CDON

Source: Wikipedia, the free encyclopedia.
CDON
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Ensembl
UniProt
RefSeq (mRNA)

NM_001243597
NM_016952
NM_001378964

NM_021339

RefSeq (protein)

NP_001230526
NP_058648
NP_001365893

Location (UCSC)Chr 11: 125.96 – 126.06 MbChr 9: 35.42 – 35.51 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Cell adhesion molecule-related/down-regulated by oncogenes is a protein that in humans is encoded by the CDON gene.[5][6]

CDON and

FNIII) repeat family involved in myogenic differentiation. CDON and BOC are coexpressed during development, form complexes with each other in a cis fashion, and are related to each other in their ectodomains, but each has a unique long cytoplasmic tail.[6]

Structure and function

Cell adhesion molecule-related/down-regulated by oncogenes (CDON) is a conserved transmembrane

hedgehog proteins: Sonic Hh, Indian Hh, and Desert Hh.[10]

Clinical significance

CDON mutations are thought to diminish

sonic hedgehog (SHH)-pathway activity which is important in stimulating cell proliferation, differentiation, and tissue patterning at multiple points in animal development. CDON was shown to play a role in differentiation of midbrain dopaminergic neurons through the interference with of Shh signaling pathway.[11] Mutations in CDON gene has been associated with Holoprosencephaly which is structural anomaly of the brain, in which the developing forebrain fails to correctly separate into right and left hemispheres.[12] CDON mutations synergistically interact with prenatal alcohol exposure to increase susceptibility to Holoprosencephaly.[13]

Gene knockdown studies

CDON knockdown using morpholinos in zebra fish altered the eye development, CDON was shown important in restraining the size of the optic stalk and ventral retina in chick embryos.[13] Additionally, double CDON knock out mice display optic nerve hypoplasia (ONH), a prominent feature of septo-optic dysplasia (SOD), the same phenotype shown by treating mice prenatally with ethanol.[14] CDON−/− animals also show cardiac dysfunction with increased fibrosis, those cardiac effects are mediated through hyperactivation of WNT/β-catenin signaling.[15]

Interactions

CDON has been shown to

CDH1[16] and BOC.[17]

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000064309Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000038119Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. PMID 9214393
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  6. ^ a b "Entrez Gene: CDON Cdon homolog (mouse)".
  7. PMID 22326621
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Further reading

External links


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