Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P80404 (GABA transaminase)
 786 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The number of cerebellar Purkinje cells is increased by over 40% in young transgenic mice that overexpress a human Bcl-2 transgene (Hu-Bcl-2). To determine whether the Bcl-2-mediated rescue of Purkinje cells persists through life, the numbers of Purkinje cells were estimated in 6-, 12-, 18-, and 24-month-old Hu-Bcl-2 transgenic mice and age-matched controls. In addition, the expression of four markers for Purkinje cell differentiation, calbindin (CaBP), the 67-kDa isoform of glutamic acid decarboxylase (GAD67), gamma-aminobutyric acid transaminase (GABA-T), and the NMDA-R1 receptor subtype (NMDA-NR1) was analyzed in 6-month-old Hu-Bcl-2 transgenics and controls to determine whether overexpression of Bcl-2 and rescue from naturally occurring cell death affects the normal differentiation of Purkinje cells. The estimates of Purkinje cell numbers showed that the number of Purkinje cells in the Hu-Bcl-2 transgenics declines after 6 months to approach wild-type values by 18 months. Although the exogenous human BCL-2 is still expressed in Purkinje cells at 24 months, the expression levels of human BCL-2 appear to decline significantly after 6 months, suggesting that survival of the supernumary Purkinje cells depends on the sustained overexpression of Bcl-2. All the Purkinje cells in the Hu-Bcl-2 transgenic mice appeared to express normal levels of the differentiation markers analyzed so there was no evidence for a class of Purkinje cells that do not differentiate normally when rescued from naturally occurring cell death.
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PMID:Cerebellar Purkinje cell loss in aging Hu-Bcl-2 transgenic mice. 1523 31

Mongolian gerbils subjected to transient global ischemia exhibit neuroprotection against ischemic neuronal cell death in the hippocampal CA1 region when treated with vanillin, 4-hydroxybenzyl aldehyde (4-HBAL) and 4-hydroxybenzyl alcohol (4-HBA), which are active components of Gastrodia elata Blume. Pre- and post-insult vanillin, 4-HBAL and 4-HBA treated-animals showed a significant increase in neuronal survival (66.32%, 43.21% and 64.58%, respectively) compared to vehicle-treated animals. Animals exhibited a gender difference in this neuroprotective effect. To study the neuroprotective mechanism of 4-HBA, we investigated N-methyl-d-aspartate (NMDA) receptor 1 (NR1), 8-hydroxy-2'-deoxyguanosine (8-OHdG), and gamma-aminobutyric acid transaminase (GABA-T) immunoreactivity at various times after ischemic insults. Treatment with 4-HBA did not affect NR1 expression levels, down-regulated 8-OHdG immunoreactivity, and increased GABA-T expression levels after global ischemia, suggesting that 4-HBA inhibited NR1 stimulation. Moreover, GABA-T was rapidly increased in the early stage after ischemia, which might enhance the survival of cells by supplying energy to the CA1 region. These results suggest that 4-HBA inhibits oxidative stress and excitotoxicity for at least 12 h and suppresses neuronal death in CA1 region. Diethyl ether fractions of GE scavenged hydroxyl radical (OH.) and showed antioxidant activity on lipid peroxidation. Vanillin and 4-HBA treatment blocked oxidative damage in PC12 cells. The neuroprotective effect has therapeutic significance and these compounds need to be evaluated for potential use in protecting against neuronal cell damage during stroke.
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PMID:Vanillin, 4-hydroxybenzyl aldehyde and 4-hydroxybenzyl alcohol prevent hippocampal CA1 cell death following global ischemia. 1794 3