Trends in Pharmacological Sciences
ReviewAntisense knockouts: molecular scalpels for the dissection of signal transduction
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Cited by (48)
GAP1(IP<inf>4</inf>BP)/RASA3 mediates Gα<inf>i</inf>-induced inhibition of mitogen-activated protein kinase
2008, Journal of Biological ChemistryCitation Excerpt :We have found that stable transfection of full-length antisense constructs in GH4 cells provides excellent specificity for knockdown individual Gαi/o subunits, which are highly (90! amino acid identity) conserved (23-25). Depletion of RASA3 in two independent clones strongly blocked dopamine D2S-induced inhibition of TRH-induced ERK1/2 activation (Fig. 9), which clearly displays the critical role of RASA3 in this pathway.
Antidepressant effects on GABA-stimulated <sup>36</sup>Cl<sup>-</sup> influx in rat cerebral cortex are altered after treatment with GABA(A) receptor antisense oligodeoxynucleotides
2000, Brain ResearchCitation Excerpt :Using antisense oligodeoxynucleotide (aODNs) treatment of rats, we sought to determine the subunit(s) that are necessary for amitriptyline and mianserin modulation of the GABA effect on chloride influx. The expression level of a particular protein can be reduced by treatment with synthetic oligodeoxynucleotides that are complementary to the mRNA encoding this protein [1,21,28]. Many studies have shown that antisense oligodeoxynucleotides effectively reduce receptor protein expression in brain tissue [2,3,30] and in cultured cells [25,29].
Involvement of calmodulin in 1α,25-dihydroxyvitamin D<inf>3</inf> stimulation of store-operated Ca<sup>2+</sup> influx in skeletal muscle cells
2000, Journal of Biological ChemistryCitation Excerpt :However, interaction of these antagonists with components of the signaling mechanism regulating SOC influx other than CAM cannot be ruled out from these data. Antisense technology allows selective inhibition of the expression of one particular protein involved in signal transduction and to investigate how its knock-out affects a determined cell function (28). This technique, used in combination with fluorimetric detection of hormone-induced changes in [Ca2+]i has proven to be a powerful tool for identifying signaling cascades involved in VDCC regulation (29, 30).