adhesion assays Developmental dynamics Low 20034073

Source papers

Stage 0 corpus · 75 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2004 TEM8 interacts with the cleaved C5 domain of collagen alpha 3(VI). Cancer research 180 14871805
2017 TEM8/ANTXR1-Specific CAR T Cells as a Targeted Therapy for Triple-Negative Breast Cancer. Cancer research 138 29183891
2012 TEM8/ANTXR1 blockade inhibits pathological angiogenesis and potentiates tumoricidal responses against multiple cancer types. Cancer cell 135 22340594
2013 ANTXR1, a stem cell-enriched functional biomarker, connects collagen signaling to cancer stem-like cells and metastasis in breast cancer. Cancer research 104 23832666
2005 TEM8 expression stimulates endothelial cell adhesion and migration by regulating cell-matrix interactions on collagen. Experimental cell research 97 15777794
2005 ATR/TEM8 is highly expressed in epithelial cells lining Bacillus anthracis' three sites of entry: implications for the pathogenesis of anthrax infection. American journal of physiology. Cell physiology 86 15689409
2013 Mutations in ANTXR1 cause GAPO syndrome. American journal of human genetics 68 23602711
2021 TEM8 marks neovasculogenic tumor-initiating cells in triple-negative breast cancer. Nature communications 61 34285210
2024 Residual ANTXR1+ myofibroblasts after chemotherapy inhibit anti-tumor immunity via YAP1 signaling pathway. Nature communications 42 38346978
2007 Antitumor activities of TEM8-Fc: an engineered antibody-like molecule targeting tumor endothelial marker 8. Journal of the National Cancer Institute 42 17925540
2011 Targeting the anthrax receptors, TEM-8 and CMG-2, for anti-angiogenic therapy. Frontiers in bioscience (Landmark edition) 41 21196249
2010 The cell surface structure of tumor endothelial marker 8 (TEM8) is regulated by the actin cytoskeleton. Biochimica et biophysica acta 38 21129411
2018 MSLN (Mesothelin), ANTXR1 (TEM8), and MUC3A are the potent antigenic targets for CAR T cell therapy of gastric adenocarcinoma. Journal of cellular biochemistry 37 30260046
2019 TEM8/ANTXR1-specific CAR T cells mediate toxicity in vivo. PloS one 35 31622431
2010 The structure of tumor endothelial marker 8 (TEM8) extracellular domain and implications for its receptor function for recognizing anthrax toxin. PloS one 35 20585457
2007 Selection of anthrax toxin protective antigen variants that discriminate between the cellular receptors TEM8 and CMG2 and achieve targeting of tumor cells. The Journal of biological chemistry 34 17251181
2005 TEM-8 and tubule formation in endothelial cells, its potential role of its vW/TM domains. Biochemical and biophysical research communications 27 15993844
2004 Tumour endothelial marker 8 (TEM-8) in human colon cancer and its association with tumour progression. European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology 26 15498639
2017 MicroRNA-493 suppresses hepatocellular carcinoma tumorigenesis through down-regulation of anthrax toxin receptor 1 (ANTXR1) and R-Spondin 2 (RSPO2). Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 25 28651234
2018 Seneca Valley Virus Exploits TEM8, a Collagen Receptor Implicated in Tumor Growth. Frontiers in oncology 24 30460197
2025 Cancer associated fibroblasts-derived lactate induces oxaliplatin treatment resistance by promoting cancer stemness via ANTXR1 lactylation in colorectal cancer. Cancer letters 20 40683418
2021 N-Myc promotes angiogenesis and therapeutic resistance of prostate cancer by TEM8. Medical oncology (Northwood, London, England) 20 34523032
2014 Whole exome sequencing identifies three novel mutations in ANTXR1 in families with GAPO syndrome. American journal of medical genetics. Part A 20 25045128
2022 TEM8 Tri-specific Killer Engager binds both tumor and tumor stroma to specifically engage natural killer cell anti-tumor activity. Journal for immunotherapy of cancer 19 36162918
2019 MicroRNA-26b-3p/ANTXR1 signaling modulates proliferation, migration, and apoptosis of glioma. American journal of translational research 18 31934301
2014 Immuno-PET imaging of tumor endothelial marker 8 (TEM8). Molecular pharmaceutics 18 24984190
2020 Overexpression of TEM8 promotes ovarian cancer progression via Rac1/Cdc42/JNK and MEK/ERK/STAT3 signaling pathways. American journal of translational research 17 32774719
2010 Dendritic cells transduced with TEM8 recombinant adenovirus prevents hepatocellular carcinoma angiogenesis and inhibits cells growth. Vaccine 17 20650339
2006 Cytotoxic activity of Bacillus anthracis protective antigen observed in a macrophage cell line overexpressing ANTXR1. Cellular microbiology 17 16882031
2019 The Anthrax Toxin Receptor 1 (ANTXR1) Is Enriched in Pancreatic Cancer Stem Cells Derived from Primary Tumor Cultures. Stem cells international 16 31191663
2016 Cell autonomous ANTXR1-mediated regulation of extracellular matrix components in primary fibroblasts. Matrix biology : journal of the International Society for Matrix Biology 16 28011198
2020 Antxr1, Which is a Target of Runx2, Regulates Chondrocyte Proliferation and Apoptosis. International journal of molecular sciences 15 32244499
2019 ANTXR1 (TEM8) overexpression in gastric adenocarcinoma makes the protein a potential target of immunotherapy. Cancer immunology, immunotherapy : CII 15 31520110
2016 Anthrax Toxin Protective Antigen Variants That Selectively Utilize either the CMG2 or TEM8 Receptors for Cellular Uptake and Tumor Targeting. The Journal of biological chemistry 15 27555325
2013 Identification of small molecules that inhibit the interaction of TEM8 with anthrax protective antigen using a FRET assay. Journal of biomolecular screening 15 23479355
2017 Effect of silencing TEM8 gene on proliferation, apoptosis, migration and invasion of XWLC‑05 lung cancer cells. Molecular medicine reports 14 29115620
2012 Broad expression analysis of human ANTXR1/TEM8 transcripts reveals differential expression and novel splizce variants. PloS one 14 22912819
2009 Detection of epithelial cells by RT-PCR targeting CEA, CK20, and TEM-8 in colorectal carcinoma patients using OncoQuick density gradient centrifugation system. The Journal of surgical research 14 19645077
2018 A biallelic ANTXR1 variant expands the anthrax toxin receptor associated phenotype to tooth agenesis. American journal of medical genetics. Part A 13 29436111
2018 GAPO syndrome in seven new patients: Identification of five novel ANTXR1 mutations including the first large intragenic deletion. American journal of medical genetics. Part A 13 30575274
2024 Mechanical strain regulates osteogenesis via Antxr1/LncRNA H19/Wnt/β-catenin axis. Journal of cellular physiology 12 38358001
2023 ANTXR1 as a potential sensor of extracellular mechanical cues. Acta biomaterialia 12 36638946
2016 New ANTXR1 Gene Mutation for GAPO Syndrome: A Case Report. Molecular syndromology 12 27587992
2021 KLF7 Promotes Gastric Carcinogenesis Through Regulation of ANTXR1. Cancer management and research 11 34285576
2006 Expression and purification of functional human anthrax toxin receptor (ATR/TEM8) binding domain from Escherichia coli. Protein expression and purification 11 16798009
2020 Low doses of deoxynivalenol inhibit the cell migration mediated by H3K27me3-targeted downregulation of TEM8 expression. Biochemical pharmacology 10 32135158
2019 Role of ANTXR1 in the regulation of RANKL-induced osteoclast differentiation and function. Biochemical and biophysical research communications 9 30686531
2010 Expression and regulation of ANTXR1 in the chick embryo. Developmental dynamics : an official publication of the American Association of Anatomists 9 20034073
2018 ANTXR1 Intronic Variants Are Associated with Fetal Hemoglobin in the Arab-Indian Haplotype of Sickle Cell Disease. Acta haematologica 8 30114697
2018 TEM8 functions as a receptor for uPA and mediates uPA-stimulated EGFR phosphorylation. Cell communication and signaling : CCS 7 30241478
2024 ANTXR1 deficiency promotes fibroblast senescence: implications for GAPO syndrome as a progeroid disorder. Scientific reports 6 38653789
2023 A Novel tRNA-Derived Fragment, tRFGlnCTG, Regulates Angiogenesis by Targeting Antxr1 mRNA. International journal of molecular sciences 6 37833999
2021 Targeted silencing of TEM8 suppresses non‑small cell lung cancer tumor growth via the ERK/Bcl‑2 signaling pathway. Molecular medicine reports 6 34165155
2015 Differential dependence on N-glycosylation of anthrax toxin receptors CMG2 and TEM8. PloS one 6 25781883
2024 DNA Methylation in Recurrent Glioblastomas: Increased TEM8 Expression Activates the Src/PI3K/AKT/GSK-3β/B-Catenin Pathway. Cancer genomics & proteomics 5 39191501
2021 miR-381-3p Involves in Glioma Progression by Suppressing Tumor-Promoter Factor ANTXR1. Computational and mathematical methods in medicine 5 34956398
2023 TEM8 in Oncogenesis: Protein Biology, Pre-Clinical Agents, and Clinical Rationale. Cells 4 37998358
2021 Imaging of anthrax intoxication in mice reveals shared and individual functions of surface receptors CMG-2 and TEM-8 in cellular toxin entry. The Journal of biological chemistry 4 34871548
2016 In situ targeting TEM8 via immune response and polypeptide recognition by wavelength-modulated surface plasmon resonance biosensor. Scientific reports 4 26822761
2011 TEM8 targeted cancer therapy. Anti-cancer agents in medicinal chemistry 4 22023048
2025 CALCR interaction with ANTXR1 drives gastric tumor growth and metastasis via AKT signaling pathway. Scientific reports 3 40195530
2017 A novel mutation at ANTXR1 in an Indian patient with growth retardation-alopecia-pseudoanodontia-optic atrophy syndrome. Oral surgery, oral medicine, oral pathology and oral radiology 3 28870703
2016 ANTXR-1 and -2 independent modulation of a cytotoxicity mediated by anthrax toxin in human cells. The Journal of veterinary medical science 3 27170489
2024 GAPO syndrome: a novel variant in ANTXR1 gene. Ophthalmic genetics 2 38691016
2024 Abnormal dental phenotypes in GAPO syndrome: A descriptive study with a new ANTXR1 variant & insights on teeth eruption. The Saudi dental journal 2 39286584
2022 Transmembrane Protein ANTXR1 Regulates γ-Globin Expression by Targeting the Wnt/β-Catenin Signaling Pathway. Journal of immunology research 2 35942209
2025 ANTXR1 blockade enhances cardiac function in preclinical models of heart failure. Nature cardiovascular research 1 41039173
2024 Prenatal onset GAPO syndrome with a novel ANTXR1 variant in an Indian child: Expansion of the phenotype & literature review. European journal of medical genetics 1 38423276
2023 Depleting ANTXR1 suppresses glioma growth via deactivating PI3K/AKT pathway. Cell cycle (Georgetown, Tex.) 1 37974357
2022 ANTXR1 Regulates Erythroid Cell Proliferation and Differentiation through wnt/β-Catenin Signaling Pathway In Vitro and in Hematopoietic Stem Cell. Disease markers 1 36065334
2026 Expression and clinical significance of TEM8 protein in triple-negative breast cancer. Science progress 0 41505341
2026 The genomic, transcriptomic, and immunologic landscape of TEM8 (ANTXR1) in neuroendocrine neoplasms (NENs) including small-cell lung cancer (SCLC). Cancer treatment and research communications 0 42061011
2026 Identification of the target ANTXR1 and covalent acylation mechanism of 8-esterified cycloberberines against cancer. European journal of medicinal chemistry 0 42143941
2026 Comprehensive multi-omics pan-cancer analysis revealed that ANTXR1 is a potential biomarker for diagnosis and immunotherapy. Biology direct 0 42251445
2025 The mechanosensitive protein ANTXR1 is involved in maintaining cartilage homeostasis in post-traumatic osteoarthritis. Frontiers in cell and developmental biology 0 40970092

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