1  demonstrated by CD4(+) T cells treated with cyclohexamide.

2   The induction of BRCA1 mRNA was blocked by cyclohexamide.

3 e DES-induced expression is not inhibited by cyclohexamide.

4                               Treatment with cyclohexamide, a potent inhibitor of protein synthesis,

5 barrier recovery occurred in the presence of cyclohexamide, an inhibitor of protein synthesis.

6 s dependent on protein synthesis, given that cyclohexamide blocks the ability of LPS to prime macroph

7 nM PAF or preincubated with PAF antagonists, cyclohexamide (CHX) or actinomycin D (AcD) before adding

8 utant exhibited proteolytic stability during cyclohexamide (CHX) or LPS treatment.

9                             Experiments with cyclohexamide-dependent block of protein synthesis showe

10  bFGF expression by ox-LDL was attenuated by cyclohexamide, indicating a requirement for continuous n

11  in the intermediate mesoderm, is blocked by cyclohexamide, indicating that the activation of Odd-1 b

12                                              Cyclohexamide or actinomycin D does not attenuate DTDP-i

13 Src expression was completely abolished with cyclohexamide or actinomycin D.

14 ild-type plants, the translational inhibitor cyclohexamide partially inhibited Ca(2+)-programmed stom

15 F-1 isoforms, and studies in the presence of cyclohexamide, provided evidence for the phosphorylation

16                                              Cyclohexamide restored Apo2L/TRAIL sensitivity in associ

17 for a diversity of genetic backgrounds under cyclohexamide stress and also detects previously unident

18 mycin D, and the protein synthesis inhibitor cyclohexamide suggest that MGP, OPN, and VCAF mRNA abund

19  knockout mice, and by treating T cells with cyclohexamide to further rule out endogenous expression

20              Protein stability studies after cyclohexamide treatment suggested an increase in the Sp1

21                                Studies after cyclohexamide treatment suggested an increase in the Sp1