Serum sulfatase activity is more elevated in colonic adenomas than cancers.

Background And Aims: Elucidation of molecular basis of the adenomatous polyps (AP) and colorectal cancer (CRC) development is crucial for their prevention, early detection, and treatment. According to the recent discoveries, sulfatases are implied in extracellular matrix remodeling and degradation and also in the regulation of certain signaling pathways. However, their exact role in carcinogenesis remains unclear.

GABA transient sets the susceptibility of mIPSCs to modulation by benzodiazepine receptor agonists in rat hippocampal neurons.

Benzodiazepines (BDZs) are known to increase the amplitude and duration of IPSCs. Moreover, at low [GABA], BDZs strongly enhance GABAergic currents suggesting the up-regulation of agonist binding while their action on gating remains a matter of debate. In the present study we have examined the impact of flurazepam and zolpidem on mIPSCs by investigating their effects on GABA(A)R binding and gating and by considering dynamic conditions of synaptic receptor activation.

Benzodiazepine receptor agonists affect both binding and gating of recombinant alpha1beta2gamma2 gamma-aminobutyric acid-A receptors.

Benzodiazepines are known to act by enhancing the effect of gamma-aminobutyric acid-A receptor agonists. Positive modulation by benzodiazepines is typically ascribed to upregulation of agonist binding affinity but their effect on gamma-aminobutyric acid-A receptor gating remain unclear. In this work, we have used the ultrafast application system to examine the impact of flurazepam and zolpidem on recombinant alpha1beta2gamma2 gamma-aminobutyric acid-A receptors.

Molecular evolution of enolase.

Enolase (EC 4.2.1.