Genes that were given a lower proportion of votes for the correct class than expected under the null hypothesis (labels permuted randomly) were excluded.
To test this hypothesis, CFSE labeled B16F10 and CD45+ cells were detected in blood 24 h after injection of B16F10 cells into the blood of RNF13-KO and WT mice.
To test this hypothesis, we labeled E. muris-infected DH82 cells with carboxyfluorescein succinimidyl ester (CFSE) and seeded the infected cell culture with non-labeled uninfected DH82 cells.
To test this hypothesis, we labeled actin filaments with phalloidin conjugated Quantum dots (Qdots) and/or Alexa 488 Phalloidin, and tracked their movement in and out of the nascent contractile ring.
As a starting hypothesis, we labeled all the sequences in the gold standard according to our previously proposed classification, based on the presence of key functional residues in the proton conducting channels (Table 1).
Once again, and in line with our predictions, the two epimeric biotinylated ThrCer analogues behaved differently in their ability to activate iNKT cells, and in accord with our hypothesis, the labeled analogue, possessing the (S -configuration at the tethering S -configurationgnificatthe betethering itsite)-epimer.
To test this hypothesis, we labelled primary DG cells with BrdU before transplantation to determine whether cells re-populating the DG were post-mitotic at the time they were transplanted.
To test this hypothesis, we labelled two pools of individual human dynein complexes with different fluorophores and mixed them in the presence of dynactin and BICD2N.
The conclusion says that after we have weighed the evidence, the scales tip to the side labeled "Hypothesis of Indifference".
In an attempt to verify this hypothesis, we first labeled cells in vivo with biotin.
