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Nontagged ubiquitin and mutants were from Boston Biochem, Cambridge, MA.
Primers for mTR3 mutants were from IDT (Coralville, IA).
Deletion mutants were from the MATa collection, created by the Saccharomyces Genome Deletion Project [ 18], and obtained from Open Biosystems.
In genotype E, pre-S2 deletions were found mainly in HCC patients, whereas in genotype D, the deletion mutants were from non-HCC patients.
Primers for DmTR mutants were from IDT (Coralville, IA), and plasmid pTYB3 and restriction enzymes were from New England Biolabs (Ipswich, MA).
The mir-8-Gal4, mir-8Δ2 and mir-8Δ3 mutants were from S.M. Cohen and described in Karres et al (2007); UAs-mir-8 was described previously in Vallejo et al (2011); UAS-mir-8 sponge in Loya et al (2009); and UAS-zfh1 Postigo et al (1999).
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The datasets of WT and oxt6 mutant were from previous studies [ 12].
For example, the concept rTg4510 P301-L mutant is from the NeuroMorpho.Org species ontology namespace NMOSp.owl#.
Data from 264 mutants were analyzed from three selection classes: forward genetic screen mutants, no-phenotype mutants, and reverse genetic screen mutants.
NMJ boutons from lin-10 mutants were indistinguishable from those in wild type, and rpm-1 lin-10 double mutants were indistinguishable from those in rpm-1 single mutants.
Seeds from atsrp2 and atsrp3 T-DNA insertion mutants were obtained from the Salk Institute Genomic Analysis Laboratory.
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