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P. Koulen, H. Xin, P. Mitchell, E.V. Gregg, O.A. Mafe, E. Nixon; Localization of Binding Proteins of Intracellular Calcium Channels in Mouse Retina Ganglion Cells . Invest. Ophthalmol. Vis. Sci. 2006;47(13):167.
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© ARVO (1962-2015); The Authors (2016-present)
Inositol–1, 4, 5–triphosphate receptors (IP3Rs) are intracellular Ca2+ release channels that are critical components for controlling cytosolic Ca2+ concentrations and intracellular signaling pathways. In neurons, including retinal ganglion cells (RGCs), these IP3R–regulated pathways include synaptic activity, gene expression, differentiation and apoptosis. The molecular substrates of such regulatory pathways controlling intracellular Ca2+ levels include IP3R binding proteins. Identifying the localization of these accessory proteins which tightly control IP3R function is critical for the understanding of RGC function under the control of Ca2+ signaling pathways.
The expression of IP3R–associated proteins CARP and FKBP12 by adult mouse RGCs was determined using immunoblotting, immunocytochemistry and specific antibodies. RGCs were identified by cell specific markers including neurofilament 68kDa Thy1.1 and Thy1.2.
Immunoreactivity for the IP3R–associated proteins CARP and FKBP12 was detected on intracellular membranes of RGCs throughout the cells. Expression was co–localized with RGC markers and IP3R subtypes 1, 2 and 3.
The presence of critical IP3R binding proteins in RGCs indicates that these proteins are localized in compartments that allow interaction with IP3Rs and play a potential role in RGC calcium signaling. Expression and differential localization of IP3R associated proteins may therefore be a molecular mechanism used by RGC Ca2+ signaling. These findings allow us to identify the involvement of IP3R–mediated Ca2+ signaling in RGC physiology and to develop neuroprotective strategies for RGCs targeting Ca2+–mediated cell toxicity.
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