Jeffrey O. Bush

Isolation and developmental expression analysis of Tbx22, the mouse homolog of the human X-linked cleft palate gene.

The T-box gene Tbx10 exhibits a uniquely restricted expression pattern during mouse embryogenesis.

The cleft lip and palate defects in Dancer mutant mice result from gain of function of the Tbx10 gene.

Development of the upper lip: morphogenetic and molecular mechanisms.

Expression of Wnt9b and activation of canonical Wnt signaling during midfacial morphogenesis in mice.

Inhibition of gap junction communication at ectopic Eph/ephrin boundaries underlies craniofrontonasal syndrome.

The TGF-beta pseudoreceptor gene Bambi is dispensable for mouse embryonic development and postnatal survival.

Ephrin-B1 regulates axon guidance by reverse signaling through a PDZ-dependent mechanism.

Ephrin-B1 forward signaling regulates craniofacial morphogenesis by controlling cell proliferation across Eph-ephrin boundaries.

Eph/ephrin signaling: genetic, phosphoproteomic, and transcriptomic approaches.

Palatogenesis: morphogenetic and molecular mechanisms of secondary palate development.

The widely used Wnt1-Cre transgene causes developmental phenotypes by ectopic activation of Wnt signaling.

Embryonic expression of EphA receptor genes in mice supports their candidacy for involvement in cleft lip and palate.

Convergence and extrusion are required for normal fusion of the mammalian secondary palate.

Neural crest defects in ephrin-B2 mutant mice are non-autonomous and originate from defects in the vasculature.

From Bench to Bedside and Back: Improving Diagnosis and Treatment of Craniofacial Malformations Utilizing Animal Models.

Unidirectional Eph/ephrin signaling creates a cortical actomyosin differential to drive cell segregation.

EPHRIN-B1 Mosaicism Drives Cell Segregation in Craniofrontonasal Syndrome hiPSC-Derived Neuroepithelial Cells.