Disease relevance of Omp

• This is evident from the behavioral and electrophysiological deficits of OMP-null mice, which can be reversed by intranasal infection of olfactory sensory neurons with an OMP-expressing adenovirus [1].
• A hybrid oncogene was constructed utilizing the regulatory elements for the olfactory marker protein gene to direct the olfactory neuronal-specific expression of simian virus 40 T-antigen, a potent oncogene [2].
• While OMP has no significant sequence homology to proteins of known structure, it has a similar fold to a domain found in a variety of existing structures, including in a large family of viral capsid proteins [3].
• This monoclonal antibody reacted specifically with Omp29 of A. actinomycetemcomitans (serotype b), but not with any Omp of Escherichia coli, including OmpA [4].
• The gene encoding an outer membrane protein A (OmpA)-like, heat-modifiable Omp of Actinobacillus actinomycetemcomitans ATCC 43718 (strain Y4, serotype b) was cloned by a PCR cloning procedure [4].

High impact information on Omp

• This adenoviral-mediated rescue of the OMP-null phenotype is consistent with involvement of OMP in olfactory transduction [5].
• Adenoviral vector-mediated rescue of the OMP-null phenotype in vivo [5].
• LIF-deficient mice display significant increases, both in the absolute amount and in the number of cells expressing olfactory marker protein, a marker of mature ORNs [6].
• The murine homologue of OMP is tightly linked to the autosomal recessive deafness gene sh-1 [7].
• Increased cell death in combination with increased expression of the early differentiation marker Neurod1, as well as reduced expression of late differentiation markers (Galphaolf and Omp), suggests that neuronal differentiation in the absence of Lhx2 is primarily inhibited at, or immediate prior to, onset of OR expression [8].

Biological context of Omp

• Haplotype analysis indicates that Omp lies proximal to sh-1 [9].
• The molecular basis for the altered phenotype following the deletion of OMP is still unclear [10].
• The OMP/Bex interaction has been confirmed by demonstrating the chemical cross-linking of recombinant rat OMP with a synthetic peptide derived from the Bex amino acid sequence [10].
• Here we report the identification of an OMP partner, Bex2, by phage-display screening of an olfactory mucosal cDNA-library [10].
• However, in contrast to the adult, where its expression is restricted to the medial sensory neuronal component of the VNO, during fetal development OMP is also present in cells located in the lateral non-sensory epithelial component [11].

Anatomical context of Omp

• Olfactory marker protein (OMP) expression is a hallmark of mature vertebrate olfactory receptor neurons (ORNs) [10].
• Our results demonstrate that Olfactory Marker Protein (OMP), a marker of differentiated chemosensory cells, is already expressed in vomeronasal neurones and their fibres projecting to the accessory olfactory bulb during the last week of gestation [11].
• This is the first anatomical mapping of Bex proteins in the mouse brain and their colocalization with OMP in ORNs and hypothalamus [12].
• Here we show, using Western blot analysis and immunocytochemistry, that unilateral naris occlusion (UNO) on postnatal day 1 alters OMP immunoreactivity (IR) differentially on the occluded and non-occluded sides of the nasal cavity in 18, 24 and 70-day-old mice [13].
• OB recovery was measured by both immunoblotting and immunohistochemical analysis of growth cone associated protein (GAP) 43 and olfactory marker protein (OMP) [14].

Associations of Omp with chemical compounds

• This behavior of carnosine is consistent with that reported for the olfactory marker protein (OMP) [15].
• Formation of a full complement of OMP-expressing neurons occurs only after peripheral lesion with TX-100 [16].
• Following treatment with either ZnSO4 or Triton X-100, the pattern of changes in steady-state levels of OMP mRNA was similar to that observed for TH [17].
• The first [3H]thymidine-labeled, OMP-containing elements have been observed 7 days after administration of the radioactive thymidine [18].
• The neurons were judged to be intact and viable by trypan blue dye exclusion, the presence of olfactory marker protein (OMP), and a variety of electrophysiological measurements indicating the presence of substantial membrane potentials, low levels of intracellular Ca2+, and the ability to fire action potentials [19].

Regulatory relationships of Omp

• Olfactory marker protein (OMP) is expressed by mature primary olfactory sensory neurons during development and in adult mice [20].

Other interactions of Omp

• The lowest amounts of mRNA for erbB-4 and NRG-1 were observed at day 7 after lesion, whilst mRNAs for TH and OMP were lowest at day 14 [21].
• Antibodies to olfactory marker protein (OMP) and neuronal cell adhesion molecule (NCAM) were used to identify OSN axons [22].
• The olfactory epithelium of the knock-out mouse was thinner and showed lower expression of olfactory marker protein and growth-associated protein 43, indicating decreases in both generation and maturation of receptor cells [23].
• The decay of betaIII-tubulin and olfactory marker protein levels and the rise of proliferating cell nuclear antigen (PCNA) levels, starting 1 and 3 days, respectively, postlesion, provided the kinetic frame of neuronal dynamics [24].
• Of particular use for this mapping were preimplantation-lethal deletions having distal breakpoints localized between pid and Omp [25].

Analytical, diagnostic and therapeutic context of Omp

• OMP is a 19 kDa protein but these immunoprecipitation studies have revealed the unexpected presence of a 38 kDa band in addition to the expected 19 kDa band [1].
• In-gel tryptic digestion, mass spectrometry, and two-dimensional gel electrophoresis indicate that the 38 kDa protein behaves as a covalently cross-linked OMP-homodimer [1].
• Double-label immunocytochemistry indicates that Bex-ir is colocalized with OMP in mature olfactory receptor neurons (ORNs) and in the OMP-positive subpopulation of neurons in hypothalamus [12].
• To ascertain the cell-type lost as well as the time course and mechanism of the loss, the current study measured changes in the number of dendritic knobs, olfactory marker protein (OMP) expression and assessed TUNEL labeling as an indicator of apoptosis [26].
• Additionally, we defined the expression of OR(+) OSNs in the OE of rats via in situ hybridization with a panel of eight ORs followed by OMP immunostaining [27].

References