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Gene Ontology Classifications
sal-like 1 (Drosophila)

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

GO curators for mouse genes have assigned the following annotations to the gene product of Sall1. (This text reflects annotations as of Tuesday, May 26, 2015.)
Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] The protein encoded by this gene is a zinc finger transcriptional repressor and may be part of the NuRD histone deacetylase complex (HDAC). Defects in this gene are a cause of Townes-Brocks syndrome (TBS) as well as bronchio-oto-renal syndrome (BOR). Two transcript variants encoding different isoforms have been found for this gene. [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 based on GO annotations supported by structural data
Summary text for additional MGI annotations
  1. Basta JM et al. (2014) Sall1 balances self-renewal and differentiation of renal progenitor cells. Development, 141:1047-58. (PubMed:24550112)
  2. Bohm J et al. (2008) Sall1, sall2, and sall4 are required for neural tube closure in mice. Am J Pathol, 173:1455-63. (PubMed:18818376)
  3. Harrison SJ et al. (2008) Sall3 is required for the terminal maturation of olfactory glomerular interneurons. J Comp Neurol, 507:1780-94. (PubMed:18260139)
  4. Harrison SJ et al. (2008) Sall1 regulates mitral cell development and olfactory nerve extension in the developing olfactory bulb. Cereb Cortex, 18:1604-17. (PubMed:18024993)
  5. Karantzali E et al. (2011) Sall1 regulates embryonic stem cell differentiation in association with nanog. J Biol Chem, 286:1037-45. (PubMed:21062744)
  6. Kawakami Y et al. (2009) Sall genes regulate region-specific morphogenesis in the mouse limb by modulating Hox activities. Development, 136:585-94. (PubMed:19168674)
  7. Kiefer SM et al. (2002) Murine sall1 represses transcription by recruiting a histone deacetylase complex. J Biol Chem, 277:14869-76. (PubMed:11836251)
  8. Kiefer SM et al. (2008) SALL1 truncated protein expression in Townes-Brocks syndrome leads to ectopic expression of downstream genes. Hum Mutat, 29:1133-40. (PubMed:18470945)
  9. Lauberth SM et al. (2006) A conserved 12-amino acid motif in Sall1 recruits the nucleosome remodeling and deacetylase corepressor complex. J Biol Chem, 281:23922-31. (PubMed:16707490)
  10. Nishinakamura R et al. (2006) Essential roles of Sall family genes in kidney development. J Physiol Sci, 56:131-6. (PubMed:16839447)
  11. Nishinakamura R et al. (2001) Murine homolog of SALL1 is essential for ureteric bud invasion in kidney development. Development, 128:3105-15. (PubMed:11688560)
  12. Sakaki-Yumoto M et al. (2006) The murine homolog of SALL4, a causative gene in Okihiro syndrome, is essential for embryonic stem cell proliferation, and cooperates with Sall1 in anorectal, heart, brain and kidney development. Development, 133:3005-13. (PubMed:16790473)
  13. Sato A et al. (2003) Zinc finger protein sall2 is not essential for embryonic and kidney development. Mol Cell Biol, 23:62-9. (PubMed:12482961)
  14. Uchiyama Y et al. (2010) Kif26b, a kinesin family gene, regulates adhesion of the embryonic kidney mesenchyme. Proc Natl Acad Sci U S A, 107:9240-5. (PubMed:20439720)
  15. Yamashita K et al. (2007) Mouse homolog of SALL1, a causative gene for Townes-Brocks syndrome, binds to A/T-rich sequences in pericentric heterochromatin via its C-terminal zinc finger domains. Genes Cells, 12:171-82. (PubMed:17295837)

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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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