AI Article Synopsis
- Neuropathy target esterase (NTE) is crucial for nerve development and is a key target of organophosphate compounds that lead to delayed neuropathy, characterized by nerve axon degeneration.
- Researchers identified that Gbeta2 and Gbeta2-like I subunits can bind to the C-terminal of NTE, implying a potential regulatory role.
- Experiments showed that reducing Gbeta2 levels through RNA interference decreased NTE activity without affecting its expression, indicating that Gbeta2 may be essential for maintaining NTE function.
Article Abstract
Neuropathy target esterase (NTE) was identified as the primary target of organophosphate compounds that cause a delayed neuropathy with degeneration of nerve axons. NTE is a novel phospholipase B anchored to the cytoplasmic face of endoplasmic reticulum and essential for embryonic and nervous development. However, little is known about the regulation of NTE. A human fetal brain cDNA library was screened for proteins that interact with NTE, Gbeta2 and Gbeta2-like I subunits were found to be able to bind the C-terminal of NTE in yeast. The interaction of Gbeta2 and NTE was confirmed by in vivo co-immunoprecipitation analysis in COS7 cells. Furthermore, depletion of Gbeta2 by RNA interference down regulated the activity of NTE but not its expression level. In addition, the activity of NTE was down regulated by the G protein signal pathway influencing factor, pertussis toxin, treatment in vivo. These findings suggest that Gbeta2 may play a significant role in maintaining the activity of NTE.
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| http://dx.doi.org/10.1016/j.biocel.2006.08.001 | DOI Listing |
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