Affinage

CDON

Cell adhesion molecule-related/down-regulated by oncogenes · UniProt Q4KMG0

Length
1287 aa
Mass
139.1 kDa
Annotated
2026-06-09
100 papers in source corpus 45 papers cited in narrative 45 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

CDON (CDO) is a cell-surface co-receptor of the immunoglobulin/fibronectin type III superfamily that integrates Hedgehog (HH) signaling and cell-adhesion cues to drive cell-fate specification and differentiation across multiple developmental contexts (PMID:9214393, PMID:16647304, PMID:20160094). As a HH co-receptor, CDON binds all three mammalian HH ligands through its third FNIII repeat in a calcium-dependent interaction whose structural details were resolved by crystallography, and it positively transduces the signal by physically associating with PTCH1 and GAS1; HPE-causing missense mutations in human CDON spare SHH binding but disrupt these inter-receptor associations, establishing CDON-PTCH1/GAS1 complexes as essential for signaling (PMID:16647304, PMID:18794898, PMID:20519495, PMID:21802063). CDON acts collectively and non-redundantly with the related co-receptors BOC and GAS1, and combinatorial mouse genetics show an obligatory requirement for these proteins in HH-dependent ventral neural patterning, craniofacial, vertebral, and limb development (PMID:17504941, PMID:21664576, PMID:36265686). Loss of CDON in mice produces holoprosencephaly, and this phenotype is exacerbated by fetal ethanol exposure through synergistic inhibition of Shh and Nodal signaling, defining a gene-environment interaction (PMID:12620190, PMID:16647303, PMID:23071453, PMID:32876567). In a ligand-specific manner CDON also scaffolds an intracellular signaling module: N-cadherin ligation (but not SHH binding) recruits the scaffold JLP together with Bnip-2, which stimulates Cdc42 and downstream TAK1/ASK1-MKK6 to activate p38α/β MAPK and drive myogenic and neuronal differentiation, in part by enhancing bHLH/E-protein heterodimerization; CDON additionally promotes AKT activation through APPL1 and PKN2 (PMID:11782431, PMID:17074887, PMID:18678706, PMID:19244314, PMID:20160094, PMID:20484574, PMID:22337877, PMID:27763641). Through its Ig2 ectodomain, CDON binds LRP6 and negatively regulates canonical Wnt/β-catenin signaling, a function required to restrain proliferation in the forebrain, prevent Cx43 dysregulation and cardiac fibrosis, and suppress osteogenic VSMC calcification (PMID:25406935, PMID:28154134, PMID:36609601). In specific tissues such as the optic vesicle and endothelium, CDON instead behaves as a Patched-independent decoy receptor that sequesters HH ligand and limits its dispersion, and in the absence of SHH it acts as a dependence receptor whose intracellular domain is proteolytically cleaved to recruit and activate caspase-9, triggering apoptosis (PMID:23940460, PMID:25001599, PMID:33028094).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 1997 Medium

    Establishing CDO as a novel adhesion-regulated Ig-superfamily surface glycoprotein defined the structural platform from which all later co-receptor functions were dissected.

    Evidence Molecular cloning and expression/adhesion analyses identifying five Ig and three FNIII repeats plus a cytoplasmic tail

    PMID:9214393

    Open questions at the time
    • No ligand or signaling partner identified at cloning
    • Functional role undefined
  2. 1998 High

    Linking CDO to a MyoD positive-feedback loop established it as a positive regulator of differentiation, not merely a structural surface protein.

    Evidence Overexpression, soluble ectodomain inhibition, and dominant-negative constructs in C2C12 myoblasts

    PMID:9786951

    Open questions at the time
    • Molecular mechanism downstream of CDO unknown
    • Cytoplasmic effectors not identified
  3. 2002 High

    Identifying cis-complex formation with BOC introduced the concept of a CDO co-receptor network acting in differentiation.

    Evidence Reciprocal co-IP and dominant-negative epistasis in myoblast differentiation assays

    PMID:11782431

    Open questions at the time
    • Shared ligand not yet known
    • Stoichiometry of CDO-BOC complex undefined
  4. 2003 High

    The holoprosencephaly-like facial phenotype of Cdon knockout mice provided the first in vivo evidence for a role in midline development, anticipating its HH connection.

    Evidence Targeted knockout and morphological analysis in mice

    PMID:12620190

    Open questions at the time
    • Causative pathway (HH) not yet established
    • Cellular basis of facial defect unresolved
  5. 2006 High

    Demonstrating that CDO/BOC bind SHH via a specific FNIII repoat and the Drosophila ortholog Ihog acts at/upstream of Patched defined CDON as a HH-pathway co-receptor operating at the level of signal reception and Gli.

    Evidence Knockout and ectopic-expression mouse genetics, binding assays, neural tube patterning, and Drosophila RNAi/epistasis

    PMID:16630821 PMID:16647303 PMID:16647304

    Open questions at the time
    • Structural basis of ligand binding unresolved
    • Mechanism of Gli-level regulation unclear
  6. 2006 High

    Mapping the CDO intracellular tail to a JLP/p38αβ MAPK module and identifying a parallel role in neuronal bHLH activation revealed a ligand-receptor-independent intracellular signaling output.

    Evidence Co-IP, kinase assays, MKK6 rescue in Cdo-/- myoblasts, and reporter/heterodimerization assays in neural cells

    PMID:16648472 PMID:17074887

    Open questions at the time
    • Upstream activating ligand for p38 axis not defined in 2006
    • Link between p38 and bHLH activity incomplete
  7. 2007 High

    Genetic cooperation between Gas1 and Cdo established that HH-binding cell-surface proteins function combinatorially rather than independently.

    Evidence Gas1;Cdo double-mutant mice with Shh target gene analysis across multiple tissues

    PMID:17504941

    Open questions at the time
    • Molecular nature of cooperation not defined
    • Whether the proteins form a physical complex unresolved
  8. 2008 High

    The ShhN-CDO crystal structure and identification of a Bnip-2-Cdc42 arm provided atomic-level and mechanistic detail for both the HH-binding and intracellular signaling functions.

    Evidence X-ray crystallography with calcium-site mutagenesis (ShhN-CDO) and co-IP/activity assays defining Cdo-Bnip-2-Cdc42-p38

    PMID:18678706 PMID:18794898

    Open questions at the time
    • How calcium-site disease mutations differentially affect each co-receptor not fully resolved
    • Spatial coordination of intracellular complex assembly unclear
  9. 2009 Medium

    Adding Abl kinase to the CDO intracellular complex and extending the Cdc42/p38 logic to neurogenesis refined the differentiation signaling cascade.

    Evidence Co-IP/domain mapping with kinase assays in myoblasts and overexpression/RNAi in neural precursors

    PMID:19244314 PMID:19470755

    Open questions at the time
    • Ordering of Abl relative to other effectors incomplete
    • Single-lab findings for neural extension
  10. 2010 High

    Defining the ligand-specific switch (N-cadherin activates p38; SHH does not) plus crystallographic confirmation of a conserved pan-HH binding mode and demonstration of collective co-receptor requirement unified the dual roles of CDON.

    Evidence N-cadherin ligation with co-IP/IF, Hh-CDO/BOC crystal structures, triple-knockout mouse genetics, and APPL1-Akt rescue assays

    PMID:20160094 PMID:20484574 PMID:20519495 PMID:21183473 PMID:21664576

    Open questions at the time
    • How the receptor switches partner assembly between ligands mechanistically unresolved
    • Divergence of vertebrate vs Drosophila co-receptor essentiality not fully explained
  11. 2011 High

    Human CDON mutations causally linked to HPE through disrupted CDON-PTCH1/GAS1 interactions established the clinical relevance and pinpointed inter-receptor binding as the critical signaling step.

    Evidence Patient mutation analysis, cell-based Shh signaling assays, and co-IP of CDON with PTCH1/GAS1; plus Gas1-Cdo p38 complex in myoblasts

    PMID:21802063 PMID:21820049

    Open questions at the time
    • How CDON physically bridges PTCH1 and GAS1 structurally undefined
    • Variant penetrance/modifiers in patients unresolved
  12. 2012 Medium

    Adding TAK1/ASK1 MAP3Ks, Stim1/NFAT, and Cx43 to the CDO complex broadened the intracellular signaling and trafficking repertoire underlying differentiation, while a gene-environment HPE model was established.

    Evidence Co-IP, knockout-cell rescue, phospho-site mutagenesis, FRET imaging, and Cdon-/- ethanol exposure with Shh readouts

    PMID:22298426 PMID:22337877 PMID:22930637 PMID:23071453

    Open questions at the time
    • Cx43 interaction lacks functional/domain validation (imaging only)
    • Integration of Ca2+/NFAT and p38 arms unresolved
  13. 2013 High

    Defining CDON as a SHH dependence receptor that triggers caspase-9 apoptosis when unbound, plus an esophageal muscle role, revealed pro-apoptotic and morphogenetic functions distinct from canonical signaling promotion.

    Evidence Apoptosis/caspase-9 assays, intracellular-domain cleavage analysis, tumor models, and Cdo-/- esophageal phenotyping

    PMID:23569214 PMID:23940460

    Open questions at the time
    • Identity of the protease cleaving the CDON intracellular domain unknown
    • Physiological contexts where dependence-receptor activity dominates undefined
  14. 2014 High

    Establishing CDON as a Patched-independent decoy receptor in the optic vesicle and as an LRP6-binding Wnt suppressor revealed negative-regulatory functions opposite to its co-receptor role.

    Evidence Zebrafish/chick localization and Hh-distribution assays; Ig2-LRP6 co-IP, Wnt reporters, and Cdo-/- forebrain analysis

    PMID:25001599 PMID:25406935

    Open questions at the time
    • What determines decoy vs co-receptor behavior in a given tissue unresolved
    • Whether Wnt inhibition and HH decoy functions are mechanistically linked unclear
  15. 2015 Medium

    Distinguishing CDON from BOC mechanistically and defining roles in neural crest migration and surface trafficking refined how the co-receptors and their adhesion functions are deployed.

    Evidence Domain dissection in chick spinal cord, zebrafish NCC knockdown/transplantation, and Stx4 co-IP/surface biotinylation

    PMID:25848697 PMID:26256768 PMID:26347807

    Open questions at the time
    • Membrane-attachment requirement of CDON mechanistically unexplained
    • Single-lab trafficking findings
  16. 2016 High

    Extending CDON to cardiac Wnt suppression, cardiomyogenesis via Shh, Kir2.1 channel surface delivery, and PKN2-AKT signaling demonstrated broad tissue deployment of its dual signaling modes.

    Evidence Cdo-/- cardiac phenotyping with Wnt-inhibitor rescue, ES/P19 cardiomyogenesis with Shh agonist rescue, electrophysiology, and PKN2 co-IP/AKT assays

    PMID:26906632 PMID:27380411 PMID:27763641 PMID:28154134

    Open questions at the time
    • How CDON simultaneously balances Wnt suppression and Shh promotion in heart unresolved
    • Mechanism of channel surface stabilization incomplete
  17. 2018 Medium

    Identifying Ash1L as a Trithorax activator of Cdon transcription placed CDON within an epigenetic regulatory circuit controlling myoblast fusion.

    Evidence RNA-seq/ChIP-seq and Ash1L loss-of-function with myoblast fusion assays

    PMID:30487570

    Open questions at the time
    • Direct vs indirect transcriptional control not fully resolved
    • Other upstream regulators of Cdon expression unknown
  18. 2020 High

    Tissue-specific knockouts linked CDON to satellite-cell FGFR/integrin signaling, endothelial Dhh decoy function, and Nodal-dependent HPE synergy, extending its roles into regeneration, vascular biology, and morphogen crosstalk.

    Evidence Conditional Cdon knockouts with co-IP/surface analysis (FGFR), EC binding/permeability assays, and Cdon-/- ethanol Nodal assays

    PMID:32103583 PMID:32876567 PMID:33028094

    Open questions at the time
    • Whether FGFR/ErbB regulation reflects a general trafficking role unresolved
    • Mechanism by which CDON discriminates Dhh decoy vs promotion in endothelium unclear
  19. 2021 Medium

    Placing BOC/CDON in a Dispatched co-receptor complex on SHH-producing cells revealed a presynaptic-side role in cytoneme-mediated ligand delivery, broadening CDON function beyond the receiving cell.

    Evidence Live imaging, Myo10 knockout mice, DISP-BOC/CDON co-IP, and time-lapse neural tube signaling

    PMID:33570491

    Open questions at the time
    • Whether CDON's producing-cell and receiving-cell roles are separable unresolved
    • Single-lab cytoneme mechanism
  20. 2023 High

    Demonstrating Ig2-dependent Wnt suppression in VSMC calcification and CDON's requirement in motor neuron survival/neurotrophin signaling consolidated its dual roles in disease-relevant tissues.

    Evidence VSMC-specific knockout with recombinant Ig2 rescue and Wnt reporters; motor neuron-specific knockout with NRG1/Akt and ErbB4/FGFR analysis

    PMID:36609601 PMID:37559423

    Open questions at the time
    • How a single Ig2 domain mediates LRP6 binding across diverse tissues structurally undefined
    • Integration of neurotrophin-receptor regulation with HH functions unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CDON selects between its opposing molecular outputs—HH co-receptor, HH decoy, Wnt suppressor, intracellular p38/AKT scaffold, and apoptotic dependence receptor—within a given cell remains unresolved at a mechanistic level.
  • No unifying model for context-dependent partner selection
  • Protease responsible for dependence-receptor cleavage unidentified
  • Structural basis of CDON-PTCH1/GAS1 and CDON-LRP6 complexes undefined

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:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 3 GO:0098631 cell adhesion mediator activity 2
Localization
GO:0005886 plasma membrane 5
Pathway
R-HSA-162582 Signal Transduction 6 R-HSA-1266738 Developmental Biology 4 R-HSA-5357801 Programmed Cell Death 1
Partners
ABL1APPL1BNIP2BOCGAS1JLPLRP6PTCH1
Complex memberships
CDON-BOC co-receptor complexCDON-JLP-Bnip-2 p38 signaling complexCDON-PTCH1-GAS1 HH receptor complexDISP-BOC/CDON cytoneme complex

Evidence

Reading pass · 45 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 CDO is a novel cell surface glycoprotein of the Ig superfamily containing five Ig-like repeats, three fibronectin type III-like repeats in the extracellular region, and a 256-amino acid intracellular region. Its mRNA is down-regulated by serum stimulation and constitutively down-regulated in oncogene-transformed cells; CDO protein levels are also regulated post-transcriptionally by cell-substratum adhesion. Molecular cloning, Northern blot, Western blot, cell adhesion assays The Journal of cell biology Medium 9214393
1998 CDO positively regulates myogenic differentiation: overexpression of CDO in C2C12 myoblasts accelerates differentiation, while soluble extracellular regions of CDO inhibit differentiation. CDO and MyoD are involved in a positive feedback loop — oncogenic Ras down-regulates MyoD, and re-expression of CDO in C2C12/Ras cells induces MyoD; conversely, MyoD induces CDO expression. Overexpression, dominant-negative constructs, differentiation assays in C2C12 myoblasts The Journal of cell biology High 9786951
2002 BOC associates with CDO to form cis-acting complexes via both their ectodomains and intracellular domains. BOC accelerates myoblast differentiation in a CDO-dependent manner (a dominant-negative form of CDO inhibits the promyogenic effects of soluble BOC), placing BOC downstream of or in complex with CDO for myogenesis. Co-immunoprecipitation, soluble fusion protein overexpression, dominant-negative CDO, myoblast differentiation assays The EMBO journal High 11782431
2003 Mice homozygous for targeted mutations of Cdon display hallmark facial defects associated with microforms of holoprosencephaly (HPE), demonstrating a role for Cdon in facial midline development in vivo. Targeted gene knockout in mice, morphological analysis Current biology : CB High 12620190
2004 CDO functions to activate myogenic bHLH factors (MyoD family) via enhanced heterodimer formation, most likely by inducing hyperphosphorylation of E proteins; mice lacking CDO display delayed skeletal muscle development and satellite cells from these mice differentiate defectively in vitro. CDO knockout mice, satellite cell cultures, co-immunoprecipitation, reporter assays for bHLH heterodimer activity Developmental cell High 15572127
2006 Cdo and Boc bind Sonic Hedgehog (Shh) through a high-affinity interaction with a specific fibronectin repeat that is essential for activity. Ectopic expression of Cdo or Boc results in Shh-dependent, cell-autonomous promotion of ventral cell fates. Loss of Cdo produces a Shh dosage-dependent reduction of the floor plate. Cdo and Boc are also transcriptional targets negatively regulated by Hedgehog signaling. Genetic loss-of-function (knockout mice), gain-of-function (ectopic expression), binding assays, neural tube patterning analysis Developmental cell High 16647304
2006 Cdo-deficient mice display holoprosencephaly with strain-specific severity without limb defects, modeling human HPE. Shh target gene expression is reduced in developing forebrains of Cdo-/- mice. Cdo positively regulates Shh signaling in vitro at multiple levels including signal reception and via a parallel mechanism required at the level of Gli transcription factors. Specific Cdo domains required for promyogenic effects are dispensable for Shh signaling. Cdo knockout mice, Shh target gene expression analysis (in situ hybridization), cell-based Shh signaling assays, domain-deletion constructs Developmental cell High 16647303
2006 CDO promotes neuronal differentiation and cotransfection of CDO enhances the activity of neurogenic bHLH factor neurogenin1 in reporter assays, enhancing heterodimerization of neurogenin1 and E47. Cdo-/- mice on C57BL/6 background display hydrocephalus and cortical thinning, and primary neural progenitors from Cdo-/- mutants show reduced proliferation. CDO knockout mice, neuronal precursor cell overexpression/RNAi, reporter assays, co-immunoprecipitation for bHLH heterodimerization Molecular and cellular biology Medium 16648472
2006 Ihog (Drosophila ortholog of CDON) binds Hedgehog protein through its first extracellular fibronectin type III (FNIII) domain; the second FNIII domain is additionally required for in vivo signaling and for Ihog-enhanced binding of Hh to cells co-expressing Patched. Epistasis analysis places ihog action at or upstream of Patched. Other Ihog family members including mammalian CDO also interact with Hh ligands via a specific FNIII domain. RNAi in Drosophila cultured cells, in vitro binding assays (pulldown), genetic epistasis analysis, loss-of-function mutations in Drosophila Cell High 16630821
2006 The intracellular region of Cdo interacts with JLP, a scaffold protein for the p38alpha/beta MAPK pathway. Cdo, JLP, and p38alpha/beta form complexes in differentiating myoblasts. Cdo and JLP cooperate to enhance levels of active p38alpha/beta. Primary myoblasts from Cdo-/- mice are deficient in p38alpha/beta activity, and expression of activated MKK6 rescues differentiation of Cdo-/- cells. Co-immunoprecipitation, kinase activity assays, Cdo-/- primary myoblasts, rescue experiments with activated MKK6 The Journal of cell biology High 17074887
2007 Gas1 and Cdo cooperate to promote Shh signaling during neural tube patterning, craniofacial, and vertebral development. Gas1;Cdo double mutant mice show more severe Shh-dependent defects than either single mutant, establishing a genetic interaction between these two Shh-binding cell surface proteins. Genetic double knockout mice, in situ hybridization for Shh target genes, ectopic expression assays Genes & development High 17504941
2008 X-ray crystallography revealed the structure of the ShhN-CDO complex; the ShhN binds to the third FNIII repeat of CDO (not the orthologous FNIII repeat used by Drosophila Ihog). The ShhN-CDO interaction requires calcium, which binds at a previously undetected site on ShhN conserved in nearly all Hh proteins. Mutations in vertebrate Hh proteins causing holoprosencephaly and brachydactyly type A1 map to this calcium-binding site and disrupt interactions with CDO, Ptc, Hip, and Gas1. X-ray crystallography, biophysical binding assays (ITC, SPR), pulldown experiments, mutagenesis Nature High 18794898
2008 Cdo also interacts with Bnip-2, a regulator of Cdc42, and with JLP; Bnip-2 and JLP are brought together through mutual interaction with Cdo. The Cdo-Bnip-2 interaction stimulates Cdc42 activity, which in turn promotes p38alpha/beta activity and myoblast differentiation. This defines a Cdo-Bnip-2-Cdc42 signaling pathway upstream of p38 MAPK. Co-immunoprecipitation, gain- and loss-of-function experiments in myoblasts, Cdc42 activity assays, p38 activity assays The Journal of cell biology High 18678706
2009 Abl tyrosine kinase associates with both Cdo and JLP during myoblast differentiation. Abl binds a proline-rich motif in the Cdo intracellular domain via its SH3 domain; these regions are required for their promyogenic effects. Cdo is important for full Abl kinase activity, and Abl is necessary for full p38 MAPK activation during myogenic differentiation. Co-immunoprecipitation, domain-deletion/mutation constructs, kinase activity assays, shRNA knockdown, differentiation rescue assays Molecular and cellular biology Medium 19470755
2009 Cdo uses similar regulatory mechanisms in neuronal differentiation as in myogenesis: Cdo-dependent activation of Cdc42 and p38 MAPK promotes neuronal differentiation of C17.2 and P19 cells. Cdc42 and p38 MAPK activities promote heterodimerization of neurogenin1 and E47, suggesting regulation of neural bHLH factor activity as a mechanism. Overexpression and RNAi knockdown in neural precursor cells, Cdc42 and p38 activity assays, bHLH heterodimerization assays FASEB journal Medium 19244314
2010 N-cadherin ligation activates p38alpha/beta MAPK in myoblasts in a Cdo-, Bnip-2-, and JLP-dependent manner; Cdo, JLP, Bnip-2, and activated Cdc42 cluster at sites of N-cadherin ligation. In contrast, Shh binding to Cdo does not activate p38alpha/beta — JLP and Bnip-2 are not associated with Cdo when bound to Shh — demonstrating mechanistically distinct signaling roles for Cdo depending on the extracellular ligand. N-cadherin ligation assays, co-immunoprecipitation, p38 MAPK activity assays, immunofluorescence clustering analysis, Shh treatment controls Proceedings of the National Academy of Sciences of the United States of America High 20160094
2010 GAS1, CDO, and BOC play overlapping and collectively essential roles during HH-mediated ventral neural patterning; they function in cell fate specification of neural progenitors and later in motor neuron progenitor maintenance. Genetic loss-of-function (triple mutant) experiments indicate an obligatory collective requirement for these coreceptors in HH pathway activity in multiple tissues. Single, double, and triple genetic knockout mice, neural tube patterning analysis, in situ hybridization for HH target genes Developmental cell High 21664576
2010 All three mammalian Hedgehog proteins (Sonic, Indian, and Desert Hh) bind CDO and BOC in the same manner via the same domain (FNIII repeat 3 of CDO). X-ray crystallography confirmed this conserved mode of binding and revealed that formation of Hh-CDO interaction is weakened at low pH. X-ray crystallography of Hh-CDO and Hh-BOC complexes, biochemical binding assays The Journal of biological chemistry High 20519495
2010 Cdo interacts with APPL1 (an interacting partner of Akt), and both Cdo and APPL1 are required for efficient Akt activation during myoblast differentiation. Constitutively active Akt rescues differentiation defects of Cdo-depleted cells, whereas APPL1 overexpression alone does not, placing Cdo upstream of Akt via APPL1 for myogenic differentiation. Co-immunoprecipitation, shRNA knockdown, constitutively active Akt rescue, Akt activity assays, differentiation assays Molecular biology of the cell Medium 20484574
2010 Boc mutation exacerbates HPE in Cdo-deficient mice, indicating that Boc is a silent HPE modifier gene. Cdo and Boc have selective roles in Shh signaling — Cdo;Boc double mutants do not phenocopy Shh-null mice, demonstrating evolutionary divergence from Drosophila where Ihog and Boi are fully essential for all Hh signaling. Cdo;Boc double-mutant mice, Shh target gene expression analysis, HPE scoring Disease models & mechanisms High 21183473
2011 Missense mutations in human CDON cause holoprosencephaly (HPE). These mutations diminish CDON's ability to support Shh-dependent gene expression in cell-based signaling assays but do not affect Shh binding. Instead, wild-type CDON associates with PTCH1 and GAS1, but the HPE-associated variants do so inefficiently, indicating that CDON-PTCH1 and CDON-GAS1 interactions are required for signaling and that disruption of these inter-receptor interactions is a mechanism of HPE. Patient mutation identification, cell-based Shh signaling assays, co-immunoprecipitation of CDON with PTCH1 and GAS1, Shh binding assays American journal of human genetics High 21802063
2011 Gas1 and Cdo are coexpressed in muscle cells, form a complex in differentiating myoblasts, and cooperate to activate p38 MAPK. Gas1 overexpression in Cdo-depleted C2C12 cells restores p38 MAPK activities and differentiation, placing Gas1 as a component of the Cdo/Cadherin multiprotein complex that activates p38. Co-immunoprecipitation, overexpression, shRNA knockdown, p38 MAPK activity assays, myoblast differentiation assays Cellular signalling Medium 21820049
2012 Cx43 (Connexin 43) physically interacts with Cdo to form dynamic complexes during myoblast differentiation, as demonstrated by co-localization and FRET-based molecular imaging approaches. Fluorescence imaging, FRET/FLIM analysis, co-immunoprecipitation Journal of biophotonics Low 22930637
2012 TAK1 and ASK1 associate with the cytoplasmic tail of Cdo and with the scaffold protein JLP, and function as MAP3Ks in Cdo-mediated p38 MAPK activation during myoblast differentiation. Overexpression of TAK1 or ASK1 in Cdo-/- myoblasts restores p38 MAPK activation and myotube formation. Co-immunoprecipitation, overexpression, shRNA knockdown, p38 kinase activity assays, rescue in Cdo-/- myoblasts The Journal of biological chemistry Medium 22337877
2012 Phosphorylation of Stim1 at serine 575 by ERK1/2 (activated via netrin-2/Cdo signaling) is required for myoblast differentiation. Cdo and Stim1 form a complex in differentiating myoblasts, and alanine substitution at S575 fails to rescue differentiation of Stim1-depleted myoblasts. Cdo-/- primary myoblasts display defective NFATc3 activation correlating with reduced Stim1 levels. Co-immunoprecipitation, site-directed mutagenesis of Stim1 S575, rescue assays, p-ERK and NFATc3 activity assays, Cdo-/- primary myoblasts Molecular biology of the cell Medium 22298426
2012 Cdon mutation synergizes with fetal ethanol exposure to produce defects in early midline patterning, inhibition of Shh signaling in the developing forebrain, and a broad spectrum of HPE phenotypes in 129S6 mice. Loss of Cdon alone or ethanol alone gives little/no phenotype, establishing a gene-environment interaction. Cdon-/- mouse model with in utero ethanol exposure, Shh target gene expression analysis, HPE scoring PLoS genetics High 23071453
2013 Cdo-/- mice are specifically defective in smooth muscle fascicular reorientation in the esophagus, resulting in an aberrantly proximal skeletal-smooth muscle boundary, megaesophagus, achalasia, and lower esophageal sphincter resistance to nitric oxide-induced relaxation. Cdo knockout mice, histochemistry, immunostaining, morphometric analysis, physiological measurements The Journal of cell biology High 23569214
2013 CDON behaves as a SHH dependence receptor: it actively triggers apoptosis in the absence of SHH. The pro-apoptotic activity of unbound CDON requires proteolytic cleavage in its intracellular domain, allowing recruitment and activation of caspase-9. SHH binding to CDON inhibits this pro-apoptotic activity, promoting tumor cell survival. Cell-based apoptosis assays, caspase-9 activation assays, CDON intracellular domain cleavage analysis, in vivo tumor growth models, SHH-CDON interaction interference experiments PLoS biology High 23940460
2014 In the zebrafish and chick optic vesicle, Cdon acts as a negative Hh signaling regulator (decoy receptor) by predominantly localizing to the basolateral side of neuroepithelial cells, promoting enlargement of the neuroepithelial basal end-foot, trapping Hh protein, and limiting its dispersion in a Patched-independent manner. This protects the retinal primordium from Hh activity. Zebrafish and chick in vivo genetics, live imaging, subcellular localization assays, Hh protein distribution analysis, genetic rescue experiments Nature communications High 25001599
2014 Cdo suppresses canonical Wnt signaling to promote neuronal differentiation. The ectodomains of Cdo and Lrp6 interact via the Ig2 repeat of Cdo and the LDLR repeats of Lrp6; the Cdo Ig2 repeat is necessary for Cdo-dependent Wnt inhibition. Cdo-deficient dorsal forebrain displays enhanced Wnt signaling, increased proliferation, and elevated Pax6, Gli3, and Axin2 expression. Co-immunoprecipitation, domain-deletion constructs, Wnt reporter assays, Cdo-/- mouse forebrain analysis, cell proliferation assays Nature communications High 25406935
2015 CDON and BOC utilize distinct molecular mechanisms to promote HH signaling. CDON requires membrane attachment while BOC does not for full activity. Separate novel extracellular motifs in CDON and BOC are identified as required for their HH-promoting effects, demonstrating non-redundant structural requirements despite functional overlap. Gain-of-function in developing chicken spinal cord, domain-deletion and mutant constructs, HH target gene expression analysis Developmental biology Medium 25848697
2015 Cdon promotes neural crest cell (NCC) migration in zebrafish; Cdon knockdown results in aberrant trunk NCC migration with reduced directedness and mispositioned protrusions. Cdon is required cell-autonomously for directed NCC migration and regulates localization of N-cadherin to the cell membrane in migratory NCCs. Morpholino knockdown in zebrafish, live cell imaging, cell transplantation, immunofluorescence for N-cadherin localization Developmental biology Medium 26256768
2015 Syntaxin 4 (Stx4) binds to the cytoplasmic tail of Cdo and is required for cell surface localization of Cdo; Stx4 depletion specifically decreases surface Cdo without altering surface N-cadherin levels. Cdo depletion in turn reduces surface GLUT4 and Stx4, and overall glucose uptake, linking Cdo surface trafficking to metabolic signaling in myoblasts. Co-immunoprecipitation, surface biotinylation, shRNA knockdown, glucose uptake assays, myoblast differentiation assays Skeletal muscle Medium 26347807
2016 Cdo forms a complex with Kir2.1 potassium channel during myoblast differentiation and is required for Kir2.1 surface expression and channel activity. Loss of Cdo reduces Kir2.1 surface levels, and this is dependent on p38 MAPK activity (MKK6(EE) expression restores Kir2.1 activity in Cdo-depleted cells). Co-immunoprecipitation, surface biotinylation, electrophysiology, shRNA knockdown, rescue with activated MKK6 PloS one Medium 27380411
2016 PKN2 forms complexes with Cdo, APPL1, and AKT via its C-terminal region; this interaction is important for AKT activation and myoblast differentiation. PKN2 levels are decreased in Cdo-depleted cells, and PKN2 overexpression compensates for Cdo deficiency in AKT activation. Co-immunoprecipitation, shRNA knockdown, overexpression, AKT activity assays, myoblast differentiation assays Cell death & disease Medium 27763641
2016 Cdo-/- mice develop cardiac dysfunction (reduced ejection fraction, ECG abnormalities), fibrosis, and up-regulation and mislocalization of Connexin 43 (Cx43) due to hyperactivation of Wnt/β-catenin signaling. Cdon is localized at intercalated discs in mouse and human hearts. Inhibition of Wnt signaling (by XAV939, IWP2, or DKK1) prevents Cdo-depletion-induced upregulation of collagen 1a and Cx43, placing Cdo as a negative regulator of Wnt/β-catenin in cardiomyocytes. Cdo-/- mice, echocardiography, histology, immunostaining for Cx43 and β-catenin, gap junction activity assays, Wnt inhibitor treatments Proceedings of the National Academy of Sciences of the United States of America High 28154134
2016 Cdo is required for efficient cardiomyogenesis of pluripotent stem cells via activation of Shh signaling. Cdo-/- ES cells display decreased expression of cardiac regulators (Gata4, Nkx2.5, Mef2c) and reduced Shh signaling; Shh agonist treatment restores cardiomyogenesis in Cdo-deficient ES cells. Cdo-/- mouse ES cells, P19 EC cell differentiation, shRNA knockdown, Shh pathway reporter assays, Shh agonist rescue Journal of molecular and cellular cardiology Medium 26906632
2018 Ash1L (a Trithorax group epigenetic activator) promotes myoblast fusion by activating Cdon expression. Ash1L is required to counteract Polycomb repressive activity at the Cdon locus; RNA- and ChIP-sequencing identified Cdon as a key target gene of Ash1L in myogenesis. RNA-seq, ChIP-seq, Ash1L loss-of-function in vitro and in vivo, myoblast fusion assays Nature communications Medium 30487570
2020 Satellite cell-specific Cdon ablation causes impaired muscle regeneration with fibrosis due to decreased satellite cell proliferation and senescence. Mechanistically, Cdon-depleted satellite cells show impaired integrin β1 activation, reduced ERK activation in response to FGF, and Cdon interacts with and regulates cell surface localization of FGFR1 and FGFR4. Inducible satellite cell-specific Cdon knockout mice (Pax7-CreERT2), cardiotoxin injury, immunostaining, EdU assay, co-immunoprecipitation, FGFR surface expression analysis, RNA-seq Journal of cachexia, sarcopenia and muscle High 32103583
2020 Nodal signaling is a major point of synergistic interaction between Cdon mutation and fetal alcohol exposure in HPE. Window-of-sensitivity experiments indicate that brief ethanol exposure during gastrulation transiently inhibits Nodal pathway activity in Cdon mutant embryos, with consequent effects on midline patterning. Cdon-/- mouse with timed ethanol exposure, Nodal pathway activity assays, genetic epistasis, in vitro Nodal assays eLife Medium 32876567
2020 In endothelial cells, Cdon prevents Desert Hedgehog (Dhh) binding to Ptch1 and thus acts as a decoy receptor for Dhh, negatively regulating Dhh signaling. Cdon deficiency in ECs promotes endothelial junction integrity and decreases inflammatory markers (VCAM-1, ICAM-1), opposite to Gas1 (which is a positive regulator of Dhh in ECs). siRNA knockdown, EC-specific conditional knockout mice, Dhh-Ptch1 binding assays, VCAM-1/ICAM-1 expression analysis, vascular permeability assays Arteriosclerosis, thrombosis, and vascular biology Medium 33028094
2021 Cytoneme-mediated delivery of SHH from ligand-producing cells requires a novel Dispatched (DISP)-BOC/CDON co-receptor complex at the producing cell membrane. Myosin 10 promotes vesicular transport of SHH in mouse cell cytonemes. Cytoneme-deposited SHH induces rapid receptor-dependent signaling within seconds; this is dependent on the DISP-BOC/CDON complex for cytoneme occurrence and ligand delivery. Live cell imaging, Myo10 knockout mice, neural tube patterning analysis, co-immunoprecipitation of DISP-BOC/CDON complex, time-lapse signaling assays eLife Medium 33570491
2022 GAS1, CDON, and BOC are collectively required for HH-dependent digit specification, limb patterning, and long bone growth. Limb-specific conditional deletion of Cdon in a Gas1;Boc null background results in digit loss and limb outgrowth defects. Limb-specific conditional Cdon knockout in Gas1;Boc null background, skeletal preparations, HH target gene expression analysis Developmental biology High 36265686
2023 Cdon deficiency in vascular smooth muscle cells (VSMCs) causes exacerbated aortic calcification via hyperactivation of Wnt/Runx2 signaling. The Ig2 domain of Cdon ectodomain is required for Wnt suppression; deletion of Ig2 abolishes Cdon-dependent Wnt inhibition and osteogenic conversion. Recombinant Ig2 domain protein suppresses Wnt signaling and VSMC calcification. Cdon conditional knockout mice (VSMC-specific), Wnt reporter assays, domain-deletion mutants, recombinant Ig2 protein treatment, aortic stiffness measurements, histological calcification analysis Experimental & molecular medicine High 36609601
2023 Motor neuron-specific Cdon ablation causes age-related motor neuron degeneration and impaired sciatic nerve repair. Mechanistically, Cdon-depleted motor neurons show altered ErbB4 and FGFR expression and impaired Akt activation in response to neuregulin-1 (NRG1), linking Cdon to neurotrophin signaling in motor neuron survival. Motor neuron-specific Cdon knockout (Hb9-Cre), sciatic nerve crush injury model, RNA-seq, immunostaining, electrophysiology, Akt activity assays in Cdon-depleted NSC34 cells Journal of cachexia, sarcopenia and muscle Medium 37559423

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 The cell surface membrane proteins Cdo and Boc are components and targets of the Hedgehog signaling pathway and feedback network in mice. Developmental cell 298 16647304
2011 Overlapping roles and collective requirement for the coreceptors GAS1, CDO, and BOC in SHH pathway function. Developmental cell 227 21664576
2007 The Hedgehog-binding proteins Gas1 and Cdo cooperate to positively regulate Shh signaling during mouse development. Genes & development 224 17504941
2006 Cdo functions at multiple points in the Sonic Hedgehog pathway, and Cdo-deficient mice accurately model human holoprosencephaly. Developmental cell 207 16647303
2006 The ihog cell-surface proteins bind Hedgehog and mediate pathway activation. Cell 179 16630821
2002 BOC, an Ig superfamily member, associates with CDO to positively regulate myogenic differentiation. The EMBO journal 126 11782431
2008 The mode of Hedgehog binding to Ihog homologues is not conserved across different phyla. Nature 124 18794898
2011 Mutations in CDON, encoding a hedgehog receptor, result in holoprosencephaly and defective interactions with other hedgehog receptors. American journal of human genetics 109 21802063
2006 Activation of p38alpha/beta MAPK in myogenesis via binding of the scaffold protein JLP to the cell surface protein Cdo. The Journal of cell biology 103 17074887
2012 Cdon mutation and fetal ethanol exposure synergize to produce midline signaling defects and holoprosencephaly spectrum disorders in mice. PLoS genetics 100 23071453
2008 A Cdo-Bnip-2-Cdc42 signaling pathway regulates p38alpha/beta MAPK activity and myogenic differentiation. The Journal of cell biology 91 18678706
2003 Microform holoprosencephaly in mice that lack the Ig superfamily member Cdon. Current biology : CB 91 12620190
2010 The cell-surface proteins Dally-like and Ihog differentially regulate Hedgehog signaling strength and range during development. Development (Cambridge, England) 89 20501592
1998 CDO, a robo-related cell surface protein that mediates myogenic differentiation. The Journal of cell biology 89 9786951
2004 Positive regulation of myogenic bHLH factors and skeletal muscle development by the cell surface receptor CDO. Developmental cell 85 15572127
1997 CDO: an oncogene-, serum-, and anchorage-regulated member of the Ig/fibronectin type III repeat family. The Journal of cell biology 81 9214393
2012 Balancing Hedgehog, a retention and release equilibrium given by Dally, Ihog, Boi and shifted/DmWif. Developmental biology 65 23276604
2010 Boc modifies the holoprosencephaly spectrum of Cdo mutant mice. Disease models & mechanisms 57 21183473
2010 N-cadherin ligation, but not Sonic hedgehog binding, initiates Cdo-dependent p38alpha/beta MAPK signaling in skeletal myoblasts. Proceedings of the National Academy of Sciences of the United States of America 55 20160094
2010 All mammalian Hedgehog proteins interact with cell adhesion molecule, down-regulated by oncogenes (CDO) and brother of CDO (BOC) in a conserved manner. The Journal of biological chemistry 54 20519495
2017 Cdon deficiency causes cardiac remodeling through hyperactivation of WNT/β-catenin signaling. Proceedings of the National Academy of Sciences of the United States of America 53 28154134
2013 Sonic Hedgehog promotes tumor cell survival by inhibiting CDON pro-apoptotic activity. PLoS biology 50 23940460
2010 Cdo interacts with APPL1 and activates Akt in myoblast differentiation. Molecular biology of the cell 50 20484574
2021 Cytoneme delivery of Sonic Hedgehog from ligand-producing cells requires Myosin 10 and a Dispatched-BOC/CDON co-receptor complex. eLife 49 33570491
2014 Cdon acts as a Hedgehog decoy receptor during proximal-distal patterning of the optic vesicle. Nature communications 48 25001599
2010 Ihog and Boi are essential for Hedgehog signaling in Drosophila. Neural development 42 21044292
2000 Developmental expression pattern of the cdo gene. Developmental dynamics : an official publication of the American Association of Anatomists 42 10974670
2009 Cdo binds Abl to promote p38alpha/beta mitogen-activated protein kinase activity and myogenic differentiation. Molecular and cellular biology 41 19470755
2009 Cdo promotes neuronal differentiation via activation of the p38 mitogen-activated protein kinase pathway. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 40 19244314
2015 A Nonsense Mutation in the Hedgehog Receptor CDON Associated With Pituitary Stalk Interruption Syndrome. The Journal of clinical endocrinology and metabolism 39 26529631
2014 Cdo suppresses canonical Wnt signalling via interaction with Lrp6 thereby promoting neuronal differentiation. Nature communications 39 25406935
2018 Sublethal effects of chronic exposure to CdO or PbO nanoparticles or their binary mixture on the honey bee (Apis millefera L.). Environmental science and pollution research international 37 30280346
1999 Inhibition of protein kinase C--do we, can we, and should we? Pharmacology & therapeutics 36 10454203
2021 ZnO-CdO nanocomposites incorporated with graphene oxide nanosheets for efficient photocatalytic degradation of bisphenol A, thymol blue and ciprofloxacin. Journal of hazardous materials 35 34607025
2016 PKN2 and Cdo interact to activate AKT and promote myoblast differentiation. Cell death & disease 35 27763641
2012 TGF-β-activated kinase 1 (TAK1) and apoptosis signal-regulating kinase 1 (ASK1) interact with the promyogenic receptor Cdo to promote myogenic differentiation via activation of p38MAPK pathway. The Journal of biological chemistry 35 22337877
2006 Cortical thinning and hydrocephalus in mice lacking the immunoglobulin superfamily member CDO. Molecular and cellular biology 35 16648472
2011 Promyogenic function of Integrin/FAK signaling is mediated by Cdo, Cdc42 and MyoD. Cellular signalling 34 21397010
2020 Satellite cell-specific ablation of Cdon impairs integrin activation, FGF signalling, and muscle regeneration. Journal of cachexia, sarcopenia and muscle 31 32103583
2020 Consequences of a short-term exposure to a sub lethal concentration of CdO nanoparticles on key life history traits in the fruit fly (Drosophila melanogaster). Journal of hazardous materials 30 33349477
2011 Gas1 cooperates with Cdo and promotes myogenic differentiation via activation of p38MAPK. Cellular signalling 29 21820049
2014 Regulation by miR181 family of the dependence receptor CDON tumor suppressive activity in neuroblastoma. Journal of the National Cancer Institute 28 25313246
2012 CdO nanoparticle toxicity on growth, morphology, and cell division in Escherichia coli. Langmuir : the ACS journal of surfaces and colloids 28 23137198
2010 Brother of cdo (umleitung) is cell-autonomously required for Hedgehog-mediated ventral CNS patterning in the zebrafish. Development (Cambridge, England) 28 21115611
2012 Phosphorylation of Stim1 at serine 575 via netrin-2/Cdo-activated ERK1/2 is critical for the promyogenic function of Stim1. Molecular biology of the cell 27 22298426
2012 Cdon and Boc: Two transmembrane proteins implicated in cell-cell communication. The international journal of biochemistry & cell biology 26 22326621
2016 Prenatal ethanol exposure in mice phenocopies Cdon mutation by impeding Shh function in the etiology of optic nerve hypoplasia. Disease models & mechanisms 25 27935818
2015 Cdon promotes neural crest migration by regulating N-cadherin localization. Developmental biology 25 26256768
2005 BOC, brother of CDO, is a dorsoventral axon-guidance molecule in the embryonic vertebrate brain. The Journal of comparative neurology 24 15776441
2013 Rescue of holoprosencephaly in fetal alcohol-exposed Cdon mutant mice by reduced gene dosage of Ptch1. PloS one 22 24244464
2009 Ocular abnormalities in mice lacking the immunoglobulin superfamily member Cdo. The FEBS journal 22 19754878
2023 Cdon suppresses vascular smooth muscle calcification via repression of the Wnt/Runx2 Axis. Experimental & molecular medicine 20 36609601
2017 Hedgehog mediated degradation of Ihog adhesion proteins modulates cell segregation in Drosophila wing imaginal discs. Nature communications 20 29097673
2013 Smooth muscle fascicular reorientation is required for esophageal morphogenesis and dependent on Cdo. The Journal of cell biology 20 23569214
2015 Distinct structural requirements for CDON and BOC in the promotion of Hedgehog signaling. Developmental biology 19 25848697
2018 The Trithorax protein Ash1L promotes myoblast fusion by activating Cdon expression. Nature communications 18 30487570
2014 Sonic Hedgehog promotes the survival of neural crest cells by limiting apoptosis induced by the dependence receptor CDON during branchial arch development. Biochemical and biophysical research communications 18 25193697
2016 Cdo Regulates Surface Expression of Kir2.1 K+ Channel in Myoblast Differentiation. PloS one 17 27380411
2020 Cdon mutation and fetal alcohol converge on Nodal signaling in a mouse model of holoprosencephaly. eLife 16 32876567
2014 Shifting redox states of the iron center partitions CDO between crosslink formation or cysteine oxidation. Archives of biochemistry and biophysics 16 24929188
2011 Identification of transmembrane protein in prostate cancer by the Escherichia coli ampicillin secretion trap: expression of CDON is involved in tumor cell growth and invasion. Pathobiology : journal of immunopathology, molecular and cellular biology 16 21849809
2021 Glypicans define unique roles for the Hedgehog co-receptors boi and ihog in cytoneme-mediated gradient formation. eLife 15 34355694
2020 Desert Hedgehog-Driven Endothelium Integrity Is Enhanced by Gas1 (Growth Arrest-Specific 1) but Negatively Regulated by Cdon (Cell Adhesion Molecule-Related/Downregulated by Oncogenes). Arteriosclerosis, thrombosis, and vascular biology 15 33028094
2016 A Shh coreceptor Cdo is required for efficient cardiomyogenesis of pluripotent stem cells. Journal of molecular and cellular cardiology 15 26906632
2014 The Shh coreceptor Cdo is required for differentiation of midbrain dopaminergic neurons. Stem cell research 15 25117422
2022 CDON contributes to Hedgehog-dependent patterning and growth of the developing limb. Developmental biology 14 36265686
2014 CDO, an Hh-coreceptor, mediates lung cancer cell proliferation and tumorigenicity through Hedgehog signaling. PloS one 14 25369201
2012 A molecular imaging analysis of Cx43 association with Cdo during skeletal myoblast differentiation. Journal of biophotonics 14 22930637
2012 The Drosophila WIF1 homolog Shifted maintains glypican-independent Hedgehog signaling and interacts with the Hedgehog co-receptors Ihog and Boi. Development (Cambridge, England) 13 23154411
2006 Mutational screening of FGFR1, CER1, and CDON in a large cohort of trigonocephalic patients. The Cleft palate-craniofacial journal : official publication of the American Cleft Palate-Craniofacial Association 13 16526918
2022 Inebilizumab-cdon: USFDA Approved for the Treatment of NMOSD (Neuromyelitis Optica Spectrum Disorder). Current drug discovery technologies 12 34011260
2016 Cdon, a cell surface protein, mediates oligodendrocyte differentiation and myelination. Glia 12 26988125
2003 Overexpression of the immunoglobulin superfamily members CDO and BOC enhances differentiation of the human rhabdomyosarcoma cell line RD. Molecular carcinogenesis 12 12720294
2021 CdO/CdCO3 nanocomposite physical properties and cytotoxicity against selected breast cancer cell lines. Scientific reports 11 33420103
1997 Human cysteine dioxygenase type I (CDO-I; EC 1.13.11.20): 5' flanking region and intron-exon structure of the gene. Molecular pathology : MP 11 9497919
2016 A mutation in the Cdon gene potentiates congenital nevus development mediated by NRAS(Q61K). Pigment cell & melanoma research 10 27155367
2015 Syntaxin 4 regulates the surface localization of a promyogenic receptor Cdo thereby promoting myogenic differentiation. Skeletal muscle 10 26347807
2013 Drosophila miR-932 modulates hedgehog signaling by targeting its co-receptor Brother of ihog. Developmental biology 10 23453925
2022 Predictive model for cytoneme guidance in Hedgehog signaling based on Ihog- Glypicans interaction. Nature communications 9 36163184
2021 CDON gene contributes to pituitary stalk interruption syndrome associated with unilateral facial and abducens nerve palsy. Journal of applied genetics 9 34235642
2019 Homozygous variants in MAPRE2 and CDON in individual with skin folds, growth delay, retinal coloboma, and pyloric stenosis. American journal of medical genetics. Part A 9 31502381
2018 Large-scale production of CdO/Cd(OH)2 nanocomposites for non-enzyme sensing and supercapacitor applications. RSC advances 8 35538943
2016 Mesocortical Dopamine Phenotypes in Mice Lacking the Sonic Hedgehog Receptor Cdon. eNeuro 8 27419218
2022 NFI transcriptionally represses CDON and is required for SH-SY5Y cell survival. Biochimica et biophysica acta. Gene regulatory mechanisms 7 35151899
2021 Enhanced photocatalytic and photodynamic activity of chitosan and garlic loaded CdO-TiO2 hybrid bionanomaterials. Scientific reports 7 34675259
2019 The Drosophila Hedgehog receptor component Interference hedgehog (Ihog) mediates cell-cell interactions through trans-homophilic binding. The Journal of biological chemistry 7 31209108
1998 Hsp27 phosphorylation is induced in alveolar macrophages exposed to CdO-coated silica particles. Biochemical and biophysical research communications 7 9675116
2023 Mutations in cdon and boc affect trunk neural crest cell migration and slow-twitch muscle development in zebrafish. Development (Cambridge, England) 6 37390228
2022 Exposure to a sublethal concentration of CdO nanoparticles impairs the vision of the fruit fly (Drosophila melanogaster) by disrupting histamine synthesis and recycling mechanisms. Environmental science and pollution research international 6 36394804
2021 Formation Mechanism of Cofactor Cys-Tyr in the Cysteine Dioxygenases (CDO and F2-CDO) and Its Influence on Catalysis: A QM/MM Study. Inorganic chemistry 6 34008401
2020 Compound heterozygous splicing CDON variants result in isolated ocular coloboma. Clinical genetics 6 32729136
2013 Growth cone dynamics in the zebrafish embryonic forebrain are regulated by Brother of Cdo. Neuroscience letters 6 23603263
2003 Effects of inhaled CdO particles on the sphingolipid synthesis of rat lungs. Inhalation toxicology 6 12635003
2023 Cdon ablation in motor neurons causes age-related motor neuron degeneration and impaired sciatic nerve repair. Journal of cachexia, sarcopenia and muscle 5 37559423
2018 Experimental and computational assessment of mycosynthesized CdO nanoparticles towards biomedical applications. Journal of photochemistry and photobiology. B, Biology 5 29448204
2018 Aerobic Conditions Enhance the Photocatalytic Stability of CdS/CdOx Quantum Dots. Chemistry (Weinheim an der Bergstrasse, Germany) 5 29750379
2016 Toxicity and efficacy of CdO nanostructures on the MDCK and Caki-2 cells. Journal of photochemistry and photobiology. B, Biology 5 27689742
2014 Ihog and Boi elicit Hh signaling via Ptc but do not aid Ptc in sequestering the Hh ligand. Development (Cambridge, England) 5 25231763
2011 Brother of CDO (BOC) expression in equine articular cartilage. Osteoarthritis and cartilage 5 21262369
2014 Detergent-solubilized Patched purified from Sf9 cells fails to interact strongly with cognate Hedgehog or Ihog homologs. Protein expression and purification 4 25261717

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