Park, H L <br/><br/>
Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation.  [electronic resource] 

 -  Development (Cambridge, England)  Apr 2000 
 - 1593-605 p.  digital 
<br/><br/> Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. 
<br/><br/><label>ISSN: </label>0950-1991 
<br/><br/><label>Standard No.: </label>10.1242/dev.127.8.1593  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Abnormalities, Multiple<br/>Alleles<br/>Animals<br/>Binding Sites<br/>Brain--embryology<br/>COS Cells<br/>DNA--metabolism<br/>DNA-Binding Proteins<br/>Diencephalon--embryology<br/>Embryonic and Fetal Development<br/>Extremities--embryology<br/>Gene Expression<br/>Hedgehog Proteins<br/>Humans<br/>Kruppel-Like Transcription Factors<br/>Lung--embryology<br/>Mice<br/>Mice, Transgenic<br/>Mutagenesis<br/>Nerve Tissue Proteins<br/>Notochord--embryology<br/>Nuclear Proteins<br/>Oncogene Proteins--genetics<br/>Proteins--genetics<br/>Repressor Proteins<br/>Signal Transduction--physiology<br/>Spinal Cord--embryology<br/>Trans-Activators<br/>Transcription Factors--genetics<br/>Xenopus Proteins<br/>Zinc Finger Protein GLI1<br/>Zinc Finger Protein Gli2<br/>Zinc Finger Protein Gli3<br/>Zinc Fingers