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The Trithorax protein Ash1L promotes myoblast fusion by activating Cdon expression
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Cdon deficiency causes hyperactive Wnt signaling leading to aberrant intercellular coupling and cardiac fibrosis.
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These results support a model whereby mutations in Cdon and prenatal ethanol exposure increase Septo-optic dysplasia risk through spatiotemporal perturbations in Shh signaling activity.
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Mutation in the Cdon gene is associated with congenital nevus development.
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Study assessed the role of the Shh receptor Cdon in the development of ventral tegmental area and substantia nigra pars compacta dopamine neurons. Results suggest that Cdon plays an important role in the encoding of diversity within the population of dopamine neurons of the midbrain, influencing both the development of the mesocortical dopamine pathway as well as behavioral outputs that involve this neural circuitry.
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Results suggest that a promyogenic cell adhesion molecule Cdo signaling is critical for Inward rectifier potassium channel Kir2.1 activities in the induction of myogenic differentiation.
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PKN2 formed complexes with Cdo, APPL1 and AKT via its C-terminal region and this interaction appeared to be important for induction of AKT activity as well as myoblast differentiation.
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that Cdon participates in oligodendrocyte differentiation and myelination, most likely in the initial stages of development
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Suggest that Cdo is required for the full Shh signaling activation to induce efficient dopaminergic neuron neurogenesis.
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Rescue of holoprosencephaly in fetal alcohol-exposed Cdon mutant mice by reduced gene dosage of Ptch1.
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Cx43 physically interacts with Cdo to form dynamic complexes during myoblast differentiation
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Stim1 protein levels were decreased in Cdo-deficient perinatal hindlimb muscles or primary myoblasts; this correlates with defective NFATc3 activation in Cdo(-/-) myoblasts upon differentiation.
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ASK1 and TAK1 function as MAP3 kinases in Cdo-mediated p38MAPK activation to promote myogenic differentiation.
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Gas1 cooperates with Cdo and promotes myogenic differentiation via activation of p38MAPK
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CDON must associate with both ligand and other hedgehog-receptor components, particularly PTCH1, for signaling to occur and disruption of the latter interactions is a mechanism of holoprosencephaly.
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the Integrin/FAK signaling pathway regulates the expression of the promyogenic factors, Cdo, MyoD and Cdc42 which are required for myoblast differentiation
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Cdo;Boc double mutants on a largely Cdo-resistant genetic background have lobar holoprosencephaly.
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The promyogenic function of Cdo involves a coordinated activation of p38MAPK and Akt via association with scaffold proteins, JLP and Bnip-2 for p38MAPK and APPL1 for Akt.
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Hedgehog proteins interact with cell adhesion molecule, down-regulated by oncogenes (CDO) and brother of CDO (BOC) in a conserved manner
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CDO has a role in regulation of myogenic bHLH factors and skeletal muscle development