1 We then asked whether 17B1.3 prevents signaling by binding to
2 Since glycosylation can enhance the function of a compound,
we then asked whether adding a glucose makes aesculin activat
3 We then asked whether BIG1 phosphorylation altered its GEP ac
4 We then asked whether complexes of these glycoproteins could
5 We then asked whether food consumption during a hypothesized
6 We then asked whether gene transfer of viral IL-10 could decr
7 We then asked whether miR-3189 was expressed in clinical samp
8 specific markers of chondrocyte differentiation in culture,
we then asked whether PKA phosphorylation could modulate the
9 We then asked whether prolonged PSAP/IntA experience would ne
10 We then asked whether such CTL escape mutations had an impact
11 We then asked whether the aberrant tangential migration of GA
12 We then asked whether the CGRP promoter in the viral vector c
13 We then asked whether the connected neurons are presynaptic o
14 We then asked whether the differences between real and appare
15 We then asked whether the replication and the mitotic phenoty
16 We then asked whether the responses in these regions reflecte
17 We then asked whether the SR protein binding sites in these e
18 Using these models,
we then asked whether this vascular defect could be rescued b
19 Using a series of recombinant X genotypes,
we then asked whether X overexpression in hybrids is controll