1 We next investigated and observed that TMP treatment induced
2 We next investigated autophagy following infection with sonic
3 We next investigated changes in synaptic plasticity with lesi
4 We next investigated how the axonal mRNA pool changes after a
5 Thus,
we next investigated if functional inactivation of Cav-1 gene
6 We next investigated if overexpression of Cx43 in Sertoli cel
7 We next investigated if warming sea temperatures have forced
8 We next investigated longitudinal plasma samples from HCV-inf
9 We next investigated physiologic levels of the T cell cytokin
10 We next investigated possible interactions between red meat a
11 stream mediator of epidermal growth factor receptor (EGFR),
we next investigated SFK phosphorylation in a panel of NSCLC
12 We next investigated the ability of the T-cell receptor/CD3 c
13 We next investigated the allosteric effect on CRF-stimulated
14 We next investigated the cellular distribution of mTOR substr
15 We next investigated the contribution of the recently discove
16 We next investigated the effect of nigrostriatal lesioning on
17 We next investigated the effect of secondary heterologous DEN
18 caveolins in the pathogenesis of cerebral ischemic injury,
we next investigated the effects of cerebral ischemia in cave
19 S3 encodes a protein implicated in autophagosome formation,
we next investigated the effects of gene silencing on this pa
20 We next investigated the effects of Ras/Raf/AP-1 signals on t
21 We next investigated the endothelial CD47-dependent signaling
22 We next investigated the evolutionary history of genes associ
23 We next investigated the expression of GLT1b in vivo.
24 We next investigated the functional relationship between an i
25 We next investigated the mechanism by which monocytic MPs act
26 ince TASK channels are modulated by extracellular pH (pHo),
we next investigated the pH sensitivity of ISO in Hepes-buffe
27 lpha3beta1 to interact with both LN5 and rat tail collagen,
we next investigated the possibility that integrin alpha3beta
28 We next investigated the requirements for ADAMTS13 and VWF in
29 We next investigated the role of CXCR3 on peripheral effector
30 of resting UCB monocytes from both groups were comparable,
we next investigated the role of epigenetic differences.
31 We next investigated the role of Ucp2 in cytokine-induced apo
32 We next investigated the signal transduction pathway responsi
33 We next investigated the signal transduction pathways control
34 causing poly-Q mutation in Htt affects synapse development,
we next investigated the synaptic connectivity in a full-leng
35 We next investigated the temporal events associated with neur
36 Thus,
we next investigated whether an isolated increase in the hepa
37 We next investigated whether beta gamma subunits play a role
38 We next investigated whether PDTC treatment altered the p53 r
39 Therefore,
we next investigated whether PMA induced translocation of SK
40 We next investigated whether reduced type I procollagen produ
41 oposed as a mediator of retinoid-induced growth inhibition,
we next investigated whether TGFbeta mediates the anti-prolif
42 We next investigated whether the ability of beta-catenin to i
43 We next investigated whether the influenza A virus NS1 protei
44 We next investigated whether the mitogenic response to specif
45 We next investigated whether there was any alternative mode t
46 We next investigated whether VFDNFVLK could be used as a reag
47 We next investigated which energy source drives the TLR-induc
48 We next investigated which signal transduction pathways trigg