Psychiatry related information on Rem1

• Mice were treated with either vehicle, SCH (0.015 mg/kg), remoxipride (Rem, 0.3 mg/kg), CPP (2.5 mg/kg) or NBQX (10.0 mg/kg), followed 30 min later by vehicle or 75 mg/kg TDF (TDF), twice a week for 7 weeks, with locomotor activity measured post-dosing once a week [1].

High impact information on Rem1

• Regulation of voltage-gated calcium channel activity by the Rem and Rad GTPases [2].
• Rem is expressed in primary skeletal myoblasts and, when overexpressed in C2C12 myoblasts, wild-type Rem inhibits L type Ca2+ channel activity [2].
• The administration of lipopolysaccharide to mice, a potent activator of the inflammatory and immune systems, results in the general repression of Rem mRNA levels in a dose- and time-dependent manner [3].
• Ribonuclease protection analysis found Rem to be expressed at comparatively high levels in cardiac muscle and at moderate levels in lung, skeletal muscle, and kidney [3].
• The activity of these compounds largely paralleled that of bis(2-chloroethyl)-N-nitrosourea (BCNU), except for those cell lines which exhibited the Rem phenotype; triazenes were more active in those lines than BCNU [4].

Biological context of Rem1

• These results suggest that 14-3-3 may allow the recruitment of distinct proteins that participate in Rem-mediated signal transduction pathways [5].
• Examination of the interaction between 14-3-3zeta and various Rem deletion mutants mapped a critical binding site to the C-terminus of Rem [5].
• Interestingly, nuclear targeting of Rad and Rem can relocalize and sequester the beta-subunit to the nucleus, thus providing a novel mechanism for Ca2+ channel downregulation [6].

Analytical, diagnostic and therapeutic context of Rem1

• Immunoprecipitation studies demonstrate an interaction that is independent of the nucleotide state of Rem [5].

References