Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of Cdon. (This text reflects annotations as of Thursday, July 24, 2014.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of December 2, 2010. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.

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Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a cell surface receptor that is a member of the immunoglobulin superfamily. The encoded protein contains three fibronectin type III domains and five immunoglobulin-like C2-type domains. This protein is a member of a cell-surface receptor complex that mediates cell-cell interactions between muscle precursor cells and positively regulates myogenesis. [provided by RefSeq, Aug 2011]

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Summary text based on GO annotations supported by experimental evidence in mouse

• Researchers have inferred from direct assay, that the gene product of Cdon
  • participates in the following biological processes:
    • positive regulation of neuron differentiation ^[11]
    • positive regulation of protein phosphorylation ^[3]
    • regulation of protein heterodimerization activity ^{[3, 11]}
• The gene product of Cdon has been shown to bind to the gene products of Abl1, Cdh2, Mapk14, Shh. ^{[2, 5, 6, 8]}
• Researchers have inferred, based on phenotypic analysis of mouse mutants, that the gene product of Cdon
  • participates in the following biological processes:
    • anterior/posterior pattern specification ^[10]
    • cerebral cortex development ^[11]
    • embryonic body morphogenesis ^[12]
    • embryonic retina morphogenesis in camera-type eye ^[10]
    • lens development in camera-type eye ^[10]
    • myoblast fusion ^[4]
    • positive regulation of MAPK cascade ^[7]
    • positive regulation of neural precursor cell proliferation ^[11]
    • positive regulation of neuron differentiation ^{[7, 11]}
    • positive regulation of skeletal muscle tissue development ^[3]
    • positive regulation of small GTPase mediated signal transduction ^[7]
    • regulation of neuron differentiation ^[11]
    • skeletal muscle satellite cell differentiation ^[3]
• Researchers have inferred, based on genetic interactions, that the gene product of Cdon
  • participates in the following biological processes:
    • cell fate specification based on interactions with Shh ^[9]
    • embryonic body morphogenesis based on interactions with Shh ^[9]
    • embryonic morphogenesis based on interactions with Gas1 ^[1]
    • positive regulation of MAPK cascade based on interactions with Bnip2, Cdh2, Spag9 ^[6]
    • positive regulation of transcription from RNA polymerase II promoter based on interactions with Myod1, Neurog1 ^{[3, 11]}
    • smoothened signaling pathway based on interactions with Shh ^[9]
    • striated muscle cell differentiation based on interactions with Bnip2, Cdh2, Mapk14, Spag9 ^[6]

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Summary text based on GO annotations supported by experimental evidence in other organisms

• From comparative sequence analysis (see table for details), MGI curators have determined that the gene product of Cdon:
  • participates in the following biological processes:
    • cell adhesion
    • regulation of striated muscle tissue development
    • smoothened signaling pathway
  • is located in the following cellular components:
    • cell surface
    • integral component of plasma membrane

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Summary text for additional MGI annotations

• Automated translation to GO terms of SwissProt keywords that describe Cdon indicates that it:
  • is located in the following cellular components:
    • integral component of membrane
    • membrane
    • plasma membrane

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References

1. Allen BL et al. (2007) The Hedgehog-binding proteins Gas1 and Cdo cooperate to positively regulate Shh signaling during mouse development. Genes Dev, 21:1244-57. (PubMed:17504941)
2. Bae GU et al. (2009) Cdo binds Abl to promote p38alpha/beta mitogen-activated protein kinase activity and myogenic differentiation. Mol Cell Biol, 29:4130-43. (PubMed:19470755)
3. Cole F et al. (2004) Positive regulation of myogenic bHLH factors and skeletal muscle development by the cell surface receptor CDO. Dev Cell, 7:843-54. (PubMed:15572127)
4. Kang JS et al. (2004) Netrins and neogenin promote myotube formation. J Cell Biol, 167:493-504. (PubMed:15520228)
5. Kang JS et al. (2002) BOC, an Ig superfamily member, associates with CDO to positively regulate myogenic differentiation. EMBO J, 21:114-24. (PubMed:11782431)
6. Lu M et al. (2010) N-cadherin ligation, but not Sonic hedgehog binding, initiates Cdo-dependent p38alpha/beta MAPK signaling in skeletal myoblasts. Proc Natl Acad Sci U S A, 107:4212-7. (PubMed:20160094)
7. Oh JE et al. (2009) Cdo promotes neuronal differentiation via activation of the p38 mitogen-activated protein kinase pathway. FASEB J, 23:2088-99. (PubMed:19244314)
8. Okada A et al. (2006) Boc is a receptor for sonic hedgehog in the guidance of commissural axons. Nature, 444:369-73. (PubMed:17086203)
9. Tenzen T et al. (2006) The cell surface membrane proteins Cdo and Boc are components and targets of the Hedgehog signaling pathway and feedback network in mice. Dev Cell, 10:647-56. (PubMed:16647304)
10. Zhang W et al. (2009) Ocular abnormalities in mice lacking the immunoglobulin superfamily member Cdo. FEBS J, 276:5998-6010. (PubMed:19754878)
11. Zhang W et al. (2006) Cortical thinning and hydrocephalus in mice lacking the immunoglobulin superfamily member CDO. Mol Cell Biol, 26:3764-72. (PubMed:16648472)
12. Zhang W et al. (2006) Cdo functions at multiple points in the Sonic Hedgehog pathway, and Cdo-deficient mice accurately model human holoprosencephaly. Dev Cell, 10:657-65. (PubMed:16647303)

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Gene Ontology Evidence Code Abbreviations:

EXP Inferred from experiment

IC Inferred by curator

IDA Inferred from direct assay

IEA Inferred from electronic annotation

IGI Inferred from genetic interaction

IMP Inferred from mutant phenotype

IPI Inferred from physical interaction

ISS Inferred from sequence or structural similarity

ISO Inferred from sequence orthology

ISA Inferred from sequence alignment

ISM Inferred from sequence model

NAS Non-traceable author statement

ND No biological data available

RCA Reviewed computational analysis

TAS Traceable author statement

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