Our own work demonstrated previously that knockdown of PI4KIIα drastically reduces HER-2 autophosphorylation (Li et al., 2010).
Using biodegradable PLGA microspheres, we demonstrated previously that, in vitro, we could inhibit the degradative effects of IL-1β on the NP for up to 20 days.
Consistent with this notion, we demonstrated previously that high-affinity, peptide-specific TCRs could be generated in vitro by mutations in the CDR3α region of the 2C TCR.
We demonstrated previously that baculovirus accumulates into EEA1-positive endosomes in HepG2 cells starting at 30 min p.t. [12], [13].
We and others demonstrated previously that mFasL is proinflammatory and proapoptotic, while sFasL is anti-inflammatory and non-apoptotic [24].
We demonstrated previously that TGF-β was an additional stimulus for inducing Egr-1 expression in normal fibroblasts [10].
Further, we demonstrated previously that M. bovis BCG induced expression of SOCS3 involved Notch1 upregulation and activation of Notch1 signaling pathway in a TLR2-MyD88 manner [36].
It has been demonstrated previously that interactions between β sheets can drive partial folding of gp120 even after a critical S-S bond has been eliminated [64], [65].
It has been demonstrated previously that L. nivale ssp.
We demonstrated previously that oxycodone has potent antinociceptive effects at supraspinal sites.
It has been demonstrated previously that intact 37LRP is insoluble upon expression in bacteria [ 39].
