1 o determine how this signaling network is altered in maize,
we first examined effects of a knockout mutation in an essent
2 To address this question,
we first examined expression patterns of Cx26 and Cx30 in the
3 We first examined HCMV entry into two EGFR-positive or -negat
4 Here,
we first examined how 11 years of warming during different se
5 To fill the void,
we first examined hybridization isotherms generated on differ
6 To evaluate the role of chemotaxis in our model,
we first examined in vivo chemotaxis in the absence of wound
7 We first examined isolated compounds (monomers) and evaluated
8 We first examined its role in established melanoma cells.
9 To evaluate whether PKCdelta regulates Rab7,
we first examined lysosomal morphology in cells with reduced
10 To validate our technique,
we first examined one modulating aromatic ligand, Congo Red,
11 We first examined p42 ERK (ERK2) activation in the NAcc after
12 In this study,
we first examined putative cargo complexes associated with sy
13 We first examined redox (oxidation/reduction) properties and
14 We first examined retinas from control, non-transplanted, age
15 In this active vaccination study,
we first examined safety and immunogenicity for a broad serie
16 To investigate the importance of SLURP2,
we first examined Slurp2 knockout mice in which exon 2-3 sequ
17 We first examined the ability of the model to predict the flo
18 We first examined the association of statin treatment with va
19 To explore these questions,
we first examined the cellular localization of endogenous myo
20 Here,
we first examined the distribution of aKIR genes and haplotyp
21 We first examined the effect of genetic deletion of MOR and D
22 We first examined the effect of the auxiliary subunits.
23 Here,
we first examined the effects of chronic EtOH on DLS neuronal
24 In this study,
we first examined the effects of MSH3 deficiency on cytotoxic
25 in regulating the proliferation and survival of RCC cells,
we first examined the expression of MAPK kinase (MKK) and MAP
26 signated PerA (for pathogenicity island-encoded regulator),
we first examined the expression of the perA gene in the orig
27 We first examined the fundamental steps by which protein comp
28 investigate early events associated with antigen exposure,
we first examined the interaction of PF4/heparin complexes wi
29 We first examined the levels of Grx1 in postmortem midbrain s
30 We first examined the location of Thy-1(+) CAFs within human
31 Using a mouse infection model,
we first examined the mouse colonization ability of an H. pyl
32 urther characterize the role of microglia in glioma growth,
we first examined the properties of Nf1+/- microglia in vitro
33 We first examined the regulation of Arc/Arg3.1 mRNA and prote
34 We first examined the relationship between fasting plasma TMA
35 se IS is an agonist of the aryl hydrocarbon receptor (AHR),
we first examined the relationship between IS levels and AHR-
36 We first examined the relationship of KF11 responses in B cla
37 We first examined the response of four fundamental motifs (po
38 To test this hypothesis,
we first examined the response of peripheral blood mononuclea
39 We first examined the role of cognitive strategies by having
40 We first examined the role of residue 283 in macrophage tropi
41 We first examined the substrate specificity of the purified t
42 We first examined the temporal relationship between GC activi
43 We first examined the transposition of Tn21Km into IncP-1beta
44 We first examined this switching process in an auditory event
45 We first examined whether autophosphorylation regulates BTK a
46 We first examined whether mice and humans experience similar
47 To explore potential genetic interactions,
we first examined whether RNAs from HIV-1 and HIV-2 can be co
48 Here
we first examined whether such deletions could occur during r
49 We first examined whether the acute-phase protein, alpha-2 ma
50 We first examined which KCNQ subunits are targeted by AKAP79