| First Author | Mendez A | Year | 2002 |
| Journal | Adv Exp Med Biol | Volume | 514 |
| Pages | 361-88 | PubMed ID | 12596933 |
| Mgi Jnum | J:91656 | Mgi Id | MGI:3050157 |
| Doi | 10.1007/978-1-4615-0121-3_22 | Citation | Mendez A, et al. (2002) Mouse models to study GCAP functions in intact photoreceptors. Adv Exp Med Biol 514:361-88 |
| abstractText | In photoreceptor cells cGMP is the second messenger that transduces light into an electrical response. Regulation of cGMP synthesis by Ca2+ is one of the key mechanisms by which Ca2+ exerts negative feedback to the phototransduction cascade in the process of light adaptation. This Ca2+ feedback to retinal guanylyl cyclases (Ret-GCs) is conferred by the guanylate cyclase-activating proteins (GCAPs). Mutations in GCAP1 that disrupt the Ca2+ regulation of Ret-GCs in vitro have been associated with severe human vision disorders. This chapter focuses on recent data obtained from biochemical and electrophysiological studies of GCAP1/GCAP2 knockout mice and other GCAP transgenic mice, addressing: 1. the quantitative aspects of the Ca2+-feedback to Ret-GCs in regulating the light sensitivity and adaptation in intact rods; 2. functional differences between GCAP1 and GCAP2 in intact rod photoreceptors; and 3. whether GCAP mutants with impaired Ca2+ binding lead to retinal disease in vivo by constitutive activation of Ret-GCs and elevation of intracellular cGMP, as predicted from in vitro studies. |
