Rabbit Anti-Human RGS16 (a.a. 141-190) Polyclonal antibody

The number and affinity of GABA(B) receptors (assayed by the specific antagonist [H-3]CGP54626A) was unchanged when compared in carefully washed cerebrocortical membranes from young (12-day-old) and adult (90-day-old) rats. In contrast, high-affinity GTPase activity, both basal and baclofen-stimulated was significantly higher (by 45% and 56%, respectively) in adult than in young rats. Similar results were obtained by concomitant determination of agonist (baclofen)-stimulated GTPgammaS binding. Under standard conditions, baclofen-stimulated GTPase activity was further considerably enhanced by exogenously added regulator of G protein function, RGS1, but not by RGS16. RGS16 was able to affect agonist-stimulated GTPase activity only in the presence of markedly increase substrate (GTP) concentrations. RGS1 alone slightly increased GTPase activity in adult rats, but neither RGS1 nor RGS16 influenced GTPase activity in membrane preparations isolated from young animals. These findings indicate increasing functional activity of trimeric G protein(s) involved in GABAergic transmission in the developing rat brain cortex and suggest a high potential of RGS1 I in regulation of high-affinity GTPase activity. (C) 2004 Elsevier B.V. All rights reserved.

Estrogen receptors (ERs), ER alpha and ER beta, mediate estrogen actions in a broad range of target tissues. With the introduction of microarray techniques, a significant understanding has been gained regarding the interplay between the ER alpha and ER beta in breast cancer cell lines. To gain a more comprehensive understanding of ER beta-dependent gene regulation independent of ER alpha, we performed microarray analysis on HEK293/mock and HEK293/ER beta cells. A total of 332 genes was identified as ER beta-upregulated genes and 210 identified as ER beta-downregulated genes. ER beta-induced and ER beta-repressed genes were involved in cell-cell signaling, morphogenesis, and cell proliferation. The ER beta repressive effect on genes related to proliferation was further studied by proliferation assays, where ER beta expression resulted in a significant decrease in cell proliferation. To identify primary ER beta target genes, we examined a number of ER beta-regulated genes using chromatin immunoprecipitation assays for regions bound by ER beta. Our results showed that ER beta recruitment was significant to regions associated with 12 genes (IL1RAP, TMSB4X, COLEC12, ENPP2, KLRC1, RERG, RGS16, TNNT2, CYR61, FER1L3, FAM108A1, and CYP4X1), suggesting that these genes are likely to be ER beta primary target genes. This study has provided novel information on the gene regulatory function of ER beta independent of ER alpha and identified a number of ER beta primary target genes. The results of Gene Ontology analysis and proliferation assays are consistent with an antiproliferative role of ER beta independent of ER alpha.