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Marcette et al. became interested in the PTRN-1 protein after conducting a screen of randomly mutated worms to look for those with abnormally developed nerve cells.
One way to discover such variants is by conducting a screen following chemical mutagenesis for new mutants that are more sensitive or resistant to radiation than wild-type flies.
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The results for both simulated and analytically relevant experimental systems show excellent agreement with previous approaches, highlighting the importance of considering potential interactions when conducting a screening search.
We conducted a screen of a collection of insertion lines for their ability to dominantly modify a misexpression eye phenotype of stbm.
We conducted a screen for genetic modifiers of an Smn phenotype using the Exelixis collection of transposon-induced mutations, which affects approximately 50% of the Drosophila genome.
We conducted a screen for anti-capsular small molecules and identified an agent designated "C7" that blocks the production of K1 and K5 capsules, unrelated polysaccharide types among the Group 2 3 capsules.
We conducted a screen for recessive mutations that block compensatory growth.
Our laboratory conducted a screen for regulators of the G1-S transition of the cell cycle (Royzman et al. 1997).
We also constructed genomic bacterial artificial chromosome (BAC) libraries for the two snakes and conducted a screen for venom genes.
Motivated by this and the success of the VYDS Opi− screen, we conducted a screen of an essential gene library driven by a titratable promoter (Mnaimneh et al. 2004).
They conducted a screen using a panel of structurally diverse chemical compounds and evaluated toxicity in embryonic development, including on the central nervous and cardiovascular systems.
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