Xin Zhang

This study shows FGF signaling is essential for mammalian retinal regeneration by enabling Muller glia to overcome transcriptional barriers through sustained ERK activation.

The paper shows that Wnt signaling, through {beta}-catenin, regulates passive cell competition in the retina by inducing a cadherin switch that segregates cells into distinct compartments.

This study identifies Shc1 as a critical collaborator with Frs2 and Shp2 in recruiting Grb2 during FGF signaling for lens development.

This study identifies an mTOR-Wnt-Rac1 signaling axis that regulates cytoskeletal tension to drive lens vesicle closure, with disruptions leading to developmental defects like Peters anomaly.

This study shows that a catalytically inactive Shp2 mutation causes hydrocephalus by altering conformation, which can be rescued by allosteric inhibition.

This study shows that Ptpn14 deficiency in mice causes female-specific Hippo pathway defects, including corneal lesions, uterine defects, and organ abnormalities, with conserved roles in humans.

This study identifies Abl kinases as regulators of FGF signaling that prevent Peters anomaly by modulating RhoA and Rac1 activity through the Ptpn12-p130Cas pathway.

This study shows that PLCgamma competes with PI3K in phosphoinositide metabolism to regulate lacrimal gland branching.

This study shows that chondroitin sulfates and heparan sulfates play distinct roles in the assembly and barrier function of the retinal basement membrane.

The paper shows that FGF and Wnt signaling gradients determine phase transitions in vertebrate eye cup development, specifying cell fates through their combinatorial code.

This study shows that FGF signaling is essential for ciliary margin development in the retina, with its disruption causing aniridia by altering the boundary between the central retina and the ciliary margin.