Figure 1.
Figure 1. GILZ expression is induced by deprivation of interleukin-2 in human PHA-stimulated peripheral blood lymphocytes, human KIT 225, human NKL, and murine CTLL-2 cells. Cells were deprived of IL-2 by washing, set back in culture in the absence of IL-2, and lysed at the indicated times. (A) Western blot analysis (WB) was performed using a polyclonal anti-GILZ antibody. Membranes were stripped and reblotted with an anti–β Tubulin antibody as a loading control. GILZ expression was quantified by densitometric analysis and normalized to the densitometric value of β Tubulin (ratio GILZ/β Tubulin). (B) Total RNA was extracted and used as a template for RT-PCR using primers specific for gilz or β actin. Gilz expression was quantified by densitometric analysis and normalized to the densitometric value of β actin (ratio GILZ/β actin). w/o indicates without.

GILZ expression is induced by deprivation of interleukin-2 in human PHA-stimulated peripheral blood lymphocytes, human KIT 225, human NKL, and murine CTLL-2 cells. Cells were deprived of IL-2 by washing, set back in culture in the absence of IL-2, and lysed at the indicated times. (A) Western blot analysis (WB) was performed using a polyclonal anti-GILZ antibody. Membranes were stripped and reblotted with an anti–β Tubulin antibody as a loading control. GILZ expression was quantified by densitometric analysis and normalized to the densitometric value of β Tubulin (ratio GILZ/β Tubulin). (B) Total RNA was extracted and used as a template for RT-PCR using primers specific for gilz or β actin. Gilz expression was quantified by densitometric analysis and normalized to the densitometric value of β actin (ratio GILZ/β actin). w/o indicates without.

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