Protein C Inhibitor (PCI) is a secreted serine protease inhibitor, belonging to the family of serpins. In addition to activated protein C PCI inactivates several other proteases of the coagulation and fibrinolytic systems, suggesting a regulatory role in hemostasis. Glycosaminoglycans and certain negatively charged phospholipids, like phosphatidylserine, bind to PCI and modulate its activity. Phosphatidylerine (PS) is exposed on the surface of apoptotic cells and known as a phagocytosis marker. We hypothesized that PCI might bind to PS exposed on apoptotic cells and thereby influence their removal by phagocytosis. Using Jurkat T-lymphocytes and U937 myeloid cells, we show here that PCI binds to apoptotic cells to a similar extent at the same sites as Annexin V, but in a different manner as compared to live cells (defined spots on ∼10-30% of cells). PCI dose dependently decreased phagocytosis of apoptotic Jurkat cells by U937 macrophages. Moreover, the phagocytosis of PS exposing, activated platelets

Deficient expression of Bak in a clonal Jurkat cell line. (A) Wild-type or the variant Jurkat cell line, Bak−, were incubated in 1% NP-40 lysis buffer for 30

We have demonstrated previously the potent activation of PLD by the chemokine IL-8 in T lymphocytes (18). We have now extended our findings to include the C-C chemokine RANTES in demonstrating that in the Jurkat T cell line, the activation of this enzyme occurs at subnanomolar concentrations and is dependent on the activation of small GTP-binding protein cofactors. RANTES-induced PLD activation is consistently maximal at 1 nM, a concentration corresponding to the optimal chemotaxis-inducing dose in normal T lymphocytes. Interestingly, PLD activation in T lymphocytes and Jurkat T cells appears to be an important biologic consequence of chemokine action and more readily measurable (at nanomolar concentrations) than readouts of receptor activation such as calcium flux. It was also apparent that RANTES is the only chemokine tested to date (RANTES, MIP-1α, MIP-1β, MCP-1, MCP-3, lymphotactin) that induces as robust a response as seen in this study, although the others listed were capable of low ...

Annexin A6 (AnxA6) is a Ca2+-dependent membrane-binding protein involved in vesicular traffic. The likely participation of AnxA6 in the response of lymphocytes to Ca2+ signals has not been investigated yet. The present study focuses on intracellular relocation of AnxA6 in human Jurkat T lymphoblasts upon stimulation followed by transient increase of intracellular [Ca2+] and exocytosis of interleukin-2 (IL-2). Stimulation of the cells under different experimental conditions (by lowering pH and/or by rising extracellular [Ca2+] in the presence of ionomycin) induced time-dependent transients of intracellular [Ca2+] and concomitant changes in AnxA6 intracellular localization and in IL-2 secretion, with only minor effects on cell viability and apoptosis. In resting conditions (in the presence of EGTA or with no ionophore) AnxA6 was localized uniformly in the cytosol, whereas it translocated to vesicular structures beneath the plasma membrane within 5 min following stimulation of Jurkat T cells and ...

Necroptosis is a form of regulated necrotic cell death mediated by receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and RIPK3. Necroptotic cell death contributes to the pathophysiology of several disorders involving tissue damage, including myocardial infarction, stroke and ischemia-reperfusion injury. However, no inhibitors of necroptosis are currently in clinical use. Here we performed a phenotypic screen for small-molecule inhibitors of tumor necrosis factor-alpha (TNF-α)-induced necroptosis in Fas-associated protein with death domain (FADD)-deficient Jurkat cells using a representative panel of Food and Drug Administration (FDA)-approved drugs. We identified two anti-cancer agents, ponatinib and pazopanib, as submicromolar inhibitors of necroptosis. Both compounds inhibited necroptotic cell death induced by various cell death receptor ligands in human cells, while not protecting from apoptosis. Ponatinib and pazopanib abrogated phosphorylation of mixed lineage kinase domain-like

TY - JOUR. T1 - Assessment of secondary necrosis of Jurkat cells using a new microscopic system and double staining method with annexin V and propidium iodide.. AU - Honda, O.. AU - Kuroda, Masahiro. AU - Joja, I.. AU - Asaumi, Jun-Ichi. AU - Takeda, Yoshihiro. AU - Akaki, S.. AU - Togami, I.. AU - Kanazawa, Susumu. AU - Kawasaki, S.. AU - Hiraki, Y.. PY - 2000/2. Y1 - 2000/2. N2 - Using a new system developed by us for acquiring microscopic images automatically, we compared the morphological changes that apoptotic cells undergo with changes in the staining pattern of annexin V-enhanced green fluorescent protein (AV-EGFP) and propidium iodide (PI) in individual cells. Jurkat cells were treated with 5 mM CaCl2 alone, anti-Fas antibody and heating at 42 degrees C for 30 min or 46 degrees C for 60 min, and then were incubated in medium with 5 mM CaCl2. Time-lapse DNA fragmentation analysis and morphological observation revealed that the anti-Fas antibody and heating at 42 degrees C for 30 min ...

The ς binding site present in the Jurkat human T lymphocyte cell line was investigated. Jurkat cell membranes were found to have a single saturable binding site for [3H]haloperidol, a ς ligand (dissociation constant, 3.9 ± 0.3 nM). The binding of [3H]haloperidol was inhibited by several ς ligands. Northern analysis and reverse transcription-polymerase chain reaction provided evidence for the expression of the recently cloned type 1 ς-receptor (ς-R1) in Jurkat cells. The ς-R1 cDNA cloned from these cells was functional in heterologous expression systems. When expressed in mammalian cells, the cDNA-induced binding was saturable with dissociation constants of 1.9 ± 0.3 nM for [3H]haloperidol and 12 ± 2 nM for (+)-pentazocine. The binding of [3H]progesterone, a putative endogenous ligand to ς-R1, to the Jurkat cell ς-receptor could be directly demonstrated by using heterologously expressed ς-R1 cDNA. The binding of [3H]progesterone was saturable, with a dissociation constant of 88 ± 7 ...

TY - JOUR. T1 - Signaling through T lymphocyte surface proteins, TCR/CD3 and CD28, activates the HIV-1 long terminal repeat. AU - Tong-Starksen, S. E.. AU - Luciw, Paul A. AU - Peterlin, B. M.. PY - 1989. Y1 - 1989. N2 - The state of T cell activation and proliferation controls HIV-1 replication and gene expression. Previously, we demonstrated that the administration of PHA and PMA to the human T cell line Jurkat activates the HIV-1 enhancer, which is composed of two nuclear factor κB (NFκB) binding sites. Here, we show that PMA alone is sufficient for this effect. In addition, activation of T cells through the surface proteins TCR/CD3 and CD28 increased gene expression directed by the HIV-1 long terminal repeat (LTR) to the same extent as PMA. Analysis of 5 deletions in the LTR revealed that the NFκB binding sites and sequences in the upstream U3 region are required for this response. Whereas cyclosporin A did not inhibit the effect of PMA, it reduced the effects of agonists to TCR/CD3 and ...

TY - JOUR. T1 - Lysophosphatidylcholine is a regulator of tyrosine kinase activity and intracellular Ca2+ level in Jurkat T cell line. AU - Légrádi, Ádám. AU - Chitu, Violeta. AU - Szukacsov, Valéria. AU - Fajka-Boja, Roberta. AU - Szücs, Kinga Székely. AU - Monostori, Éva. PY - 2004/1/30. Y1 - 2004/1/30. N2 - Lysophospholipids, particularly lysophosphatidylcholine (lyso-PC), have been implicated in modulating T cell functions at the sites of inflammation and atherosclerosis. Although the chemotactic and immunomodulatory effects are well documented, the exact signaling pathway of lyso-PC action is poorly defined. In this work, we studied the earliest biochemical events in T cells triggered by lyso-PC. A marked and immediate tyrosine phosphorylation was induced in the leukemic T cell line, Jurkat. Phosphorylation of cellular substrates included src family kinase, p56lck and syk family kinase, ZAP70. The lyso-PC induced tyrosine phosphorylation was largely dependent on the presence of ...

Jurkat E6.1 Cell Line human from human blood(leukemic T-cell lymphoblast), 88042803; find null-null MSDS, related peer-reviewed papers, technical documents, similar products & more at Sigma-Aldrich.

Calcium release-activated calcium channels (CRAC) control influx of calcium in human T lymphocytes. Hour-long calcium elevations are necessary for efficient gene expression during T cell activation and proliferation. We report here that, the time course for store-operated Ca2+ entry is short-lived (3-4 min) and therefore, cannot account for the prolonged Ca2+ elevations necessary for NFAT translocation into nucleus. Previous findings strongly suggest that T cell activation is accompanied by cytosolic alkalinization. Here, we show that pH changes in Jurkat T cells following activation with mitogenic lectin, phytohemagglutinin (PHA), depends on the length of time of exposure and the concentration (potency) of the mitogen. For full understanding of ion fluxes involved in this process, it is important to distinguish CRAC channel subtype functions in these cells during activation as well as elucidate the pH mediated changes in Ca2+. In some experiments we show low pH with high concentrations of PHA. We also

Ca2+ release from intracellular stores is one of the major events transducing extracellular signals into living cells. Recently, a metabolite of nicotinamide adenine dinucleotide+ (NAD+), termed cyclic adenosine diphosphate-ribose (cADPr), has been described to release Ca2+ from caffeine-sensitive internal stores of cells. Jurkat T cells possess intracellular Ca2+ stores sensitive to caffeine, so a potential involvement of cADPr in Ca2+ signaling was investigated. cADPr released Ca2+ in a dose-dependent manner from intracellular stores of permeabilized Jurkat T cells. Half maximal release was obtained at 2.25 microM cADPr. Prior addition of D-myo-inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) or thapsigargin did not influence cADPr-induced Ca2+ release, indicating the presence of different Ca2+ pools sensitive to Ins(1,4,5)P3 and cADPr. The specificity of the response was confirmed using the inhibitors ruthenium red, 8-NH2-cADPr, and 8-Br-cADPr. All three compounds blocked cADPr-induced, but not Ins(1,4

© 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. T lymphocytes need to detect rare cognate foreign peptides among numerous foreign and self-peptides. This discrimination seems to be based on the kinetics of TCRs binding to their peptide-MHC (pMHC) ligands, but there is little direct information on the minimum time required for processing elementary signaling events and deciding to initiate activation. Here, we used interference reflection microscopy to study the early interaction between transfected human Jurkat T cells expressing the 1G4 TCR and surfaces coated with five different pMHC ligands of 1G4. The pMHC concentration required for inducing 50% maximal IFN-γ production by T cells, and 1G4-pMHC dissociation rates measured in soluble phase or on surface-bound molecules, displayed six- to sevenfold variation among pMHCs. When T cells were dropped onto pMHC-coated surfaces, rapid spreading occurred after a 2-min lag. The initial spreading rate measured during the first 45 s, and the contact area

Our previous experiments have shown that MMTV Rem functions in nuclear export of unspliced viral RNA in rodent cells [5]. In this manuscript, we have shown that Rem functions in human cell lines. Our results also indicate that Rev and Rex can increase reporter gene expression by interaction with the MMTV RmRE in human Jurkat T cells (Figures 2 and 4). Rex also could function on the RmRE in 293T HEK cells. Prior data indicate that some retroviral export proteins function on heterologous retroviral RNAs. For example, Rex can bind and function on both the RRE and the RxRE [43, 44]. However, the interaction is not reciprocal since Rev cannot act on the RxRE [43]. In this respect, the RmRE is quite permissive since it is required for enhancement of luciferase activity by Rem, Rev and Rex in human T cells. No effect of Rem was observed on the HIV and HTLV response elements (Figure 8). Surprisingly, the Rec export protein from the human retrovirus most closely related to MMTV, HERV-K/HML, had no effect ...

HIV-1 is transcriptionally active in activated T helper (Th)-cells and inactive in naive or resting memory Th-cells. Ets-2 is a preinduction transcriptional repressor of the IL-2 gene in naive Th-cells and a candidate transcriptional repressor of HIV-1 in the same cells, because the −279 to −250 upstream region of HIV-1-LTR [repressor-activator target sequence (RATS)], that participates in HIV-1-LTR transcriptional silencing, encompasses the AAGGAG Ets-2 binding site. In this proof of concept study, we investigated whether Ets-2 represses the expression of HIV-1. To assess whether Ets-2 can repress HIV-1 transcriptional activation acting through RATS, we transfected Jurkat cells with an Ets-2 overexpression plasmid (pCDNA3-ets-2) or Ets-2 silencing plasmids (ets-2-shRNA) and, as target genes, plasmids carrying the whole HIV-1-LTR sequence (HIV-1-LTR-CAT) or two copies of the RATS sequence (2× RATS-CAT) or a point mutation in the Ets-2 binding site (2× mutantRATS-CAT) or CMV-CAT (control). Ets-2

TY - JOUR. T1 - Determination of cytokine regulated glycan expression by using molecularly imprinted polymers targeting sialic acid. AU - Shinde, Sudhirkumar. AU - El-Schich, Zahra PY - 2019/7/11. Y1 - 2019/7/11. N2 - Cancer cells often have an increased amount of glycans, such as sialic acid (SA), on the cell surface, which normallyplay an important role in cell growth, proliferation and differentiation. In this study, SA expression is determinedby fluorescent nanoprobes, molecularly imprinted polymers, SA-MIPs. The nanoprobes are synthesized with animprinting approach to produce tailor-made fluorescent core-shell particles with high affinity for cell surface SA.Inflammation and cytokine production are well known tumor promoters, modulating the cellular microenvironment,including an aberrant cell surface glycan pattern. The recombinant cytokines IL-4, IL-6, IL-8 and a cocktail ofcytokines collected from stimulated T leukemia Jurkat cells were used to induce in vitro inflammation in two ...

The mechanism through which CD28 costimulation potentiates TCR-driven gene expression is still not clearly defined. Vav-1, an exchange factor for Rho GTPases thought to regulate, mainly through Rac-1, various signaling components leading to cytokine gene expression, is tyrosine phosphorylated upon CD28 engagement. Here, we provide evidence for a key role of Vav-1 in CD28-mediated signaling. Overexpression of Vav-1 in Jurkat cells in combination with CD28 ligation strongly reduced the concentration of staphylococcus enterotoxin E/MHC required for TCR-induced NF-AT activation. Surprisingly, upon Vav-1 overexpression CD28 ligation sufficed to activate NF-AT in the absence of TCR engagement. This effect was not mediated by overexpression of ZAP-70 nor of SLP-76 but necessitated the intracellular tail of CD28, the intactness of the TCR-proximal signaling cascade, the Src-homology domain 2 (SH2) domain of Vav-1, and SLP-76 phosphorylation, an event which was favored by Vav-1 itself. Cells overexpressing Vav-1

Chang PY, Draheim K, Kelliher MA, Miyamoto S. NFKB1 is a direct target of the TAL1 oncoprotein in human T leukemia cells. Cancer Res. 2006 Jun 15; 66(12):6008-13 ...

hi! is anyone out there tried electroporating Jurkat cells? If so, can you post the electroporation conditions please. cheers venkat -- Venkat Pisupati Lab -44-01223-334131 Wellcome/CRC Institute Fax -44-01223-334134 Dept. of Genetics E.mail. vnp at mole.bio.cam.ac.uk University of Cambridge UK CB2 1QR ...

For three years, I worked at NIH, in the NICHD. I took part in the research being conducted in the lab of Dr. Brant Weinstein, working with vascular morphogenesis in embryonic zebrafish. From Jan 2008-Jan 2009, I worked with Dr. Andreas Herrlich in the Lodish lab at the Whitehead. We performed a large-scale high-throughput screen to test the effects a set of shRNAs designed to knock-down most human kinases and phophatases has on ectodomain cleavage. Specifically, we used osmotic stress as a cleavage stimulus to the EGF ligand TGF-alpha. We worked in human Jurkat cells, and mouse Baf3 cell lines. Previous 20.109 labwork [1] Currently, I work in the lab of Dr. Ed Boyden. I am involved in the Epilepsy research group, an attempt to cause and then silence seizure activity in mice using optically controlled neurons. Over the summer, I am also working with the molecular biology group, to clone multiple new mutants of rhodopsins into usable backbones, which will then be used to generate virus capable of ...

Fingerprint Dive into the research topics of Biotin requirements are lower in human Jurkat lymphoid cells but homeostatic mechanisms are similar to those of HepG2 liver cells. Together they form a unique fingerprint. ...

Anti-Cancer Properties. A team of Iranian researchers at the Vaccine and Serum Research Institute in Mashhad conducted in vitro tests to evaluate the ability of dried jujube extract to inhibit growth or induce cell death in a variety of human tumor cell lines. Scientists used the MTT colorimetric assay to measure the degree to which water extract of dried jujube reduced the proliferation of tumor cells. Although the jujube extract inhibited tumor cell proliferation in all lines, it displayed the greatest effect against Jurkat leukemia cells. In a report in the February 2008 issue of Cytotechnology, researchers said their findings confirm dried jujubes cytotoxic properties against a variety of cancer cell lines and urged further study to identify the mechanisms through which jujube works.. Anti-Inflammatory. Diabetics can benefit from jujube fruit when it is used as a medicinal rub for cuts and sores. Many diabetics suffer from poor circulation and neuropathy, which causes nerve damage, ...

The I 9.2 cell line is a caspase-8 mutant of the wild-type Jurkat cell line A3 (see ATCC CRL-2570). Wild-type A3 cells were made neomycin resistant and treated with three cycles of exposure to the frameshifting mutagen ICR-191 to isolate clones harboring recessive mutations that were resistant to killing by Fas antibody.  Ref ICR-191 treated clones were serially diluted in 96-well plates in the presence of Fas Antibody for 3 to 5 weeks. Ref  Two of these ICR-191 treated clones have been deposited at the ATCC . They are I 9.2 (ATCC CRL-2571), a clone with a mutation in the cysteine protease caspase-8/FLICE and I 2.1 (ATCC CRL-2572), a clone with a mutation in the adaptor FADD.  

One cryopreserved vial of immortalised human T lymphocyte cells stably expressing a nuclear restricted red fluorescent protein (1.5 x 106 cell/vial) Jurkat Incucyte® NucLight Red Cells are supplied as 1 mL cryopreserved vials (1.5 x 106 cells/mL in 90% FBS and 10% DMSO) containing a stable population of human T lymphoc

Plasmid NFAT/AP-1 3x luciferase from Dr. Anjana Raos lab contains the insert NFAT/AP-1 3x and is published in EMBO J. 2000 Sep 1. 19(17):4783-95. This plasmid is available through Addgene.

Thank you for your interest in spreading the word about The Journal of Immunology.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.. ...

DOK3 Antibody 15749-1-AP has been identified with ELISA, WB, IHC. 15749-1-AP detected 53kd band in Jurkat cells with 1:500-1:1000 dilution...

NOD2 Antibody 20980-1-AP has been identified with ELISA, IF, IHC, WB. 20980-1-AP detected 100-110 kDa band in Jurkat cells with 1:500-1:1000 dilution...

WMF: please dont send me spam-mails again. Dont ever ask me again to translate articles into a language I do not speak. Especially if I have no clue what they are about (en:Cell migration, en:Subject-matter jurisdiction, en:Jurkat cells) and I am totally not interest in (en:Connie Sawyer, en:House of Kamehameha). This is not the kind of mail I left my e-mail-address for. I am interested in pigeons and poultry. If I ever felt like translating something, this would be the very good czech-pigeon-articles into de-wikipedia. ...

Mayya V., Lundgren D.H., Hwang S.-I., Rezaul K., Wu L., Eng J.K., Rodionov V., Han D.K.. Protein phosphorylation events during T cell receptor (TCR) signaling control the formation of complexes among proteins proximal to the TCR, the activation of kinase cascades, and the activation of transcription factors; however, the mode and extent of the influence of phosphorylation in coordinating the diverse phenomena associated with T cell activation are unclear. Therefore, we used the human Jurkat T cell leukemia cell line as a model system and performed large-scale quantitative phosphoproteomic analyses of TCR signaling. We identified 10,665 unique phosphorylation sites, of which 696 showed TCR-responsive changes. In addition, we analyzed broad trends in phosphorylation data sets to uncover underlying mechanisms associated with T cell activation. We found that, upon stimulation of the TCR, phosphorylation events extensively targeted protein modules involved in all of the salient phenomena associated ...

The protein-tyrosine kinase ZAP-70 is implicated, together with the Src kinase p56(lck), in controlling the early steps of the T-cell antigen receptor (TCR) signaling cascade. To help elucidate further the mechanism by which ZAP-70 regulates these initial events, we used a dominant-negative mutant approach. We overexpressed in the Jurkat T-cell line ZAP-70 mutated on Tyr-492 and Tyr-493 in the putative regulatory loop of its kinase domain. This mutant inhibited TCR-induced activation of nuclear factor of activated T cells by interfering with both intracellular calcium increase and Ras-regulated activation of extracellular signal-regulated kinases. Moreover, TCR-induced phosphorylation of pp36-38, thought to play a role upstream of these pathways, was found to be reduced. In contrast, overexpression of wild-type ZAP-70 induced constitutive activation of nuclear factor of activated T cells. The ZAP-70 mutant studied here could be phosphorylated on tyrosine when associated to the TCR zeta chain and was

Cell-cell interactions through direct contact are very important for cellular communication and coordination especially for immune cells. The human immunodeficiency virus type I (HIV-1) induces immune cell interactions between CD4(+) cells to shuttle between T cells via a virological synapse. A goal to understand the process of cell-cell transmission through virological synapses is to determine the cellular states that allow a chance encounter between cells to become a stable cell-cell adhesion. We demonstrate the use of optical tweezers to manipulate uninfected primary CD4(+) T cells near HIV Gag-iGFP transfected Jurkat T cells to probe the determinants that induce stable adhesion. When combined with fast 4D confocal fluorescence microscopy, optical tweezers can be utilized not only to facilitate cell-cell contact, but also to simultaneously track the formation of a virological synapse, and ultimately to probe the events that precede virus transfer. [GRAPHICS] HIV-1 infected T cell (green) ...

BioAssay record AID 541028 submitted by ChEMBL: Induction of apoptosis in bovine BL3 cells assessed as early apoptotic cells after 24 hrs by annexin V/propidium iodide staining-based FACS analysis.

Apoptosis,Blotting, Western,Caspases/metabolism,Cell Survival,Coloring Agents/pharmacology,Comet Assay,*DNA Damage,DNA Fragmentation,Enzyme Activation,Flow Cytometry,Humans,Hydrogen Peroxide/*pharmacology,Jurkat Cells,Poly(ADP-ribose) Polymerases,Tetrazolium Salts/pharmacology,Thiazoles/pharmacology,Time ...

Abstract: Zinc deficiency causes immune dysfunction. In T lymphocytes, hypozincemia promotes thymus atrophy, polarization imbalance, and altered cytokine production. Zinc supplementation is commonly used to boost immune function to prevent infectious diseases in at-risk populations. However, the molecular players involved in zinc homeostasis in lymphocytes are poorly understood. In this paper, we wanted to determine the identity of the transporter responsible for zinc entry into lymphocytes. First, in human Jurkat cells, we characterized the effect of zinc on proliferation and activation and found that zinc supplementation enhances activation when T lymphocytes are stimulated using anti-CD3/anti-CD28 Abs. We show that zinc entry depends on specific pathways to correctly tune the NFAT, NF-κB, and AP-1 activation cascades. Second, we used various human and murine models to characterize the zinc transporter family, Zip, during T cell activation and found that Zip6 was strongly upregulated early ...

Our previous genetic, pharmacological and analogue protection studies identified the glycosphingolipid, Gb3 (globotriaosylceramide, Pk blood group antigen) as a natural resistance factor for HIV infection. Gb3 is a B cell marker (CD77), but a fraction of activated peripheral blood mononuclear cells (PBMCs) can also express Gb3. Activated PBMCs predominantly comprise CD4+ T-cells, the primary HIV infection target. Gb3 is the sole receptor for Escherichia coli verotoxins (VTs, Shiga toxins). VT1 contains a ribosome inactivating A subunit (VT1A) non-covalently associated with five smaller receptor-binding B subunits. The effect of VT on PHA/IL2-activated PBMC HIV susceptibility was determined. Following VT1 (or VT2) PBMC treatment during IL2/PHA activation, the small Gb3+/CD4+ T-cell subset was eliminated but, surprisingly, remaining CD4+ T-cell HIV-1IIIB (and HIV-1Ba-L) susceptibility was significantly reduced. The Gb3-Jurkat T-cell line was similarly protected by brief VT exposure prior to HIV-1IIIB

transfecting Jurkat with Fugene HD: does not work? - posted in Molecular Cloning: Hi all, We are busy doing luciferase assays (dual). We would like to do a transient transfection of Jurkat. Since Promega has a protocol in its database we bought Fugene HD as transfection agent. It works extremely well on HepG2, but we have absolute zero success with Jurkat. We tried 1.5:1 -8:1 ratios in +1 steps, tried 3x105 and 5x105 cells, and both 24h incubation and 36h incubat...

Jurkat Cell Slide (Human (14yrs, Male) T lymphocyte acute T cell leukemia) (5 slides/pk) Slide for ICC HCLS-17005 Jurkat Cell Slide (Human (14yrs, Male) T lymphocyte acute T cell leukemia) (5 slides/pk) Slide for ICC HCLS-17005

Protein Kinase C Theta Type (nPKC Theta or PRKCQ or EC 2.7.11.13) - Pipeline Review, H1 2017 Size and Share Published in 2017-05-30 Available for US$ 3500 at Researchmoz.us

TY - JOUR. T1 - Selective Identification of Macrophages and Cancer Cells Based on Thermal Transport through Surface-Imprinted Polymer Layers. AU - Eersels, Kasper. AU - van Grinsven, Bart. AU - Ethirajan, Anitha. AU - Timmermans, Silke. AU - Monroy, Kathia L. Jimenez. AU - Bogie, Jeroen F. J.. AU - Punniyakoti, Sathya. AU - Vandenryt, Thijs. AU - Hendriks, Jerome J. A.. AU - Cleij, Thomas J.. AU - Daemen, Mat J.A.P.. AU - Somers, Veerle. AU - De Ceuninck, Ward. AU - Wagner, Patrick. PY - 2013/8/14. Y1 - 2013/8/14. KW - heat transfer resistance. KW - surface-imprinted polymer. KW - biomimetic sensors. KW - macrophages. KW - NR8383. KW - RAW 264.7 cell lines. KW - MCF-7 cell lines. KW - Jurkat cell lines. U2 - 10.1021/am401605d. DO - 10.1021/am401605d. M3 - Article. VL - 5. SP - 7258. EP - 7267. JO - ACS Applied Materials & Interfaces. JF - ACS Applied Materials & Interfaces. SN - 1944-8244. IS - 15. ER - ...

The major barrier to a HIV-1 cure is the persistence of latent genomes despite treatment with antiretrovirals. To investigate host factors which promote HIV-1 latency, we conducted a genome-wide functional knockout screen using CRISPR-Cas9 in a HIV-1 latency cell line model. This screen identified I …

Although the activation of immune cells is the first and thereby pivotal step in the immunological cascade, the current knowledge about the details of this process is quite limited. Recent studies have shown that aromatic compounds, such as B[a]P, influence the immune system even at low concentrations. We investigated the effect of a subtoxic B[a]P concentration (50 nM) on the proteome and the metabolome of non-activated and activated Jurkat T cells. The GeLC-MS/MS analysis yielded 2624 unambiguously identified proteins. In addition to typical regulatory pathways associated with T cell activation, pathway analysis by Ingenuity IPA revealed several metabolic processes, for instance purine and pyruvate metabolism. The activation process seems to be influenced by B[a]P suggesting an important role of the mTOR pathway in the cellular adaptation. B[a]P exposure of non-activated Jurkat cells induced signaling pathways such as protein ubiquitination and NRF2 mediated oxidative stress response as well ...

Our first experiment consisted in incubating Jurkat and 3T3 cells with TRAIL for 4h and 6h (see protocol about apoptosis sensibility). Concentrations of 0, 50 and 100 ng/mL of TRAIL were used with each cell line. A positive control for Jurkat cells was applied by incubating these cells with PMA and ionomycin overnight Park et al, 2001 . After that, FACS analysis was performed. To differentiate between apoptosis and necrosis, PI dye was used to stain necrotic cells Rieger et al, 2011 . Apoptotic cells were detected by using Annexin V labelled with Alexa 4881).. Unfortunately, despite doing several trials in which we incremented the number of hours for incubation (up to 48h) and tried different concentrations of TRAIL, we were not able to replicate the results we found in the literature [Johnstone et al, 2008; Zhang et al, 2005]. To see where the problem was, we decided to incubate the cells with 1000 ng/mL of TRAIL over a period of 48 h. If our TRAIL was functional, we would expect to see a ...

Guo A (2011) CST Curation Set: 11889; Year: 2011; Biosample/Treatment: cell line, Jurkat/calyculin_A & pervanadate; Disease: T cell leukemia; SILAC: -; Specificities of Antibodies Used to Purify Peptides prior to LCMS: p[ST]P ...

Mulhern D (2011) CST Curation Set: 12711; Year: 2011; Biosample/Treatment: cell line, Jurkat/calyculin_A & pervanadate; Disease: T cell leukemia; SILAC: -; Specificities of Antibodies Used to Purify Peptides prior to LCMS: p[ST]XP ...

ITK抗体试剂datasheet (ab14510).Abcam抗体、ELISA、激动剂拮抗剂、表观遗传试剂、蛋白多肽，使用效果保证，中国70%以上现货。

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Loss of the mitochondrial membrane potential results in a significant inhibition of calcium influx through calcium release-activated channels (CRAC) in Jurkat cells suspended in the medium of pH lower than 7.4. This effect disappears when the medium pH increases. Alkalinisation of the cytosol achieved by the addition of NH(4)Cl to the cells pretreated with thapsigargin, CCCP and CaCl(2), suspended in the medium of pH 7.2, does not affect CRAC activity, while alkalisation of the extracellular milieu by NaOH results in a strong stimulation of calcium entry. Thus, the mitochondrial effect on CRAC is exclusively related to the extracellular pH. Coupled mitochondria are able to take up Ca(2+) accumulated in the close proximity of CRAC. This protects these channels against feedback inhibition exerted by high [Ca(2+)](c). We conclude that CRAC may exist in two conformations: inhibitable and not inhibitable by cytosolic Ca(2+). Lower extracellular pH promotes the former one. This explains a much higher

GPI-anchored surface proteins mediate many important functions, including transport, signal transduction, adhesion, and protection against complement. They cluster into glycolipid-based membrane domains and caveolae, plasmalemmal vesicles involved in the transcytosis and endocytosis of these surface proteins. However, in lymphocytes, neither the characteristic flask shaped caveolae nor caveolin, a transmembrane protein typical of caveolae, have been observed. Here, we show that the GPI-anchored CD59 molecule on Jurkat T cells is internalized after cross-linking, a process inhibited by nystatin, a sterol chelating agent. Clustered CD59 molecules mostly accumulate in non-coated invaginations of the lymphocyte membrane before endocytosis, in marked contrast with the pattern of CD3-TCR internalization. Cytochalasin H blocked CD59 internalization in lymphocytes, but neither CD3 internalization nor transferrin uptake. Confocal microscopy analysis of F-actin distribution within lymphocytes showed that ...

Live-cell imaging allows for the in-depth study of activities occurring within living cells. The understanding of these complex interactions has wide ranging implications to many biomedical applications [1]. As the techniques used in live-cell imaging have improved, they have become an important component of monitoring the interactions within and among cells throughout their lifecycle [2, 3] . Several probes have been developed in relation to these endeavors, [4-6], and in turn, we have created T-Time, a repository of T cell images using a novel tag developed in [7].. T cells are lymphocytes that play a central role in cell-mediated immunity to foreign pathogens. Dysregulated T cell responses are implicated in numerous chronic conditions ranging from severe combined immunodeficiency (SCID) to autoimmunity and cancer. T cells migrate extensively throughout the body to enable proper immune function. This migration is the focus of extensive research and has motivated the development of ...

The incorporation properties of ceramide analogues for click chemistry in Jurkat T cells were investigated. The analogues varied in the acyl chain length and the position of the functional group for click chemistry. Fluorescence microscopy studies including anisotropy and quenching experiments showed signifi

The T-cell antigen receptor (TCR) complex is composed of a ligand-binding subunit, the α and β chains, and a signaling subunit, namely the CD3ε, γ and δ chains and the TCRζ chain. This complex participates in T-cell activation upon the presentation of the antigen peptide (derived from the foreign antigen) bound to the MHC (Class I and Class II) residing on antigen-presenting cells (APCs), including dendritic cells, macrophages and B cells. Co-stimulatory receptors, such as CD2, CD28, CD4, CD8, and integrin molecules, contribute to signal transduction by modulating the response threshold. All the above components along with accessory proteins essential for MHC are a part of the immunological synapse that initiates T-cell activation. Protein tyrosine phosphorylation mediated by the Src family kinases Lck and Fyn, in turn regulated by CD45, is the initial event in TCR signaling. Lck is activated by the interaction of MHC and CD4 or CD8. It then induces the phosphorylation and activation of ...

We investigated the expression differences of the TEL-AML1 fusion gene in a leukemia glucocorticoid (GC)-sensitive cell line (CEM) and a GC-resistant cell line (Jurkat). Changes in TEL-AML1 expression before and after GC exposure were analyzed. Expression of GC-sensitive and GC-resistant leukemia cells following initial diagnosis and during treatment was simulated. Leukemia cells were divided into a GC-unexposed or a GC-exposed group.

data have suggested that activation of the inducible T-cell kinase (ITK) requires an connection with the adaptor protein SLP-76. site and manifestation of Th2 cytokines. The inhibition is definitely specific as indicated by lack of effects from the polyarginine vehicle only or a scrambled sequence of the cargo peptide. In view of the part of ITK like a regulator of Th2 cytokine manifestation the data underscore the significance Obeticholic Acid of ITK like a target for pharmacological treatment. The Tec family of tyrosine kinases takes on a critical part in lymphocyte development and activation through antigen receptors (4 40 The inducible T-cell kinase (ITK) a member of the Tec family regulates selection during thymocyte development and settings the generation of effective Th2 reactions (15 40 Phosphorylation of ITK on Tyr 511 from the Src family kinase LCK happens early upon the engagement of the T-cell antigen receptor (TCR) and is critical for the enzymatic activation of ITK (18 44 Upon its ...

Opopanax chironium is a rich source of furano- and dihydrofuranocoumarins, whose accumulation in all plant parts and especially the roots is presumably responsible for the poisonous properties of the species. The presence of two distinct chemotypes was evidenced, with the one from Sicily affording the new dihydrofuranocoumarins 5d and 5e, while extracts from the Sardinian chemotype showed powerful apoptotic activity, which was traced to the prenylated furanocoumarins heraclenin (2a) and imperatorin (2b). Despite a close structural similarity, compounds 2a and 2b induced apoptosis in Jurkat leukemia cells in mechanistically different ways.

TY - CONF. T1 - Magneto-microfluidic device for apoptotic cell separation. AU - Kim, Hyun Seok. AU - Son, Oh Taek. AU - Kim, Kunhong. AU - Kim, Sang Hyeob. AU - Maeng, Sung Lyul. AU - Jung, Hyo Il. PY - 2006. Y1 - 2006. N2 - Separation of magnetically labeled cell has been a popular technique in cytometry. Normal Jurkat cells were treated with Chlorohexamide (CHX) and TRAIL to induce apoptosis. Apoptotic cells were treated with biotin functionalized fusion protein, C2A and streptavidin coated magnetic beads. The force balance between magnetic and drag force acting on the cells were calculated. The microfluidic device was designed accordingly. Results from our device were in a good agreement with those of the conventional flow cytometer, indicating our device can be used to sort apoptotic cells in a miniaturized system.. AB - Separation of magnetically labeled cell has been a popular technique in cytometry. Normal Jurkat cells were treated with Chlorohexamide (CHX) and TRAIL to induce apoptosis. ...

2019 Elsevier B.V. There is strong demand for cell separation methods that do not decrease cell activity or modify cell surfaces. Here, new temperature-modulated cell-separation columns not requiring cell-surface premodification are described. The columns were packed with temperature-responsive cationic polymer hydrogel-modified silica beads. Poly(N-isopropylacrylamide-co-n-butyl methacrylate-co-N,N-dimethylaminopropyl acrylamide) hydrogels with various cationic moieties were attached to silica-bead surfaces by radical polymerization using N,Nʹ-methylenebisacrylamide as a crosslinking agent. The beads were packed into solid-phase extraction columns, and temperature-dependent cell elution from the columns was found using HL-60 and Jurkat cells. The retention HL-60 and Jurkat cells in columns containing cationic beads at 37 °C was 95.3% to 99.6% and 95.0% to 98.8%, respectively. By contrast, beads without cationic properties exhibited low cell retention (20.6% for HL-60 and 32.5% for Jurkat ...

Epstein Barr trojan latent membrane proteins 1 (LMP1) induces NF-B activation through change effector sites (TES) 1 and 2, both which are crucial for B-lymphocyte change. These data offer further proof the essential part for Baricitinib NEMO in LMP1 TES2 NF-B activation and spotlight the need for exclusive domains within NEMO for sensing unique NF-B stimuli. and and and and and Fig. S2and had been analyzed for LMP1, p100/p52 NF-B2, and tubulin manifestation by Traditional western blot evaluation. NEMO Zn Finger and Residues 133C224 Are Separately Dispensable for LMP1 TES2-Mediated NF-B Activation, but Residues 303C372, Encompassing the UBAN Domain name, ARE CRUCIAL. To delineate which domains of NEMO are necessary for LMP1 TES2-mediated NF-B activation, NEMO? MEFs had been stably transfected with FLAG-HACtagged NEMO or among six deletion mutants, like the two isolated from your A45 and 2C Jurkat cell lines (Fig. 6as indicated. ( 0.01). **Not really significant ( 0.05) in College student check ...

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The effects of launch vibrations and microgravity on the cytoskeletal organization of a Jurkat leukemic cell line flown in space have been identified using a microarray approach.

T-cell chemiluminescence. A novel aspect of T-cell membrane activation studied with a Jurkat tumour cell line. Scand J Immunol. 1989 Aug; 30(2):265-9 ...

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The general goal of this laboratory is to elucidate the mechanism of activation, differentiation and function, and its regulation of T cells which play central roles in the regulation of immune responses and homeostasis. These include the regulation of immunological synapse, T cell receptor-induced signal transduction, co-stimulation regulation and signaling in T cell development. Particularly, the mechanism to induce autoimmune diseases and inflammations caused by aberrant regulation of T cell function and activation will be analyzed to aim to overcome the diseases.. ...

Lei Wu, Xin Guo, Steven Hartson, Abby Davis, Hui He, Denis M Medeiros, Weiqun Wang, Stephen L. Clarke, Edralin A. Lucas, Brenda J. Smith, Johannes von Lintig, Dingbo Lin. 2016. Lack of β,β-carotene -9, 10-oxygenase leads to hepatic mitochondrial dysfunction and cellular oxidative stress in mice. Mol Nutr Food Res. DOI: 10.1002/mnfr.201600576. [Epub ahead of print ...

Western blot analysis using Anti-TST antibody detects protein at predicted molecular weight using Jurkat Cells as a positive control. Tissue/Lysate Concentration: 1.0ug/ml Antibody Concentration: 1.0ug/ ...

Method of treatment of diseases caused by retroviruses which comprises administering therapeutically effective amount of a natural or synthetic oligo- or polysaccharide having at least one S-oxoacid group attached to the saccharic carbon atom through a linking group of lower molecular weight or a pharmaceutically acceptable salt thereof to a subject in need of such treatment.

The above parameters are from one study. For further information on this cell line and other parameters, including different strains, vendors, implant type and location and/or standards of care, please contact Covance.). ***Please note that cell lines are not for sale and unavailable for purchase from Covance.***. Fill out our tumor models contact form to get started setting up your next preclinical study with us.. Histotype: Leukemia [T-ALL]. Tumor Line: Human. REF# 3856. ...

Cytotoxic (aka killer, CD8+ T lymphocyte) cells attack directly, bind to antigen-bearing cells, punch holes in membrane, cause cell death. ...

Pendedahan sel Jurkat kepada ekstrak biji anggur - GSE mengakibatkan peningkatan dose- dan masa yang bergantung kepada di apoptosis dan pengaktifan caspase,

Orac recently lost his rag over JOHN WEEKS, editor of JCAM (see also here, here, here and here), and was less than appreciative of his recent comments on the