Thus, if a model has strong phylogenetic signal, it is expected to have a high W score similar to the model with λ fixed at 1 (e.g. both estimated and λ = 1 model might have a score of 0.49) and a high W score compared to the model with λ = 0 (e.g. this model would have a score of 0.02).
Since the amplitude scaling does not affect the TF structure of the signal, it is expected that JLNMF does not identify any discriminant TF bases.
Thus, if specifically involved in signal propagation, it is expected that these domains (hereby named signal-propagating domains, or SP domains) should be extremely mobile, quickly shifting between conformations in order to better propagate the signal between monomers.
Our data therefore suggests that there is a correlation between Myc and the InR signaling and it is expected that the InR pathway also shares some transcriptional targets with Myc.
As phosphorylation happens close to the beginning of the signaling cascade, it is expected that the response at a fixed early time point should be more conserved between the two species.
As stated by Doppler et al. [20], their proposed method has significant signaling load though it is expected to be feasible in low mobility scenarios.
Since OsAP77 can be induced by PBZ, SA, INA, H2O2 or ABA, which play important roles in signal defense responses, it is expected that OsAP77 is also responsive to pathogen infection.
Chr8, on the other hand, had a positive influence on signal transduction, so it is expected that these QTLs will specifically change Pb1-mediated resistance single handedly or in combination with others (Fig. 4).
As far as p75NTR signaling is concerned, it is expected that the lower binding affinity of hNGFR100E mutants for p75NTR results in a reduction of downstream signaling.
If epidermal ICs behave as D-N signal-sending cells, it is expected that excessive epidermal ICs will be detected in X-Su(H DBM mRNA-injected embryos (with reduced Notch activity).
