Different activities of viral enhancer elements before and after stable integration of transfected DNAs

Analysis of the RNA and DNA levels of a selectable gene linked to a murine retroviral enhancer demonstrated a correlation between RNA levels and tissue-specific enhancer activity during transient expression in T cells but not in stably transformed cell lines.

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Fas transduces activation signals in normal human T lymphocytes.

Journal of Experimental Medicine ◽

10.1084/jem.178.6.2231 ◽

1993 ◽

Vol 178 (6) ◽

pp. 2231-2235 ◽

Cited By ~ 372

Author(s):

M R Alderson ◽

R J Armitage ◽

E Maraskovsky ◽

T W Tough ◽

E Roux ◽

...

Keyword(s):

T Cells ◽

T Cell ◽

Cell Lines ◽

Interleukin 2 ◽

Tumor Necrosis Factor Receptor ◽

Lymphoid Cells ◽

Culture Vessel ◽

Cell Surface Molecule ◽

Transformed Cell ◽

Transformed Cell Lines

The Fas gene encodes a cell surface molecule that is a member of the the nerve growth factor/tumor necrosis factor receptor family of proteins and can mediate programmed cell death (apoptosis) in certain transformed cell lines. To characterize further the biological function of Fas, particularly with regard to its function in normal cells, a panel of monoclonal antibodies (mAbs) was generated against the extracellular portion of human Fas. Some of these mAbs induced apoptosis in transformed cell lines expressing Fas, but only when immobilized on the culture vessel. One of the new Fas mAbs (M38) was used for studies on normal lymphoid cells and found to stimulate the proliferation of purified human T cells and thymocytes when immobilized on culture wells along with CD3 antibody. T cell proliferation induced by Fas mAb was largely interleukin 2 independent and was demonstrated to be due to a direct effect on the precursor T cell. Thus, the data demonstrate that in addition to a role in the induction of apoptosis in certain transformed cell lines, the Fas protein may also play an important role in the activation and proliferation of normal T cells.

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Jasplakinolide Induces Apoptosis in Various Transformed Cell Lines by a Caspase-3-Like Protease-Dependent Pathway

Clinical and Diagnostic Laboratory Immunology ◽

10.1128/cdli.7.6.947-952.2000 ◽

2000 ◽

Vol 7 (6) ◽

pp. 947-952 ◽

Cited By ~ 76

Author(s):

Chikako Odaka ◽

Miranda L. Sanders ◽

Phillip Crews

Keyword(s):

T Cells ◽

Cell Death ◽

Cell Lines ◽

Caspase 3 ◽

Dependent Manner ◽

Jurkat T Cells ◽

Transformed Cell ◽

Induced Apoptosis ◽

Transformed Cell Lines ◽

Dependent Pathway

ABSTRACT To clarify the mechanisms underlying the antiproliferative effects of jasplakinolide, a cyclic depsipeptide from marine sponges, we examined whether jasplakinolide induces apoptosis in a variety of transformed and nontransformed cells. Jasplakinolide inhibited proliferation of human Jurkat T cells, resulting in cell death. This was accompanied by chromatin condensation and DNA cleavage at the linker regions between the nucleosomes. When caspase-3-like activity in the cytosolic extracts of Jurkat T cells was examined with a fluorescent substrate, DEVD-MAC (N-acetyl-Asp-Glu-Val-Asp-4-methyl-coumaryl-7-amide), the activity in the cells treated with jasplakinolide was remarkably increased in a time-dependent manner. Pretreatment of Jurkat T cells with the caspase inhibitor zVAD [benzyloxycarbonyl(Cbz)-Val-Ala-β-Asp(OMe)-fluoromethylketone] or DEVD-CHO (N-acetyl-Asp-Glu-Val-Asp-1-aldehyde) prevented the induction of apoptosis by jasplakinolide. Moreover, exposure of various murine transformed cell lines to jasplakinolide resulted in cell death, which was inhibited by zVAD. Although it has been well established that murine immature thymocytes are sensitive to apoptosis when exposed to various apoptotic stimuli, these cells as well as mature T lymphocytes were resistant to jasplakinolide-induced apoptosis. The results suggest that jasplakinolide induces apoptotic cell death through a caspase-3-like protease-dependent pathway. Another important outcome is that transformed cell lines were more susceptible to jasplakinolide-induced apoptosis than normal nontransformed cells.

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Down-regulation of SHP1 and up-regulation of negative regulators of JAK/STAT signaling in HTLV-1 transformed cell lines and freshly transformed human peripheral blood CD4+ T-Cells

Leukemia Research ◽

10.1016/s0145-2126(03)00158-9 ◽

2004 ◽

Vol 28 (1) ◽

pp. 71-82 ◽

Cited By ~ 17

Author(s):

Jihua Cheng ◽

Dongsheng Zhang ◽

Changhong Zhou ◽

Wayne A Marasco

Keyword(s):

T Cells ◽

Cell Lines ◽

Peripheral Blood ◽

Cd4 T Cells ◽

Human Peripheral Blood ◽

Negative Regulators ◽

Down Regulation ◽

Transformed Cell ◽

Stat Signaling ◽

Transformed Cell Lines

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Histone Deacetylase Inhibitors (HDACis) That Release the Positive Transcription Elongation Factor b (P-TEFb) from Its Inhibitory Complex Also Activate HIV Transcription

Journal of Biological Chemistry ◽

10.1074/jbc.m113.464834 ◽

2013 ◽

Vol 288 (20) ◽

pp. 14400-14407 ◽

Cited By ~ 60

Author(s):

Koen Bartholomeeusen ◽

Koh Fujinaga ◽

Yanhui Xiang ◽

B. Matija Peterlin

Keyword(s):

T Cells ◽

Histone Deacetylase ◽

Cell Lines ◽

Histone Deacetylase Inhibitors ◽

Elongation Factor ◽

Factor B ◽

Transformed Cell ◽

Positive Transcription Elongation Factor ◽

Transcription Elongation Factor ◽

Transformed Cell Lines

Numerous studies have looked at the effects of histone deacetylase inhibitors (HDACis) on HIV reactivation in established transformed cell lines and primary CD4+ T cells. However, their findings remain confusing, and differences between effects of class I- and class II-specific HDACis persist. Because no clear picture emerged, we decided to determine how HDACis reactivate HIV in transformed cell lines and primary cells. We found that neither histone H3 nor tubulin acetylation correlated with HIV reactivation in Jurkat and HeLa cells. Rather, HDACis that could reactivate HIV in chromatin or on episomal plasmids also released free positive transcription elongation factor b (P-TEFb) from its inhibitory 7SK snRNP. In resting primary CD4+ T cells, where levels of P-TEFb are vanishingly low, the most potent HDACi, suberoylanilide hydroxyamic acid (SAHA), had minimal effects. In contrast, when these cells were treated with a PKC agonist, bryostatin 1, which increased levels of P-TEFb, then SAHA once again reactivated HIV. We conclude that HDACis, which can reactivate HIV, work via the release of free P-TEFb from the 7SK snRNP.

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