8. Maxime Monfort, Belgium, Leopard Trek, 1 37.
Recent studies have suggested that the activation of TREK channels including TREK-1 mediates neuroprotection.
Because the absence of TREK-1 contributeributo to preterm labor, we also determined TREK-1 expression in samples from women in labor at 28 33 weeks gestation.
Electrophysiological analysis of two polypeptides engineered by mutagenesis (TREK-1[M53I], TREK-1[ΔN52]) revealed reduced current amplitude and K+ selectivity of the truncated TREK-1 isoform.
K2P2.1 (TREK-1) channels are expressed in the human heart.
The sensitivity of TREK-1[ΔN52] to fluoxetine decreased by 70%, indicating that the first 52 amino acids are essential for TREK-1 sensitivity to this drug.
Alternative translation initiation (ATI) generates two different protein products from a single transcript of TREK-1.
Down-regulation of TREK-1 message was seen by Q-PCR in laboring tissues consistent with a role for TREK-1 in maintaining uterine quiescence prior to labor.
Functional studies are consistent with a role for TREK-1 in uterine quiescence.
TREK-1 and TREK-2 are respectively inhibited and activated by extracellular acidification [11], [12].
Human brain was utilized as a positive for both TREK-1 and TRAAK protein expression.
