Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The alpha-esterase cluster of D. melanogaster contains 11 esterase genes dispersed over 60 kb. Embedded in the cluster are two unrelated open reading frames that have sequence similarity with genes encoding ubiquitin-conjugating enzyme and tropomyosin. The esterase amino acid sequences show 37-66% identity with one another and all but one have all the motifs characteristic of functional members of the carboxyl/cholinesterase multigene family. The exception has several frameshift mutations and appears to be a pseudogene. Patterns of amino acid differences among cluster members in relation to generic models of carboxyl/cholinesterase protein structure are broadly similar to those among other carboxyl/cholinesterases sequenced to date. However the alpha-esterases differ from most other members of the family in: their lack of a signal peptide; the lack of conservation in cysteines involved in disulfide bridges; and in four indels, two of which occur in or adjacent to regions that align with proposed substrate-binding sites of other carboxyl/cholinesterases. Phylogenetic analyses clearly identify three simple gene duplication events within the cluster. The most recent event involved the pseudogene which is located in an intron of another esterase gene. However, relative rate tests suggest that the pseudogene remained functional after the duplication event and has become inactive relatively recently. The distribution of indels also suggests a deeper node in the gene phylogeny that separates six genes at the two ends of the cluster from a block of five in the middle.
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PMID:Duplication and divergence of the genes of the alpha-esterase cluster of Drosophila melanogaster. 870 90

Outer hair cells (OHCs) are the source of otoacoustic emissions, following a tropomyosin-miosin-dependent contraction, which are regulated by the olivocochlear bundle via the release of acetylcholine (ACh). ACh acts on ACh receptors (AChR) located on the OHC post-synaptic membrane. In myasthenia gravis (M.G.) neuromuscular transmission is reduced due to the action of AChR autoantibodies. It has previously been shown that M.G. induces a reduction in transient evoked otoacoustic emissions (TEOAEs), which is reversed after administration of a cholinesterase (AChE) inhibitor. Distortion product otoacoustic emissions (DPOAEs) were recorded before and 60 min after oral administration of 60 mg pyridostigmine bromide in 25 patients with normal hearing affected by M.G. The results were compared with those from 25 age-matched normal controls. Mean values of DPOAE amplitude in myasthenic patients were significantly (p < 0.05) lower at all frequencies before drug administration. All patients showed an overall significant (p < 0.05) increase in DPOAE amplitude after drug administration, although without reaching the control values. Such a recovery was more evident and highly significant (p < 0.01) for middle and high frequencies and could be explained by a higher concentration of ACh receptors in the basal and middle cochlear turns. These data seem to confirm the role of ACh in the neurotransmission of the auditory efferent system and may represent a new in vivo model for the investigation of the physiology of this system.
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PMID:The role of cholinergic transmission in outer hair cell functioning evaluated by distortion product otoacoustic emissions in myasthenic patients. 1134 60