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Gene Ontology Classifications
SRY (sex determining region Y)-box 18

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

GO curators for mouse genes have assigned the following annotations to the gene product of Sox18. (This text reflects annotations as of Tuesday, May 26, 2015.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of February 25, 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.
Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a member of the SOX (SRY-related HMG-box) family of transcription factors involved in the regulation of embryonic development and in the determination of the cell fate. The encoded protein may act as a transcriptional regulator after forming a protein complex with other proteins. This protein plays a role in hair, blood vessel, and lymphatic vessel development. Mutations in this gene have been associated with recessive and dominant forms of hypotrichosis-lymphedema-telangiectasia. [provided by RefSeq, Jul 2008]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text for additional MGI annotations
  1. Downes M et al. (2009) Vascular defects in a mouse model of hypotrichosis-lymphedema-telangiectasia syndrome indicate a role for SOX18 in blood vessel maturation. Hum Mol Genet, 18:2839-50. (PubMed:19429912)
  2. Francois M et al. (2008) Sox18 induces development of the lymphatic vasculature in mice. Nature, 456:643-7. (PubMed:18931657)
  3. Hosking B et al. (2009) Sox7 and Sox17 are strain-specific modifiers of the lymphangiogenic defects caused by Sox18 dysfunction in mice. Development, 136:2385-91. (PubMed:19515696)
  4. Hosking BM et al. (1995) Trans-activation and DNA-binding properties of the transcription factor, Sox-18. Nucleic Acids Res, 23:2626-8. (PubMed:7651823)
  5. Hosking BM et al. (2001) Cloning and functional analysis of the Sry-related HMG box gene, Sox18. Gene, 262:239-47. (PubMed:11179689)
  6. Hosking BM et al. (2004) The VCAM-1 gene that encodes the vascular cell adhesion molecule is a target of the Sry-related high mobility group box gene, Sox18. J Biol Chem, 279:5314-22. (PubMed:14634005)
  7. Hosking BM et al. (2001) SOX18 directly interacts with MEF2C in endothelial cells. Biochem Biophys Res Commun, 287:493-500. (PubMed:11554755)
  8. Hwang CK et al. (2003) Mouse mu opioid receptor distal promoter transcriptional regulation by SOX proteins. J Biol Chem, 278:3742-50. (PubMed:12446692)
  9. Matsui T et al. (2006) Redundant roles of Sox17 and Sox18 in postnatal angiogenesis in mice. J Cell Sci, 119:3513-26. (PubMed:16895970)
  10. Ng CK et al. (2012) Deciphering the Sox-Oct partner code by quantitative cooperativity measurements. Nucleic Acids Res, 40:4933-41. (PubMed:22344693)
  11. Pennisi D et al. (2000) Mutations in Sox18 underlie cardiovascular and hair follicle defects in ragged mice. Nat Genet, 24:434-7. (PubMed:10742113)
  12. Pennisi D et al. (2000) Mice null for sox18 are viable and display a mild coat defect Mol Cell Biol, 20:9331-6. (PubMed:11094083)
  13. Sakamoto Y et al. (2007) Redundant roles of Sox17 and Sox18 in early cardiovascular development of mouse embryos. Biochem Biophys Res Commun, 360:539-44. (PubMed:17610846)
  14. Serrano AG et al. (2010) Contrasting effects of Sox17- and Sox18-sustained expression at the onset of blood specification. Blood, 115:3895-8. (PubMed:20228271)
  15. Swailes NT et al. (2006) Non-muscle myosins 2A and 2B drive changes in cell morphology that occur as myoblasts align and fuse. J Cell Sci, 119:3561-70. (PubMed:16895968)
  16. Wallace ME. (1979) Analysis of genetic control of chylous ascites in ragged mice. Heredity (Edinb), 43:9-18. (PubMed:291594)

Go Annotations in Tabular Form (Text View) (GO Graph)

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Gene Ontology Evidence Code Abbreviations:

  EXP Inferred from experiment
  IAS Inferred from ancestral sequence
  IBA Inferred from biological aspect of ancestor
  IBD Inferred from biological aspect of descendant
  IC Inferred by curator
  IDA Inferred from direct assay
  IEA Inferred from electronic annotation
  IGI Inferred from genetic interaction
  IKR Inferred from key residues
  IMP Inferred from mutant phenotype
  IMR Inferred from missing residues
  IPI Inferred from physical interaction
  IRD Inferred from rapid divergence
  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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