cdk-2 : cye-1

"Cyclin/CDK expression in muscle leads to cell cycle re-entry during larval development."

cdk-2 : cye-1

"Cyclin/CDK expression in muscle leads to cell cycle re-entry during larval development."

mec-15 : smg-4

Animals doubly mutant for the mec-15 allele and smg-4(ma116), which prevents nonsense-mediated mRNA decay (Pulak and Anderson 1993), exhibited no additional phenotypes (data not shown).

mec-15 : smg-4

Animals doubly mutant for the mec-15 allele and smg-4(ma116), which prevents nonsense-mediated mRNA decay (Pulak and Anderson 1993), exhibited no additional phenotypes (data not shown).

mec-15 : mec-7

Animals doubly mutant for the mec-15 allele and smg-4(ma116), which prevents nonsense-mediated mRNA decay (Pulak and Anderson 1993), exhibited no additional phenotypes (data not shown).

mec-15 : smg-4

Animals doubly mutant for the mec-15 allele and smg-4(ma116), which prevents nonsense-mediated mRNA decay (Pulak and Anderson 1993), exhibited no additional phenotypes (data not shown).

mec-15 : smg-4

Animals doubly mutant for the mec-15 allele and smg-4(ma116), which prevents nonsense-mediated mRNA decay (Pulak and Anderson 1993), exhibited no additional phenotypes (data not shown).

eea-1 : mtm-6

GFP::2XT10G3.5-FVYE localized to a number of subcellular vesicles at the periphery of intestinal cells in wild type worms. Following treatment with mtm-6 (RNAi), a portion of GFP::2XT10G3.5-FVYE was found to re-localize to apical membranes.

lit-1 : wrm-1

Authors prepared lysates from embryos derived from wrm-1(tm514)/+ mothers that had been fed with wrm-1(RNAi) bacteria. The anti-T220-P re- activity was greatly reduced in these wrm-1- embryo extracts, compared with wild-type embryo extracts (Fig. 1D), demon- strating that in C. elegans embryos WRM-1 activity is required for LIT-1 phosphorylation at T220.

ced-3 : hsp-90

"we were able to recover HSP-90 but not HSP-70 with both CED-4::GFP and CED-3::GFP, but not from worms expressing GFP alone. Crucially, we found that the levels of HSP-90 recovered with CED-3::GFP, but not CED-4::GFP, increased in response to mtch-1(RNAi), suggesting that HSP-90 is re-directed away from existing HSF-1-repressing complexes and toward CED-3 upon loss of MTCH-1."