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Akira Imamoto reports exciting results in two articles in the January, 2006 issue of Molecular Cell

Akira Imamoto, D.D.S., Ph.D., is Associate Professor in the Ben May Department for Cancer Research. Download a PDF or Flash Paper document about his lab's results:

Crkl Deficiency disrupts Fgf8 Signaling in a Mouse Model of 22q11 Deletion Syndromes

This study demonstrates genetic interaction of Fgf8 and the mouse homologue of the 22q11 gene CRKL through a direct role of Crkl in Fgf8-induced signaling.

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Dose-Dependent interaction of Tbx1 and Crkl and Locally Aberrant RA Signaling in a Model of del22q11 Syndrome

This study provide the first experimental evidence that 22q11 deletion syndrome is a contiguous syndrome in which combined heterozygosity of two 22q11 genes TBX1 and CRKL plays a critical role. This study also demonstrates that the phenotype is attributable to at least partly from aberrant retinoic acid homeostasis during early development of the pharyngeal apparatus.

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