A Mutation inSyne2Causes Early Retinal Defects in Photoreceptors, Secondary Neurons, and Müller Glia
Investigative Ophthalmology & Visual Science2015Vol. 56(6), pp. 3776–3776
Citations Over Time
Dennis M. Maddox, Gayle B. Collin, Akihiro Ikeda, C. Herbert Pratt, Sakae Ikeda, Britt Johnson, R.E. Hurd, Lindsay S. Shopland, Jürgen Κ. Naggert, Bo Chang, Mark P. Krebs, Patsy M. Nishina
Abstract
SYNE2 is important for normal retinal development. We have determined that not only is photoreceptor nuclear migration affected, but also the positions of Müller glia and secondary neurons are disturbed early in retinal development. The cpfl8 mouse model will serve as an important resource for further examining the role of nuclear scaffolding and migration in the developing retina.
Related Papers
- → Outer Retinal Dysfunction in the Absence of Structural Abnormalities in Multiple Sclerosis(2018)34 cited
- → Age-Related Changes in the Mouse Outer Retina(2001)86 cited
- → The effects of iodoacetic acid on the mouse retina(2014)17 cited
- → Monitoring Morphological Changes in the Retina of Rhodopsin−/−Mice with Spectral Domain Optical Coherence Tomography(2012)20 cited
- → Role of transcription factor Tgif2 in photoreceptor differentiation in the mouse retina(2016)5 cited