Deletion of GLI3 supports the homology of the human Greig cephalopolysyndactyly syndrome (GCPS) and the mouse mutant extra toes (Xt).
Vortkamp
A
A
Institut für Humangenetik der Philipps-Universität, Marburg, FRG.
Franz
T
T
Gessler
M
M
Grzeschik
K H
KH
D000015:Abnormalities, Multiple / Q000235:genetics*; D000818:Animals; D002872:Chromosome Deletion; D004268:DNA-Binding Proteins / Q000235:genetics*; D006801:Humans; D051741:Kruppel-Like Transcription Factors; D051379:Mice; D008817:Mice, Mutant Strains; D009154:Mutation; D009419:Nerve Tissue Proteins; D010641:Phenotype; D012097:Repressor Proteins; D012886:Skull / Q000002:abnormalities; D013576:Syndactyly / Q000235:genetics*; D013577:Syndrome; D014157:Transcription Factors; D029867:Xenopus Proteins; D000074290:Zinc Finger Protein Gli3; D016335:Zinc Fingers
D004268:DNA-Binding Proteins; C108003:GLI3 protein, Xenopus; C065683:GLI3 protein, human; C465571:Gli3 protein, mouse; D051741:Kruppel-Like Transcription Factors; D009419:Nerve Tissue Proteins; D012097:Repressor Proteins; D014157:Transcription Factors; D029867:Xenopus Proteins; D000074290:Zinc Finger Protein Gli3