Sentences with phrase «phosphorylation level»

(H) Spleen CD4 + T cells harvested from VPA recipients and control mice on day 21 were analyzed by Western blot assay for the expression and phosphorylation level of Akt and downstream target proteins.

Laboratory measurements of receptor phosphorylation levels — which indicate the level of their activity — showed that, in fact, deactivation rates were roughly the same for both the internal and surface receptors.

The team then performed the validation laboratory tests to determine the actual EGFR phosphorylation levels in cells, both for all the cell receptors and for only the internal receptors.

The idea that both STAT2 and IRF - 9 were basic components necessary for RIG - G expression was also supported by the fact that ATRA could not only induce the total amounts of STAT2 and IRF - 9 proteins but also increase the tyrosine phosphorylation level of STAT2 in NB4 cells (Fig. 1A).

(F) Spleen CD4 + T cells isolated from BMT recipients on day 21 were treated with different concentrations of VPA for 24 h and analyzed by Western blot assay for the expression and phosphorylation level of Akt and downstream target proteins.

The model was constructed to predict the receptor phosphorylation levels in a cell under specific conditions for the immediate - to - short (minute - to - hours) response durations.

p - rpS6 was detected in 24 of 31 (77.4 %) cases and its phosphorylation level was significantly associated with the phosphorylation level of p - 4E - BP1 and total eIF4E (P = 0.016 and 0.029, respectively, χ2 test).

Treatment of these cell lines with the PI3K inhibitor, LY294002, resulted in a concentration - dependent decrease of the phosphorylation levels of AKT, mTOR, 4E - BP1, p70S6K, and S6K (Fig. 2A and B).

The phosphorylation levels of p - mTOR and p - p70S6K as detected by immunohistochemistry were significantly associated (P = 0.0026, χ2 test), consistent with previous studies on the causal association of these molecules (24).

We observed that the phosphorylation level of AKT significantly correlated with the phosphorylation level of mTOR and rpS6 as well as with expression of total 4E - BP1 and eIF4E in ALK + ALCL tumors.

Treatment of the Karpas 299 and SU - DHL1 cell lines with increasing concentrations of rapamycin, an inhibitor of the mTOR - raptor complex, resulted in a marked concentration - dependent decrease of the phosphorylation levels of mTOR, p70S6K, 4E - BP1, and total eIF4E (Fig. 4A).

Thus, we concluded that VPA regulates the immune function of Th1 and Th17 cells by directly modulating the phosphorylation level of Akt.

Spleen CD4 + T cells were harvested from mice 21 d after transplantation and cultured or not with VPA for 24 h. Western blot assay showed that VPA attenuated the phosphorylation level of Akt in a dose - dependent manner (Fig. 4F).

We isolated spleen CD4 + T cells from VPA recipients and vehicle recipients and assessed the phosphorylation level of Akt.

In this study, we demonstrate that VPA treatment ameliorated GVHD in a mouse BMT model by downregulating Th1 and Th17 cells and reducing inflammatory cytokine levels via inhibition of the phosphorylation level of Akt in CD4 + T cells.

The phosphorylation levels of downstream target proteins of Akt also were downregulated in parallel (Fig. 4F).

As shown in Fig. 4H, the phosphorylation levels of Akt, as well as the downstream target proteins, were reduced in the VPA - treated group compared with vehicle - control group.

In the current study, VPA dose dependently decreased the phosphorylation level of Akt, as well as the downstream target proteins in CD4 + T cells, in vitro and in vivo.

Thus, we examined whether VPA treatment could increase the acetylation level of Akt and, in turn, decrease the phosphorylation level of Akt.