Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation. [electronic resource]
Producer: 20000630Description: 1593-605 p. digitalISSN:- 0950-1991
- Abnormalities, Multiple
- Alleles
- Animals
- Binding Sites
- Brain -- embryology
- COS Cells
- DNA -- metabolism
- DNA-Binding Proteins
- Diencephalon -- embryology
- Embryonic and Fetal Development
- Extremities -- embryology
- Gene Expression
- Hedgehog Proteins
- Humans
- Kruppel-Like Transcription Factors
- Lung -- embryology
- Mice
- Mice, Transgenic
- Mutagenesis
- Nerve Tissue Proteins
- Notochord -- embryology
- Nuclear Proteins
- Oncogene Proteins -- genetics
- Proteins -- genetics
- Repressor Proteins
- Signal Transduction -- physiology
- Spinal Cord -- embryology
- Trans-Activators
- Transcription Factors -- genetics
- Xenopus Proteins
- Zinc Finger Protein GLI1
- Zinc Finger Protein Gli2
- Zinc Finger Protein Gli3
- Zinc Fingers
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
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