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We evaluated the performance of alamarBlue-, BrdU-, and sulforhodamine B-based cell proliferation assays using the 96-well format.
Transcription factor assays, using the luciferase reporter plasmids of AP-1, CRE, and NF-κB were conducted to explore the signaling pathway(s) that may be regulated by CMTM2.
The percentages of beta 1- and beta 2-adrenergic receptors were determined in three cocaine users and four control patients by performing competition binding assays using the beta 2 antagonist ICI 118,551.
Then, we carried out in vitro transcription assays using the immunodepleted NEs.
Fig. 1B shows representative results of the in vitro transcription assays using the wild-type and mutant templates.
Consequently, we conducted in vitro migration assays using the various Mitostatin-overexpressing or Mitostatin-depleted prostate cancer cells.
AD performed the assays using the SNPstream system.
Contraction assays using the URA3 reporter have been described previously.
Binding assays using the fluorescence reporter N-phenyl-1-naphtylamine (NPN) were inconclusive.
ALP assays using the neutralizing BMPR-IA antibody were performed in two independent experiments.
Chemotactic assays using the Boyden chamber were performed as described previously (Hernández-Miranda et al., 2011).
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