Disease relevance of Rcvrn

• It is not present in neurons postsynaptic to rods, yet we found that light-evoked responses of rod bipolar and ganglion cells were shortened when measured in recoverin-deficient retinas [1].
• This cell culture system will be useful for investigating environments and factors which participate in the expression of the recoverin gene, and may identify regulatory features of the recoverin gene which cause it to be illicitly expressed in small-cell lung carcinomas in cancer-associated retinopathy (CAR) [2].
• CONCLUSIONS: Inhibition of the CTLA4 pathway is essential for the development of recoverin-induced murine CAR, suggesting that strengthening negative T cell signaling through CTLA4 may lessen the retinal degenerations in CAR-affected subjects [3].

High impact information on Rcvrn

• Instead, it is an effect of recoverin downstream of phototransduction in rods that prolongs signal transmission and enhances visual sensitivity [1].
• However, the terminal differentiation of OFF-CB cells in the retina of Vsx1(tauLacZ)/Vsx1(tauLacZ) mice was incomplete, as demonstrated by a substantial reduction in the expression of at least four markers (recoverin, NK3R, Neto1, and CaB5) for these interneurons [4].
• Our major finding is that light causes a significant reduction of recoverin in rod outer segments, accompanied by its redistribution toward rod synaptic terminals [5].
• Recoverin undergoes light-dependent intracellular translocation in rod photoreceptors [5].
• The Ca2+-binding protein recoverin may regulate visual transduction in retinal rods and cones, but its functional role and mechanism of action remain controversial [6].

Biological context of Rcvrn

• Unique retina cell phenotypes revealed by immunological analysis of recoverin expression in rat retina cells [2].
• Many important questions related to rhodopsin phosphorylation remain unanswered and new strategies and methods are needed to address issues such as the roles of Ca2+ and recoverin [7].
• Evaluation of the contributions of recoverin and GCAPs to rod photoreceptor light adaptation and recovery to the dark state [8].

Anatomical context of Rcvrn

• Recoverin immunoreactive cells, presumably the photoreceptors, were observed embryonically (E 18.5) and their number increased until PN 14 [9].
• The main findings show that whereas the recoverin antibody labels both rod and cone photoreceptors in all species, calbindin consistently labels cones, but not rods, in the haplorhine primates marmoset, macaque and human, but none of the photoreceptors in the mouse lemur [10].
• RESULTS: After they were grafted to the degenerating retina of mature mice, a subset of the retinal progenitor cells developed into mature neurons, including presumptive photoreceptors expressing recoverin, rhodopsin, or cone opsin [11].
• Melanocytes also express mRNA of all photoreceptor genes besides transducin, but were devoid of the corresponding protein, which was tested for rhodopsin, cGMP-phosphodiesterase, guanylyl cyclase and recoverin [12].
• The morphologies of photoreceptors, horizontal cells, recoverin-positive OFF-cone bipolar cells, rod bipolar cells, dopaminergic amacrine cells, and Müller cells appeared normal [13].

Associations of Rcvrn with chemical compounds

• In contrast to the SNP-induced cGMP accumulation, cGMP levels in response to particulate guanylate cyclase activator atriopeptin II were equal to or greater in cultured human cells than in fresh human vascular tissue [14].
• Mouse brain was found by immunoblot analysis to have a protein of Mr 23,000 (P23k) that was clearly different from recoverin and was labeled with an antiserum raised against the NH2-terminus of recoverin [15].
• Effects of cytotoxic T lymphocyte antigen 4 (CTLA4) signaling and locally applied steroid on retinal dysfunction by recoverin, cancer-associated retinopathy antigen [3].
• PURPOSE: To assess the cytotoxic T lymphocyte antigen 4 (CTLA4) pathway in the recoverin peptide (R64; AYAQHVFRSF) mouse model of cancer-associated retinopathy (CAR) and to assess the protective effects of subconjunctival triamcinalone injections in this model [3].
• RESULTS: We detected gene transcripts of S-Antigen (S-Ag), interphotoreceptor retinoid-binding protein, opsin, recoverin, lens major intrinsic protein (MIP), alphaA-, alphaA(-ins)- and gamma-crystallins in the thymi of BALB/c and FVB/N mouse strains [16].

Other interactions of Rcvrn

• In this study, we describe the expression of markers for photoreceptors (recoverin), horizontal cells (calbindin), bipolar cells (protein kinase C; PKC) and cytoskeletal elements pivotal to axonogenesis (beta-tubulin and actin) during perinatal development of mouse retina [9].
• These results provide a developmental timeframe for the expression of recoverin, calbindin, synaptophysin, beta-tubulin and actin [9].
• We show by immunocytochemistry analysis that a subpopulation of differentiated cells was committed to the photoreceptor lineage given that these cells expressed the photoreceptor proteins recoverin, peripherin, and rhodopsin in a same ratio [17].
• These inner nuclear layer (INL) rods contained markers of early rod differentiation: rod opsin, arrestin, and recoverin [18].
• Anti-CTLA4 antibody treatment did not give any significant differences in T cell proliferation and humoral reaction against recoverin [3].

References