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The N/OFQ-induced ANP secretion was completely antagonized by antagonists of NOP, 1 μM each of [Phe1 (CH2-NH) Gly2] nociceptin (1 13 -NH2 1 13 -NH2Q(1–13)NH2) or naloxone benzoylhydrazone.
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In both series of experiments, reported intensity was significantly influenced by NoP [ F 1, 63) = 92.0, p <.001, for Series 1, and F 1, 126) = 340, p <.001, for Series 2], but the increase in intensity score between NoP = 1 and NoP = 5 was higher for Series 2 than for Series 1 (an increase of 1.01 for Series 1 and 1.89 for Series 2).
The kinetics of furrow ingression in cyk-4 WT ::gfp; nop-1 it142) nop-1 it142t142); ced-10(n1993) embryos and nop-1 it142 nop-1 it142
The effect of electrode type on reported intensity was significant for the NoP = 5 stimuli [ F 1, 81) = 8.73, p =.004], but not for NoP = 1 [ F 1, 81) < 1.0, p =.87].
Crucially, nop-1; ced-10 embryos complete cytokinesis.
Cytokinetic contractility, on the other hand, involves both NOP-1 and centralspindlin.
Due to its role in RhoA activation, polarization in NOP-1-deficient embryos is also delayed.
To distinguish between these models, we reduced RhoA levels by mutationally inactivating NOP-1.
Class IX includes the microbial opsins NOP-1 and ORP-1.
Mutational inactivation of NOP-1 permits direct analysis of centralspindlin-dependent furrow formation.
This increase in nop-1 was significant at a q-value <0.2 in each case.
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