INT250283
From wiki-pain
|
|
|
|
|
Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The marked loss of EAAT2 described in this report parallels loss of AQP4 in lesioned NMO spinal cord tissue and contrasts with the increases in EAAT2 and AQP4 reported in both active and chronic MS lesions (20). | |||||||||||||||
| |||||||||||||||
|
For example, it might be feasible to ameliorate tissue damage in both gray and white matter if therapeutic upregulation of EAAT2 can be achieved in patients whose neurological dysfunction is attributable to AQP4 autoimmunity.
| |||||||||||||||
| |||||||||||||||
|
We did not detect EAAT2 in GFP vector-transfected cells (Fig. 3 B), but EAAT2 was strikingly upregulated in the plasma membrane of cells transgenically expressing either AQP4 or AQP5 (Fig. 3 B). | |||||||||||||||
| |||||||||||||||
|
We confirmed that upregulated EAAT2 protein in GFP-AQP4 transfected cells was functional by demonstrating that GFP-AQP4 cells imported two- to threefold more glutamate via the Na+-dependent pathway relative to GFP vector cells (P < 0.0002; Fig. 3 F). | |||||||||||||||
| |||||||||||||||
|
Furthermore, both the mRNA and protein levels of EAAT 1 and EAAT 2 were found to be significantly increased in the autistic cerebellum (Purcell et al., 2001). | |||||||||||||||
| |||||||||||||||
|
Since the protein level and activity of glutamate transporters are controlled by the extracellular glutamate concentration or by activity-dependent mechanisms (Levy et al., 1995), increased EAAT 1 and EAAT 2 protein levels may be due to increased extracellular glutamate concentrations in autism. | |||||||||||||||
| |||||||||||||||
|
General Comments
This test has worked.