2015-03-01

Jurkat Cells and Relevant Research Topics

Jurkat cells are an immortalized line of T lymphocyte cells that can be used to study acute T cell leukemia, T cell signaling, and the expression of various chemokine receptors susceptible to viral entry, particularly HIV. Those cells are very useful in science because of their ability to produce interleukin 2. Their primary use is to determine the mechanism of differential susceptibility of cancers to drugs and radiation.

The Jurkat cell line was firstly established in the late 1970s from the peripheral blood of a 14 year old boy with T cell leukemia. Now different derivatives of the Jurkat cell line can be obtained from cell culture banks that have been mutated to lack certain genes.

Disease relevance of Jurkat Cells

l Noncytotoxic concentrations of the drug pentoxifylline (PTX) inhibited interaction of NF-kappa B with its motif and the stimulation ofHIV-1 LTR-driven gene expression in Jurkat cells
l Co-immunoprecipitation analysis revealed the presence of endogenous TAL1/E2A complexes in Jurkat cells, a leukemic line derived from a T-ALL patient.

High impact information on Jurkat Cells

l FR-alpha expression in Jurkat cells facilitated MBG or EBO entry, and FR-blocking reagents inhibited infection by MBG or EBO.
l To explore the potential of human IL-16 for gene therapy, this portion was transfected into HIV-1-susceptible CD4+ jurkat cells by means of a mammalian expression vector.

Biological context of Jurkat Cells

l FADD/MORT1- and caspase-8-deficient Jurkat cells expressing only TRAIL-R2 were resistant to TRAIL-induced apoptosis.
l Transfection of thymidine kinase-chloramphenicol acetyltransferase constructs containing the 21-bp c-myc sequence into Jurkat cellsdemonstrated increased chloramphenicol acetyltransferase activity upon phorbol ester and phytohemagglutinin treatment.
l A cell permeant peptide derived from this sequence displaces cytochrome c from IP3R and abrogates cell death induced by staurosporine treatment of HeLa cells and Fas ligand stimulation of Jurkat cells.

Anatomical context of Jurkat Cells

l The gene encoding human interleukin-2 (IL-2) has been cloned from human spleen cells, peripheral blood lymphocytes, and the Jurkat cell line .
l Isolated melanosomes express FasL, as detected by Western blot and cytofluorimetry, and they can exert Fas-mediated apoptosis in Jurkat cells.
l Overexpression of wild-type 14-3-3 tau also inhibited phorbol ester-induced PKC theta translocation from the cytosol to the membrane inJurkat cells, while a membrane-targeted form of 14-3-3 tau caused increased localization of PKC theta in the particulate fraction in unstimulated cells.

Gene context of Jurkat Cells

l Studies in which p56lck associates with PLC gamma 1 as a result of TCR stimulation of Jurkat cells, suggesting that p56lck plays a central role in coupling the TCR to the activation of PLC gamma 1.
l A caspase 8-deficient subline (JB6) of human Jurkat cells can be killed by the oligomerization of Fas-associated protein with death domain (FADD).
l CD95L resistant myeloma cells were found to be sensitive to TRAIL, displaying apoptotic features similar to those of the CD95L- and TRAIL-sensitive T leukemia cells Jurkat.
l VLA-4 on Jurkat cells is of constitutively high avidity and interfered with migration across barriers expressing VCAM-1.

Analytical, diagnostic and therapeutic context of Jurkat Cells

l Using immunoblotting and immune complex PLC assays, CD3 stimulation of Jurkat cells can induce the association ofPLC gamma 1 enzyme with CD3 complex.
l Northern blot analysis indicated the expression of human PEBP2 alpha A, alpha B (AML1), and beta genes in Jurkat cells.
l The cytotoxicity of neutrophil-derived TRAIL against Jurkat cells was determined by flow cytometry using FITC-conjugated annexin.
l Immunoblot analyses demonstrated that TCR ligation dramatically increased the level of tyrosine-phosphorylated PLC-gamma 1 present in anti-Tyr(P) antibody immunoprecipitates from stimulated Jurkat cells.
l Nuclear cAMP-responsive element (CRE) binding activity in electrophoretic mobility shift assays was constitutive in unstimulated Jurkat cells, showing only a small increase upon Tat treatment.

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