Halford, S <br/><br/>
Isolation of a putative transcriptional regulator from the region of 22q11 deleted in DiGeorge syndrome, Shprintzen syndrome and familial congenital heart disease.  [electronic resource] 

 -  Human molecular genetics  Dec 1993 
 - 2099-107 p.  digital 
<br/><br/> Publication Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't 
<br/><br/><label>ISSN: </label>0964-6906 
<br/><br/><label>Standard No.: </label>10.1093/hmg/2.12.2099  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Abnormalities, Multiple--genetics<br/>Amino Acid Sequence<br/>Animals<br/>Base Sequence<br/>Cell Cycle Proteins<br/>Chromosome Mapping<br/>Chromosomes, Human, Pair 22<br/>Consensus Sequence<br/>DiGeorge Syndrome--genetics<br/>Embryonic and Fetal Development<br/>Enhancer Elements, Genetic<br/>Genomic Library<br/>Heart Defects, Congenital--genetics<br/>Histone Chaperones<br/>Humans<br/>In Situ Hybridization, Fluorescence<br/>Mice<br/>Molecular Sequence Data<br/>Multigene Family<br/>Polymerase Chain Reaction<br/>Sequence Deletion<br/>Sequence Homology, Amino Acid<br/>Transcription Factors--genetics<br/>Transducin--genetics<br/>Translocation, Genetic