Disease relevance of OPN3

• A conventional electrophysiological study performed in the same patients was used to classify them according to the presence or absence of electrophysiological criteria for peripheral polyneuropathy (ECPN) [1].
• We report a female patient, 11 years old, of Japanese ancestry and living in North Brazil, who developed NMO 1 week after having had a benign form of dengue fever [2].

High impact information on OPN3

• Furthermore, the human OPN3 gene overlaps with the neighboring KMO gene on a genomic as well as on an RNA level, whereas the corresponding genes in mouse lie close together but do not overlap [3].
• Based on RT-PCR data and comparative genomic sequence analysis, we show that the human OPN3 gene consists of six exons and expresses various splice variants, while the murine homologue contains four exons and produces just one splice form [3].
• As part of an ongoing search to identify novel mammalian photopigments that may mediate nonvisual tasks such as circadian entrainment and acute suppression of pineal melatonin levels, a number of recently cloned nonvisual opsin sequences were used to search dbEST. panopsin (OPN3) was one of the clones identified using this approach [4].
• Reverse-transcription polymerase chain reaction analysis showed that NMO1 mRNA levels did not differ in growth-arrested confluent cell and growing cells, suggesting that the increased NMO1 activity with cell density was due to posttranslational events [5].
• We also found that NMO1 activity was related to osteoblastic cell growth [5].

Biological context of OPN3

• Assignment of panopsin (OPN3) to human chromosome band 1q43 by in situ hybridization and somatic cell hybrids [6].
• NMO1 activity increased with osteoblastic cell density [5].
• We examined the ability of normal human trabecular osteoblastic cells to express NAD(P)H:quinone oxidoreductase (NMO1) and studied its modulation during cell proliferation and growth arrest [5].
• Opsin 3 was identified by quantitative PCR expression analysis as the putative light receptor molecule for light-induced exocytosis [7].

Anatomical context of OPN3

• NMO1 activity does not appear to be related to induction of osteoblast differentiation because treatment with the differentiating agent 1,25(OH)(2) vitamin D(3) had no effect on NMO1 activity [5].

Associations of OPN3 with chemical compounds

• We found that confluent primary human trabecular osteoblastic cells derived from healthy individuals constitutively express NMO1 activity, measured using 2-6 dichlorophenol indophenol (DCI) or menadione (vitamin K3) as substrate, and NADPH or NADH as electron donor [5].
• TCDD-activated nuclear extracts from both mouse Hepa 1c1c7 cells and human MCF-7 cells specifically bound to the hERO with relative binding affinities of 15.5 nM and 5.6 nM, respectively [8].

Other interactions of OPN3

• During hNMO1 therapy effects were observed on CD4 cell counts and plasma viral loads and further dose finding trials are necessary to better determine the therapeutic activity of hNM01 in HIV-infected individuals [9].
• Analysis of NADPH:quinone oxidoreductase (NMO-1) and plasminogen activator inhibitor-2 (PAI-2) mRNA expression revealed a dose-dependent induction of both genes in MDA-MB 231 cells after TCDD-treatment [10].

References