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Our observations that the proliferation of cells expressing these mTOR mutants was sensitive to rapamycin and that AKT was not activated in these cells suggest that such mutants exert their transforming action through mTORC1.
Like that of the wild-type UCP3, mitochondrial Ca2+ uptake by both UCP3 mutants was sensitive to mitochondrial depolarization, while under these conditions their principal differences in responsiveness remained.
Although each of the eight RAD52 group mutants was sensitive to gamma radiation as expected, a surprisingly small fraction of the other EcoRIs mutants exhibited this phenotype (32/73).
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We next investigated whether any of these pmt3 mutants were sensitive to HU or other toxins.
These results indicate that sod1Δ mutants are sensitive to even mild deficiency.
Previous studies reported that spb1DA mutants were sensitive to paromomycin, and that sparsomycin had no effect [19].
Strikingly, ccr4Δ and dhh1Δ mutants are sensitive to IR only as diploids and not as haploids, indicating that the radiation sensitive IR defect lies in G1 [39].
Surprisingly, the behaviours of ΔrecG ΔclpX and Δruv ΔclpX mutants were very different from each other despite both mutants being sensitive to 2-AP.
SUMO chain mutants are sensitive to the DNA synthesis inhibitor, hydroxyurea (HU), but not to other genotoxins, such as UV, MMS or CPT.
Recently, Schneider and colleagues showed that eiger mutants are sensitive to systemic infection by gram-positive cocci, a type of extracellular bacteria [17].
(A ) GARP mutants are sensitive to IPC synthase inhibition.
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