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1 n hematopoietic cells by treatment with TPA (12-O-tetradecanoyl phorbol-13-acetate).
2 d following starvation and/or treatment with 12-O-tetradecanoyl phorbol-13-acetate.
3 d by repeated exposure to the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate.
4 ted with PEITC-NAC alone; cells treated with 12-O-tetradecanoyl phorbol-13-acetate alone showed activ
5 e BK component of K+ current was enhanced by 12-O-tetradecanoyl-phorbol-13-acetate, an activator of P
6 horiocarcinoma BeWo cells, the PKC activator 12-O-tetradecanoyl phorbol 13-acetate and PKC inhibitor
7 , cells that were pretreated with 100 nmol/L 12-O-tetradecanoyl phorbol-13-acetate, and then treated
8 nal PKC (cPKC) by pretreatment of cells with 12-O-tetradecanoyl phorbol-13-acetate cannot block UVB-i
9 eatment of these double transgenic mice with 12-O-tetradecanoyl-phorbol-13-acetate caused rapid migra
10 in X-irradiated HL60 cells but unaffected by 12-O-tetradecanoyl phorbol-13-acetate, forskolin, or cyc
11 inase inhibitors) in the acquisition of TPA (12-O-tetradecanoyl phorbol-13-acetate)-independent growt
12 ocked the PAF effect but not that induced by 12-O-tetradecanoyl phorbol-13-acetate, indicating the sp
13 EGgamma, exhibit a marked resistance to TPA (12-O-tetradecanoyl-phorbol-13-acetate)-induced keratinoc
14 lock UVB-induced AP-1 activity, it can block 12-O-tetradecanoyl phorbol-13-acetate-induced AP-1 activ
15 also evident in 7,12-dimethylbenzanthracene/12-O-tetradecanoyl-phorbol-13-acetate-induced tumors fro
19 challenge by 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoyl-phorbol-13-acetate resulted in delaye
21 ibit neutrophil adhesion induced by FMLP and 12-O-tetradecanoyl-phorbol-13-acetate to resting and TNF
22 regulation of LPL, we studied the effect of 12-O-tetradecanoyl phorbol 13-acetate (TPA) on adipocyte
23 tment of fibroblasts with the phorbol ester, 12-O-tetradecanoyl phorbol 13-acetate (TPA), specificall
25 rsenic treatment, offspring received topical 12-O-tetradecanoyl phorbol-13-acetate (TPA) through adul
26 mouse keratinocytes treated with calcium and 12-O-tetradecanoyl phorbol-13-acetate (TPA), two agents
31 hibits in vivo acute inflammation induced by 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and arachido
32 sion of these genes and apoptosis induced by 12-O-tetradecanoyl-phorbol-13-acetate (TPA) in several h
33 IRmt-infected LCLs with the chemical inducer 12-O-tetradecanoyl-phorbol-13-acetate (TPA) led to much
34 er topical application of the tumor promotor 12-O-tetradecanoyl-phorbol-13-acetate (TPA) was observed
36 tment of human tumour cell lines with serum, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), or okadaic
37 application of Lupeol to CD-1 mouse against 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced conv
39 ead of 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced squa
42 ermis in untreated skin and after short-term 12-O-tetradecanoyl-phorbol-13-acetate treatment and acut
43 Direct activation of protein kinase C by 12-O-tetradecanoyl-phorbol-13-acetate was also sufficien
44 f lytic-phase infection by the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate was blocked by pro
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