Jurkat cell

Jurkat cells Aggregation-dependent cytotoxicity Contaminant-dependent cytotoxicity [163]... 

De Nicola, M. et al. (2008) Carbon nanotubes on Jurkat cells effects on cell viability and plasma membrane potential. Journal of Physics Condensed Matter,... 

Nakagawa, H. etal., Generation of hydrogen peroxide primarily contributes to the induction of Fe(II)-dependent apoptosis in Jurkat cells by (-)-epigallocatechin gallate, Carcinogenesis, 25, 1567, 2004. 

Espinoza, L.A. and Smulson, M.E., Macroarray analysis of the effects of JP-8 jet fuel on gene expression in Jurkat cells, Toxicol., 189, 181, 2003. 

Somlyo We did some work with David Trentham in which we looked for this in terms of modelling the lag phases, and at best we could come up with a Hill coefficient of 2. This was in smooth muscle, not Jurkat cells. My belief is that it is closer to 1. David wanted to be more conservative and said that it could be 2, but never 4 (Somlyo et al 1992). 

The cytotoxic and photocytotoxic effects of two water-soluble fullerene derivatives, a dendritic CL mono-adduct and the malonic acid CL tris-adduct were tested on Jurkat cells when irradiated with UVA or UVB light (Rancan et al., 2002). The cell death was mainly caused by membrane damage and it was UV dose-dependent. Tris-malonic acid fullerene was found to be more phototoxic than the dendritic derivative. This result is in contrast to the singlet oxygen quantum yields determined for the two compounds. 

Rancan F, Rosan S, Boehm F, Cantrell A, Brellreich M, Schoenberger H, Hirsch A, Moussa F (2002) Cytotoxicity and photocytotoxicity of a dendritic C(60) mono-adduct and a malonic acid C(60) tris-adduct on Jurkat cells. J Photochem Photobiol B 67 157-162. 

Rancan F, Helmreich M, Molich A, JuxN, Hirsch A, Roder B, Witt C, Bohm F (2005) Fullerene-pyropheophorbide a complexes as sensitizer for photodynamic therapy uptake and photo-induced cytotoxicity on Jurkat cells. J Photochem Photobiol B 80 1-7. 

Integrin receptor-binding peptides have been used to enhance liposome binding, uptake, and expression (25,47 9). The inclusion of an 0(5pi integrin-targeted peptide into a liposomal complex enhanced transfection efficiency four- to five-fold in Jurkat cells and 10- to 13-fold in TF-1 cells (48). Confocal and electron microscopy revealed that the mechanism of cell entry conferred by RGD peptides on liposomes is predominantly by clathrin-coated endocytosis rather than by phagocytosis (50). 

Incubate the cells at 37°C in the CO2 incubator and take absorbance measurements at 465 nm after the coloured product starts developing. For HeLa, A549, A2058, MCF-7 and Caco2 cells, 2 or 3 h of incubation is sufficient. For Jurkat cells, 18 h (overnight) incubation is required before absorbance measurements should be made. 

PARP binds to DNA surrounding single- or double-strand breaks and attaches polymers of ADP-ribose to itself and other proteins. This increases the negative charge in this area, thus facilitating DNA repair. Payne et al. reported increased poly(ADP-ribose) polymerase (PARP) activity in Jurkat cells treated with sodium deoxycholate. Activation of PARP in colonic cells was similarly reported by Glinghammer et al " following treatment with this bile acid. 

Armed with this new tool, Schena et al. (1996) created a microarray of 1,046 human cDNAs of unknown sequence. They were derived from human peripheral blood lymphocyfes fransformed wifh Epsfein-Barr virus. Suitably sized inserts [>600 base pairs (bp)] were cloned into a lambda vector, subsequently infected into an Escherichia coli strain, and finally amplified by polymerase chain reaction (PCR) using 5 -amino-modified primers. The resulting 5 -amino-modified cDNA amplicons were then arrayed onto sily-lated microscope slides. Next, the expression levels in human Jurkat cells undergoing heat shock or phorbol ester induction were examined. 

Donovan, J. A., R. L. Wange, W. Y. Langdon, and L. E. Samelson. The protein product of the c-cbl protooncogene is the 120-kDa tyrosine-phosphorylated protein in Jurkat cells activated via the T cell antigen receptor. J Biol. Chem. 269 22921-22924.1994. 

Meisner, H., B. R. Conway, D. Hartley, and M. P. Czech. Interactions ofCbl with Grb2 and phosphatidylinositol 3 - kinase in activated Jurkat cells. Mol Cell Biol. 15 3571-3578.1995. 

Mixture of HDAC isoforms from human T cell Jurkat cell extract... 

Previous studies have reported that ERKs are characteristically associated with cell proliferation and protection from apoptosis (Bl, XI), while activation of JNK and p38 MAPK can promote apoptosis in many systems, including B lymphocytes (G5), cerebellar granule cells (K3), hematopoietic cells (K8), and neuronal cells (M3, XI). On the other hand, a recent report found that a pyridinyl imidazole, SB 202190, the specific inhibitor of p38 MAPK, by itself was sufficient to induce apoptosis in T lymphocyte Jurkat cells (N2). Moreover, Th-2-derived cytokine IL-5, the ERK activator and antiapoptotic factor for eosinophils, could also activate p38 MAPK in human eosinophils (BIO). We recently reported that cytokine IL-3, IL-5, and GM-CSF could prolong survival of human eosinophilic leukemic (EoL-1) cells through the transient activation of ERK (W15). On the other hand, activation of p38 MAPK in EoL-1 cells by the NSAID sodium salicylate (NaSal) could lead to apoptosis (W15). We also found that the suppression of ERK using ERK antisense phosphorothioate oligodeoxynucleotides could promote the apoptosis of peripheral blood eosinophils (W16). Moreover, we found that dexamethasone-induced apoptosis and activation of JNK and p38 MAPK activity in eosinophils are regulated by caspases (Z2). 

Progressive Stages at Different Times of Anti-Fas-Induced Apoptosis in Jurkat Cells (A3)... 

Fig. 11. Flow cytometric detection of apoptotic cell deadi using the annexin V method after treatment with IgM anti-Fas mAb. The vacant retrovirus vector (LXSN)-transfected Jurkat cell clone of LX-2 clearly exhibits annexin V binding at 3 h after treatment (56.8%), and the binding cell population is further increased at 5 h (77.2%), whereas only faint annexin V binding is observed in LdelSN-transfected Jurkat cell clone RJ-14. This means diat endogenous wild-type mFas in the LX-2 cells is functional in Fas-mediated apoptosis, but transfected aberrant mFas in die RJ-14 cells interferes with die signaUng in a dominant negative manner.

The dimers were studied more closely in HL-60 leukaemia and Jurkat cell lines, and it was found that they have activities comparable to the clinically nsed anticancer drng doxorubicin. In terms of general toxicity to normal cells, it was observed that dimers 115 and 116 were not toxic to lymphocytes at doses approaching 100 p,M. In preliminary studies, apoptotic cell death was observed on exposnre to these componnds and further studies are ongoing to elucidate the underlying mechanism of apoptosis. For purposes of comparison, the corresponding phosphate ester monomers 117 and 118 were prepared and proved to have no antitumour activity in the cell lines examined. This result is important, because it rules out any role of the phosphate ester functionality in mediating the observed cytotoxic effects and emphasizes the necessity for a bivalent unit. 

Haux J, Lam M, Marthinsen ABL, Stricken T, Lundgren S. Digitoxin, in non toxic concentrations, induces apoptotic cell death in Jurkat cells in vitro. Z Onkol 1999 31 14-20. 

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