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 EPA improved murine hyperinsulinemia
5 We next investigated how the axonal mRNA pool changes after a
6 Thus,
we next investigated if functional inactivation of Cav-1 gene
7 We next investigated if overexpression of Cx43 in Sertoli cel
8 We next investigated if warming sea temperatures have forced
9 ld still bind a single GalNAc monosaccharide on this array,
we next investigated its binding characteristics to Tn-contai
10 We next investigated longitudinal plasma samples from HCV-inf
11 We next investigated physiologic levels of the T cell cytokin
12 We next investigated possible interactions between red meat a
13 stream mediator of epidermal growth factor receptor (EGFR),
we next investigated SFK phosphorylation in a panel of NSCLC
14 We next investigated the allosteric effect on CRF-stimulated
15 We next investigated the cellular distribution of mTOR substr
16 We next investigated the contribution of the recently discove
17 We next investigated the effect of nigrostriatal lesioning on
18 We next investigated the effect of secondary heterologous DEN
19 caveolins in the pathogenesis of cerebral ischemic injury,
we next investigated the effects of cerebral ischemia in cave
20 S3 encodes a protein implicated in autophagosome formation,
we next investigated the effects of gene silencing on this pa
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 fibrotic responses of tendon-derived
25 We next investigated the functional relationship between an i
26 We next investigated the mechanism by which monocytic MPs act
27 ince TASK channels are modulated by extracellular pH (pHo),
we next investigated the pH sensitivity of ISO in Hepes-buffe
28 lpha3beta1 to interact with both LN5 and rat tail collagen,
we next investigated the possibility that integrin alpha3beta
29 ymptoms, and because they seem to precede traumatic events,
we next investigated the relationship between NTRK2 methylati
30 We next investigated the requirements for ADAMTS13 and VWF in
31 We next investigated the role of CXCR3 on peripheral effector
32 of resting UCB monocytes from both groups were comparable,
we next investigated the role of epigenetic differences.
33 We next investigated the role of Ucp2 in cytokine-induced apo
34 We next investigated the signal transduction pathway responsi
35 We next investigated the signal transduction pathways control
36 causing poly-Q mutation in Htt affects synapse development,
we next investigated the synaptic connectivity in a full-leng
37 We next investigated the temporal events associated with neur
38 We next investigated their relatedness to cDC1 and cDC2 and d
39 Thus,
we next investigated whether an isolated increase in the hepa
40 We next investigated whether intrinsic leukocyte posttranscri
41 We next investigated whether PDTC treatment altered the p53 r
42 Therefore,
we next investigated whether PMA induced translocation of SK
43 We next investigated whether reduced type I procollagen produ
44 oposed as a mediator of retinoid-induced growth inhibition,
we next investigated whether TGFbeta mediates the anti-prolif
45 We next investigated whether the influenza A virus NS1 protei
46 We next investigated whether the mitogenic response to specif
47 We next investigated whether there was any alternative mode t
48 We next investigated whether VFDNFVLK could be used as a reag
49 We next investigated which energy source drives the TLR-induc
50 We next investigated which signal transduction pathways trigg