Jeffrey M. Gross

N-Ethylmaleimide-Sensitive Factor b (nsfb) Is Required for Normal Pigmentation of the Zebrafish Retinal Pigment Epithelium.

A GAL4-inducible transgenic tool kit for the in vivo modulation of Rho GTPase activity in zebrafish.

Eye development and photoreceptor differentiation in the cephalopod Doryteuthis pealeii.

The hyaloid vasculature facilitates basement membrane breakdown during choroid fissure closure in the zebrafish eye.

Tet-mediated DNA hydroxymethylation regulates retinal neurogenesis by modulating cell-extrinsic signaling pathways.

The RNA-binding protein Celf1 post-transcriptionally regulates p27Kip1 and Dnase2b to control fiber cell nuclear degradation in lens development.

Using GAL4-Inducible Transgenics to Modulate Rho GTPase Activity in Zebrafish.

Regeneration of the zebrafish retinal pigment epithelium after widespread genetic ablation.

Zebrafish mab21l2 mutants possess severe defects in optic cup morphogenesis, lens and cornea development.

Genetic and epigenetic control of retinal development in zebrafish.

Lysyl hydroxylase 3 is required for normal lens capsule formation and maintenance of lens epithelium integrity and fate.

Mitf-family transcription factor function is required within cranial neural crest cells to promote choroid fissure closure.

dnmt1 function is required to maintain retinal stem cells within the ciliary marginal zone of the zebrafish eye.

Evolution and development of complex eyes: a celebration of diversity.

Epigenetic regulation of retinal development.

The retinal pigment epithelium: Development, injury responses, and regenerative potential in mammalian and non-mammalian systems.

The immune response is a critical regulator of zebrafish retinal pigment epithelium regeneration.

Retinal ganglion cell survival after severe optic nerve injury is modulated by crosstalk between Jak/Stat signaling and innate immune responses in the zebrafish retina.

Serotonin transporter-mediated molecular axis regulates regional retinal ganglion cell vulnerability and axon regeneration after nerve injury.