Irene E. Zohn

Cell polarity pathways converge and extend to regulate neural tube closure.

Using genomewide mutagenesis screens to identify the genes required for neural tube closure in the mouse.

p38 and a p38-interacting protein are critical for downregulation of E-cadherin during mouse gastrulation.

The flatiron mutation in mouse ferroportin acts as a dominant negative to cause ferroportin disease.

The Hectd1 ubiquitin ligase is required for development of the head mesenchyme and neural tube closure.

Modeling neural tube defects in the mouse.

Transformation by a nucleotide-activated P2Y receptor is mediated by activation of Galphai, Galphaq and Rho-dependent signaling pathways.

The visceral yolk sac endoderm provides for absorption of nutrients to the embryo during neurulation.

The iron exporter ferroportin 1 is essential for development of the mouse embryo, forebrain patterning and neural tube closure.

The coiled-coil domain containing protein CCDC40 is essential for motile cilia function and left-right axis formation.

Hectd1 regulates intracellular localization and secretion of Hsp90 to control cellular behavior of the cranial mesenchyme.

Mouse as a model for multifactorial inheritance of neural tube defects.

Does the cranial mesenchyme contribute to neural fold elevation during neurulation?

HectD1 E3 Ligase Modifies Adenomatous Polyposis Coli (APC) with Polyubiquitin to Promote the APC-Axin Interaction.