Relevant bibliographies by topics / Jurkat cells

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Jurkat cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Jurkat cells"

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Lu, Shuqing, Jianmin Wang, Jianmin Yang, Shenglan Gong, Hong Zhou, Li Chen, and Xianmin Song. "Amplification and Mutation of PSMB5 Gene in Bortezomib Resistant Lymphoblastic Leukemia Cells Derived from Jurkat Line." Blood 110, no. 11 (November 16, 2007): 2373. http://dx.doi.org/10.1182/blood.v110.11.2373.2373.

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Abstract Bortezomib, the first selective proteasome inhibitor in this new category of anti-cancer drug, inhibits chymotrypsin-like activity sited at beta 5 subunit of proteasome (PSMB5). To study the mechanism of proteasome inhibitor resistance in tumor cells, we established a series of bortezomib resistant lymphoblastic leukemia cell lines, named JurkatBs, from Jurkat line by repeated drug induction. There were no significant differences observed in the growth curves, colony formation rates, or cell cycle distribution between the JurkatBs and Jurkat cells. However, the effects of bortezomib, namely cytotoxicity, cell cycle arrest at G2 phase and induction of apoptosis, were decreased significantly in JurkatBs cells. There were no significant differences of intracellular mean fluorescence intensities of daunorubicin between JurkatBs and Jurkat cells (P>0.05) after treated with daunorubicin. Accordingly, the JurkatBs showed no cross-resistance to anthracycline, alkaloid and topoisomerase inhibitor. Quantitative PCR analysis showed no significant overexpression of MDR1 gene in JurkatB1, JurkatB2, JurkatB5 cells in comparison with that of Jurkat cells (22.77±5.58, 1.17±0.23, 8.30±2.62 vs 1.00±0.50; P>0.05). P-gp expression analysis was also negative in JurkatBs and Jurkat cells by Western bloting. By using quantitative PCR, we found that the PSMB5 gene was significantly amplified in JurkatB1 (5.82±0.60) and JurkatB5 cells (6.78±1.21) in comparison with that of Jurkat cells (1±0.49)(P<0.001), but not in JurkatB2 cells(0.16±0.03, P=1.000). A specific chromosome abnormality, i(14q), was found in all JurkatB5 cells (highly resistant to bortezomib), 4/16 JurkatB1 cells (moderately resistant), but not in JurkatB2 cells (slightly resistant). This results suggested that i(14q) may be resulted from the amplification of PMSB5 gene, which is located at 14q11. The chymotrypsin-like activities, determined by measuring the release of the fluorescent AMC from the substrate N- Suc-Leu-Leu-Val- Tyr-AMC, increased significantly in JurkatB1 (relative activity 3.27±0.12) and JurkatB5 cells (5.75±0.22) in comparison with that in Jurkat cells (1.00±0.14; P<0.001), but not in JurkatB2 cells (0.92±0.09; P>0.05). These results were coincident with the amplication of PSMB5, which may partly elucidated the bortezomib resistance in JurkatB cells. We then cloned and sequenced the full-length cDNA product of the PSMB5 gene from JurkatBs and Jurkat cells. A mutation at position 322 (G322A) of PSMB5 gene, causing an an amino acid substitution (Ala108Thr), was found in all selected JurkatB clones. The inhibition of chymotrypsin-like activities in JurartB2 (39.66±2.89) and JurartB5 cells (1.71±3.51), incubated with 10nM bortezomib up to 18h, were decreased significantly in comparison with that of Jurkat cells (86.87±0.97; P<.001), suggesting a decreased binding affinity of bortezomib to the chymotrypsin-like active site caused by Ala108Thr in JurkatB cells, which may resulted in conformation change in β5 subunit. In conclusion, we established bortezomib resistant leukemia cell lines with a different mechanism from that of multi-drug resistance (MDR). Both amplification and G322A mutation of PSMB5 gene are the important mechanisms of bortezomib resistance, by increasing chymotrypsin-like activity, and decreasing binding affinity of bortezomib to the chymotrypsin-like site, respectively.
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Li, M., S. Zhou, X. Liu, and G. Li. "The role of alpha-fetoprotein in maintaining the growth of human hepatoma cells." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 14081. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.14081.

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14081 Background: This study was to explored the functional mechanism of alpha-fetoprotein (AFP) in maintaining the proliferation of human hepatoma cells line Bel 7402 and the immunsuppression of lymphocyte Jurkat cells. Methods: Western blot was used to detecting the expression of some apoptosis-related gene, fluorescence labeled AFP and confocal microscopy scanning for receptor binding assay in the membrane in Jurkat cells. Results: It showed that AFP could enhance the expression of survivin and c-ras, but restrain caspase-3 express in Bel 7402 cells by Western blotting analysis. It also showed that AFP could bind to the membrane of Jurkat cells by confocal microscopy scanning, and when treated Jurkat with AFP, it indicated that AFP could repress the expression of survivin and Livin and elevated the activity of caspase-3 in the cells; Co-cultured Bel 7402 cells with Jurkat cells, the expression of tumor necrosis related-apoptosis induced ligand (TRAIL) in Jurkt cells was inhibited, when pretreatment with monoclonal antibody of AFP (Anti-AFP), the restrained effect of TRAIL express and the activity of caspase-3 was elevated in Jurkat cells was removed. It also indicated that Anti-AFP had an ability to block these functions of AFP. Conclusions: AFP has a capability to promote the growth and escape from immune surveillance of human hepatoma cells through enhancing the expression of ras and survivin gene in Bel 7402 cells, suppressing TRAIL, survivin and Livin expressed and upregulated activity of caspase-3 in Jurkat cells. No significant financial relationships to disclose.
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Yoon, Jinsun, Eun Shil Kim, Sujung Kim, and Young Lee. "In Vitro and in Vivo Effect of Sodium Metaarsenite (KML001) in Non-Hodgkin's Lymphoma." Blood 120, no. 21 (November 16, 2012): 1656. http://dx.doi.org/10.1182/blood.v120.21.1656.1656.

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Abstract Abstract 1656 Arsenic trioxide has been used for treatment of hematological malignancies including acute promyelocytic leukemia (APL), multiple myeloma. Sodium metaarsenite (NaAs2O3: code name KML001) is an orally bio-available arsenic compound with potential anti-cancer activity. However, the effect of KML001 has not been well studied in non-Hodgkin's lymphoma. The aim of this study is to determine the anti-tumoral effect of KML001 and to investigate the mechanism of anti-tumoral effect of KML001 in malignant lymphoma. KML001 inhibited the cellular proliferation in all lymphoma cell lines as well as JurkatR cells (adriamycin-resistant Jurkat cells) in a dose-dependent manner with IC50 of 5 × 10−8M. KML001 induced G1 cell cycle arrest which was associated with decreased expression of cyclin B1, cyclin E1, CDK1 (cdc2p34), CDK2, CDK4, and CDK6. KML001- induced p27 was bound to CDK4 and CDK6 in Jurkat cells, and bound to CDK2, CDK4 and CDK6 in JurkatR cells. CDK4 and CDK6 kinase activities were reduced in Jurkat and JurkatR cells. KML001 increased early apoptotic fraction using annexin V-PI staining in a time-dependent manner. In addition, Apoptotic molecules of Bcl-2, Bcl-XL, Mcl-1, proform of caspase-3, caspase-8, and caspase-9 were decreased; in contrast, expressions of PARP active form and Bax, were increased in Jurkat and JurkatR cells treated with KML001 in a dose-dependent manner. In addition, KML001 inhibited the activation of STAT1, 3, 5, NF-κB (p65 and p50 subunits), pAKT, p-mTOR, p-GSK3 ß in a dose-dependent manner, but p-PTEN was up-regulated in KML001-treated Jurkat and JurkatR cells. In MAP kinase signaling, pERK was down regulated, while pp38 and pJNK were increased in a dose-dependent manner. Real-time PCR with RNA extracted from KML001-treated Jurkat and JurkatR cells showed a reduction of catalytic subunit of telomerase, hTERT, in a time- dependent manner. When treated KML001, DNA damage molecule (p-γ-H2AX) was increased in a time-dependent manner, and the telomere length was shorten in Jurkat and JurkatR cells. In vivo anti-tumoral activity of KML001 was confirmed using a xenograft-murine model of human lymphoma cell. Tumor burden was significantly reduced (P < 0.01) for 42 days. Especially, in-vivo anti-tumoral effect of 3.5 mg/Kg KML001 was comparable to that of doxorubicin (2.5 mg/Kg, P < 0.05). Furthermore, three refractory or relapsed malignant lymphoma patients (Diffuse large cell lymphoma, Follicular lymphoma. Mantle cell lymphoma) were treated with 10 mg of KML001 daily, resulting in decrease of lymphoma mass in 4 weeks without severe toxicities. In summary, KML001(sodium metaarsenite) demonstrated anti-tumoral effect via various mechanisms including cell cycle arrest, induction of apoptosis, and inhibition of JAK/STAT, PI3K and MAPK pathways. Especially, KML001 might target telomerase with DNA damage. Furthermore, it is probable that KML001 may overcome the resistance of chemotherapeutic agents. Collectively, KML001 may be a candidate agent for the treatment of de novo, refractory and relapsed malignant lymphoma. Disclosures: No relevant conflicts of interest to declare.
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BRAGADIN, MARCANTONIO, ANTONIO TONINELLO, ALBERTO BINDOLI, MARIA PIA RIGOBELLO, and MARCELLA CANTON. "Thallium Induces Apoptosis in Jurkat Cells." Annals of the New York Academy of Sciences 1010, no. 1 (December 2003): 283–91. http://dx.doi.org/10.1196/annals.1299.049.

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Scaringi, L., P. Cornacchione, E. Ayroldi, L. Corazzi, E. Capodicasa, R. Rossi, and P. Marconi. "Omeprazole Induces Apoptosis in Jurkat Cells." International Journal of Immunopathology and Pharmacology 17, no. 3 (September 2004): 331–42. http://dx.doi.org/10.1177/039463200401700313.

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Buenz, Eric J. "Aloin induces apoptosis in Jurkat cells." Toxicology in Vitro 22, no. 2 (March 2008): 422–29. http://dx.doi.org/10.1016/j.tiv.2007.10.013.

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Di Pasqua, Anthony J., Jerry Goodisman, Deborah J. Kerwood, Bonnie B. Toms, and James C. Dabrowiak. "Modification of carboplatin by Jurkat cells." Journal of Inorganic Biochemistry 101, no. 10 (October 2007): 1438–41. http://dx.doi.org/10.1016/j.jinorgbio.2007.06.018.

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Singhal, Pravin C., Aditi A. Kapasi, Krishna Reddy, Nicholas Franki, Nora Gibbons, and Guohua Ding. "Morphine promotes apoptosis in Jurkat cells." Journal of Leukocyte Biology 66, no. 4 (October 1999): 650–58. http://dx.doi.org/10.1002/jlb.66.4.650.

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Acharya, Tathagata, and Ram V. Devireddy. "Cryomicroscopic Investigations of Freezing Processes in Cell Suspensions." Open Biotechnology Journal 4, no. 1 (May 11, 2010): 26–35. http://dx.doi.org/10.2174/1874070701004010026.

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This study evaluates the freezing response of three different cell types, Pacific oyster embryos (~50 µm in diameter), Jurkat cells and HeLa cells (~12 to 15 µm’s in diameter), using cryomicroscopy. Freezing experiments were performed on oyster embryos at cooling rates of either 5 or 10 °C/min, while Jurkats were cooled at either 1 or 10 °C/min and HeLa cells were cooled at either 1, 15 or 20 °C/min, respectively. The experiments with oyster embryos were primarily designed to investigate the phenomena of intracellular ice formation (IIF) while the experiments for Jurkat and HeLa cells were designed to investigate both cellular dehydration and IIF during freezing. IIF was characterized by the abrupt black flashing during the cooling steps while the cellular dehydration experiments were characterized by the volumetric (projected area) shrinkage of the cells during the cooling steps. Mathematical models were fit to the cellular dehydration data to obtain the Jurkat and HeLa cell membrane permeability (Lpg) at the reference temperature (273.15 K), the apparent activation energy of the cellular dehydration process (ELp) or the temperature dependence of Lpg. The temperature dependence of IIF in the oyster embryos, the Jurkat cells and the HeLa cells were also determined.
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Sokolovskaya, Alisa, Ekaterina Korneeva, Danila Zaichenko, Edward Virus, Dmitry Kolesov, Aleksey Moskovtsev, and Aslan Kubatiev. "Changes in the Surface Expression of Intercellular Adhesion Molecule 3, the Induction of Apoptosis, and the Inhibition of Cell-Cycle Progression of Human Multidrug-Resistant Jurkat/A4 Cells Exposed to a Random Positioning Machine." International Journal of Molecular Sciences 21, no. 3 (January 28, 2020): 855. http://dx.doi.org/10.3390/ijms21030855.

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Experiments from flight- and ground-based model systems suggest that unexpected alterations of the human lymphoblastoid cell line Jurkat, as well as effects on cell growth, metabolism, and apoptosis, can occur in altered gravity conditions. Using a desktop random positioning machine (RPM), we investigated the effects of simulated microgravity on Jurkat cells and their multidrug-resistant subline, Jurkat/A4 cells. The viability of Jurkat/A4 cells decreased after simulated microgravity in contrast with the Jurkat cells. At the same time, the viability between the experimental Jurkat cells and control Jurkat cells was not significantly different. Of note, Jurkat cells appeared as less susceptible to apoptosis than their multidrug-resistant clone Jurkat/A4 cells, whereas cell-cycle analysis showed that the percentage of Jurkat/A4 cells in the S-phase was increased after 72 and 96 h of RPM-simulated microgravity relative to their static counterparts. The differences in Jurkat cells at all phases between static and simulated microgravity were not significant. The surface expression of the intercellular adhesion molecule 3 (ICAM-3)—also known as cluster of differentiation (CD)50—protein was changed for Jurkat/A4 cells following exposure to the RPM. Changes in cell morphology were observed in the Jurkat/A4 cells after 96 h of RPM-simulated microgravity. Thus, we concluded that Jurkat/A4 cells are more sensitive to RPM-simulated microgravity as compared with the parental Jurkat cell line. We also suggest that intercellular adhesion molecule 3 may be an important adhesion molecule involved in the induction of leukocyte apoptosis. The Jurkat/A4 cells with an acquired multidrug resistance phenotype could be a useful model for studying the effects of simulated microgravity and testing anticancer drugs.
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Dissertations / Theses on the topic "Jurkat cells"

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Hoffmann, Ruth. "Investigation of helenalin-induced cell death in Bcl-2 overexpressing Jurkat cells." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-122215.

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Fruasaha, Petronilla A. "Regulation of Calcium Entry Pathway in Jurkat T Cells." Wright State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=wright1231558093.

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Joensuu, Jenny. "Online Image Analysis of Jurkat T Cells using in situ Microscopy." Thesis, Linköpings universitet, Institutionen för fysik, kemi och biologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-153313.

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Cell cultivation in bioreactors would benefit from developed monitoring systems with online real-time imaging to evaluate cell culture conditions and processes. This opportunity can be provided with the newly developed in situ Microscope also called ISM. The ISM probe is mounted into the wall of a bioreactor and consists of a measurement zone with an illuminating light source to obtain real-time images of moving cells in suspension. The instrument is linked to advanced imaging analysis software which can be specifically adapted for the objects in study. The aim of this project is to analyze the T lymphocyte cell line Jurkat T cells using the ISM equipment and identify specific features of the cells that can be obtained. The results show that the equipment and linked software are suitable for monitoring cell density, cell size distribution and cell surface analysis of the Jurkat cells during cultivation. The ISM could also detect induced changes in cell size caused by osmotic shifts and the course of an infection occurring in the cell suspension using a developed software for online real-time monitoring.
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Jabur, Soumya. "Design and optimisation of a microfluidic system for single cell encapsulation." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/design-and-optimisation-of-a-microfluidic-system-for-single-cell-encapsulation(6c4b7877-1339-45a9-90e7-b23b7e622621).html.

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This thesis describes a novel approach for cell encapsulation in alginate gel microbeads. The main aim of the thesis was to optimise a microfluidic setup and chip to encapsulate cells in monodisperse alginate gel microbeads. A number of cytotoxicity tests were therefore carried out to determine the effect of formulations used for the production, degradation and gelation of calcium alginate gel beads. Results from these tests revealed that the formulations used had little or no significant effect on cell growth, and therefore, alginate was deemed to be a suitable cell encapsulating material for further investigations. Alginate gel microbeads were produced using hydrodynamic focusing techniques. For this purpose two different microfluidic setups were constructed. Fluids (oil, acidified oil and samples) were driven through the microfluidic setup by gravity. However, a number of drawbacks using this setup arose, such as polydispersity and reproducibility. Syringe pumps were introduced into the design of the second microfluidic setup as a means of driving fluids through the setup. In addition three different microfluidic chips were fabricated with the aim of producing the ideal alginate gel microbead. The first microfluidic chip (PMMA MC1) was fabricated from PMMA and involved producing alginate gel microbeads that were internally gelified. This chip suffered from a number of drawbacks such as continuous blockages within the microfluidic channels, which led to the development of the second microfluidic chip. This chip was also fabricated from PMMA (PMMA MC2) but in contrast to PMMA MC1, gelification occurred externally, i.e. gelation took place off chip, and in this case the alginate microdroplets were dropped into a well containing 1 mL of acidified oil. This encapsulating procedure caused immediate cell death, which indicated that the internal gelation of alginate gel microbeads was favoured. These results also indicated that the design of the microfluidic chip needed developing in order to produce the ideal microbeads that can be used for cell encapsulation. This led to the fabrication of a novel microfluidic chip (PC MC3) which was fabricated from polycarbonate (PC) and involved internal gelation of the calcium alginate gel microbeads. The combination of using the optimised microfluidic setup and PC MC3, in addition to alternations in some of the solutions used to make the alginate microbeads, resulted in the production of the desired ideal gel microbeads containing cells. Snap shots of the encapsulated cells obtained using fluorescence microscopy after 24 hours of encapsulation, revealed that the cells showed some characteristics of living cells, yet at the same time they also showed some characteristics of dead cells. These findings demonstrate the potential use of the optimised microfluidic setup and PC MC3 chip for many biological and medical applications.
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Al-Saffar, Nada M. Salman. "Investigations of Fas- and chemotherapy induced apoptosis in Jurkat T-cells using MRS." Thesis, Institute of Cancer Research (University Of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271613.

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Clay, Charles Michael. "Synthesis of Isatin Derivatives Used for the Inhibition of Pro-Apoptotic Jurkat T Cells." Wright State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=wright1315518391.

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Mellott, Alayna N. "Divalent Metal Cation Entry and Cytotoxicity in Jurkat T Cells: Role of TRPM7 Channels." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1597319673881729.

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Bush, Jennifer E. "Synergistic interactions of chlorambucil, DHA, and TRAIL in Jurkat and H460 human cancer cells." Huntington, WV : [Marshall University Libraries], 2003. http://www.marshall.edu/etd/descript.asp?ref=348.

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Shaw, Jeremy Joseph Porter. "The Implications Of Gap Junction Inhibition In Jurkat Cell-CellCommunication And Proliferation." Kent State University Honors College / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ksuhonors1398988837.

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Johnson, Victoria Louise. "Regulation of biochemical and morphological features of chemical- and receptor-mediated apoptosis in Jurkat T cells." Thesis, University of Leicester, 2000. http://hdl.handle.net/2381/29651.

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Evidence suggests that the signalling events which occur after apoptotic stimulation, define two basic mechanisms for the induction of apoptosis. The first is dependent on signalling via the mitochondria and the second is dependent upon signalling directly from the death receptors. After induction of apoptosis, there is a convergence in signalling at the level of caspase activation and subsequent biochemical and morphological changes. Therefore the efficacy of various inhibitors of apoptosis is dependent upon the initiating signal. In order to understand the apoptotic pathway, the mechanisms by which these inhibitors regulate chemical- and receptor-mediated apoptosis must be understood. The anti-apoptotic oncoprotein, Bcl-2, was shown to inhibit both staurosporine and Fas-mediated apoptosis in a manner which was partially dependent upon the level of Bcl-2 protein expressed. During both staurosporine and Fas-induced apoptosis Bcl-2 acted downstream of caspase-8 activation. High levels of Bcl-2 expression did not effectively inhibit apoptosis induced by anti-Fas but inhibited AICD by inhibiting the secretion of sFasL at a level above caspase-8 activation. The peptide based caspase inhibitor z-VAD-FMK resulted in a novel nuclear morphological change, characterized by partially condensed nuclear morphology and could be dissociated from the externalisation of PS, HMW DNA fragmentation and preceded the appearance of a condensed nuclear morphology during staurosporine-induced apoptosis. Furthermore, the appearance of the partially condensed nuclear morphology was independent of effector caspases. The nuclear morphological change occurred downstream of cytochrome c release, disruption of mitochondrial membrane potential and could be inhibited by Bcl-2. Finally the role of caspase-3 and DFF40/45 were examined in staurosporine- and Fas-mediated apoptosis. Using the MCF-7 cell line, it was found that caspase-3 and DFF40/45 were dispensable for the formation of HMW DNA fragments. Furthermore, the serine protease inhibitor, TPCK which has been previously shown to inhibit oligonucleosomal-length DNA fragmentation, was found to exert this effect by acting downstream of DFF40 activation.
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Books on the topic "Jurkat cells"

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Hauser, Claude, Sylviane Messerli, and Laurent Tissot. Un foyer intellectuel et artistique dans le Jura bernois, 1780-1850. Charles-Ferdinand Morel et Isabelle Morel-de Gélieu. Éditions Alphil-Presses universitaires suisses, 2021. http://dx.doi.org/10.33055/alphil.03166.

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Le XIXe siècle a un an lorsque Charles-Ferdinand Morel et Isabelle de Gélieu unissent leur destinée. Dès lors, ils formeront un couple en vue grâce à leurs multiples activités sociales, religieuses, politiques, artistiques et littéraires. De nombreuses personnalités de passage dans le Jura bernois s’arrêtent dans leur demeure, un lieu de rencontres, d’échanges sur l’art et la littérature, de débats sur les idées nouvelles. Les réalisations auxquelles le Doyen Morel a contribué – la création d’une caisse centrale des pauvres, d’une caisse d’épargne et d’un orphelinat, la rédaction d’une constitution, l’élevage de mérinos – amorcent des évolutions qui marqueront les sociétés futures par leur audace. Quant à Isabelle de Gélieu, notoriété lui est acquise par ses romans et ses traductions littéraires. Mais derrière cette façade de vie mondaine, qu’en est-il de l’intimité du couple ? Interrogeant les frontières entre vie privée et vie publique, vie cachée et vie visible, sept historiennes et historiens offrent une approche renouvelée de ces deux personnages et de leur siècle. L’image qui en ressort est plus contrastée que celle présentée jusqu’à aujourd’hui. Mari et femme vivent côte à côte mais à la lecture des écrits d’Isabelle, on saisit que l’amour n’est plus présent. Dès lors, comment continuer à vivre ensemble sans s’aimer ? Comment trouver l’énergie pour créer, lorsque les difficultés financières, les disputes et une forme d’indifférence envahissent le quotidien ?
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Book chapters on the topic "Jurkat cells"

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Alais, Sandrine, Hélène Dutartre, and Renaud Mahieux. "Quantitative Analysis of Human T-Lymphotropic Virus Type 1 (HTLV-1) Infection Using Co-Culture with Jurkat LTR-Luciferase or Jurkat LTR-GFP Reporter Cells." In Methods in Molecular Biology, 47–55. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6872-5_4.

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Chimienti, F., M. Sève, S. Richard, J. Mathieu, and A. Favier. "Characterisation of the Different Steps During Zinc Chelation Induced Apoptosis in Jurkat and HeLa Cells." In Trace Elements in Man and Animals 10, 1035. New York, NY: Springer US, 2002. http://dx.doi.org/10.1007/0-306-47466-2_316.

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Gewies, Andreas, Carina Graß, and Daniel Krappmann. "Methods to Study CARD11-BCL10-MALT1 Dependent Canonical NF-κB Activation in Jurkat T Cells." In Methods in Molecular Biology, 125–43. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1669-7_8.

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Michel, Sève, Chimienti Fabrice, Richard Sandrine, Mathieu Jacques, and Favier Alain. "Intracellular Zinc Chelation Induces Apoptosis, Caspases Activation, and Transcription Factors Degradation in Jurkat and HeLa Cells." In Trace Elements in Man and Animals 10, 1003–7. New York, NY: Springer US, 2002. http://dx.doi.org/10.1007/0-306-47466-2_309.

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Carretta, María D., María A. Hidalgo, and Rafael A. Burgos. "Indirect Measurement of CRAC Channel Activity Using NFAT Nuclear Translocation by Flow Cytometry in Jurkat Cells." In The CRAC Channel, 83–94. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8704-7_7.

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Bi, Bao Yuan, Elisabeth Elass, Dominique Legrand, Florence Deplace, Geneviève Spik, and Joël Mazurier. "Difference in Binding and Fate of Lactotransferrin in Jurkat Human Lymphoblastic T-Cells and in T-47D Human Breast Cancer Cells." In Lactoferrin, 193–209. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3956-7_13.

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Legrand, D., P. H. C. van Berkel, V. Salmon, H. A. van Veen, M. C. Slomianny, J. H. Nuijens, and G. Spik. "Role of the First N-Terminal Basic Cluster of Human Lactoferrin (R2R3R4R5) in the Interactions with the Jurkat Human Lymphoblastic T-Cells." In Advances in Lactoferrin Research, 49–55. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4757-9068-9_6.

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Antoni, Sven-Thomas, Omar M. F. Ismail, Daniel Schetelig, Björn-Philipp Diercks, René Werner, Insa M. A. Wolf, Andreas H. Guse, and Alexander Schlaefer. "Systematic Analysis of Jurkat T-Cell Deformation in Fluorescence Microscopy Data." In Informatik aktuell, 275–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-54345-0_63.

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Rodari, Anthony, Guido Poli, and Carine Van Lint. "Jurkat-Derived (J-Lat, J1.1, and Jurkat E4) and CEM-Derived T Cell Lines (8E5 and ACH-2) as Models of Reversible Proviral Latency." In Methods in Molecular Biology, 3–15. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1871-4_1.

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Duthille, Isabelle, Maryse Masson, Geneviève Spik, and Joël Mazurier. "Lactoferrin Stimulates the Mitogen-Activated Protein Kinase in the Human Lymphoblastic T Jurkat Cell Line." In Advances in Lactoferrin Research, 257–60. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4757-9068-9_31.

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Conference papers on the topic "Jurkat cells"

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Acharya, Tathagata, and Ram V. Devireddy. "A Study of Intracellular Ice Formation in Jurkat Cells." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192334.

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The objective of this study was to characterize the IIF behavior of Jurkat cells in isotonic conditions in the absence of any cryoprotective agents. The Jurkat cells were collected from culture and then washed and re-suspended in Dulbecco’s Phosphate Buffered Saline (PBS). The freezing experiments were carried out at defined freezing protocols and at various freezing rates of 5, 20, 30 and 50 °C/min. The results suggest there was no substantial evidence of intracellular ice formation at lower cooling rates of 5, 20 and 30° C/min. The first conspicuous indication of intracellular ice formation (IIF) was observed at a freezing rate of 50 °C/min. At this cooling rate, unlike the usual sudden blackening of cells, the cells suddenly grew and exploded suggesting the formation of intracellular ice, which was reminiscent of a prior observed phenomenon for IIF.
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Dutta, Surjendu Bikash, Anders Kokkvoll Engdahl, Stefan Belle, Wolfgang Hübner, Mark Schüttpelz, Thomas Huser, and Francesco Dell'Olio. "Waveguide chip based super-resolution microscopy for T cell imaging." In Integrated Photonics Research, Silicon and Nanophotonics. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/iprsn.2022.itu1b.6.

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Imaging and the quantitative estimation of T cell actin cytoskeletal dynamics are important to describe immunological processes. This study presents waveguide chip based super-resolution imaging of the filamentous actin cytoskeleton of Jurkat T cells.
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Li, H., X. Ma, X. Du, X. Cheng, and J. C. M. Hwang. "High-frequency continuous-wave electroporation of Jurkat human lymphoma cells." In 2016 IEEE/MTT-S International Microwave Symposium (IMS). IEEE, 2016. http://dx.doi.org/10.1109/mwsym.2016.7540431.

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Khakshour, Samaneh, Timothy V. Beischlag, Carolyn Sparrey, and Edward J. Park. "Mechanical characterization of ART-treated Jurkat cells using optical tweezers." In 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6945191.

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Barrowcliffe, T. W., D. A. Marshall, L. P. Trickett, A. R. Hubbard, and R. Thorpe. "PRQOOAGULANT ACTIVITY OF HUMAN T LYMPHOCYTES IN INTRINSIC AND EXTRINSIC SYSTEMS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643156.

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Cells of the monocyte/macrophage series develop thromboplastin procoagulant activity (PCA) when activated. This activity may be enhanced by T lymphocytes, but there have been few studies of the PCA of T lymphocytes themselves. In the present study, we have measured the PCA of four T lymphoma cell lines (JURKAT, CEM, HSB2 and MQLT4) as well as normal peripheral blood T lymphocytes, before and after stimulation with phyto-haemag-glutinin (PHA), using clotting and amidolytic methods.Of the four cell lines only one, JURKAT, gave enhanced PCA. after stimulation with PHA., with recalcification times in plastic tubes being shortened from 200 secs, to 90 secs, at a cell concentration of 4 × 106 ml. This activity was shown to be thromboplastin-like by its dependence on Factor VII in plasma and in an amidolytic assay with purified Factors VII and × . JURKAT was also the only one of the four cell lines to secrete interleukin-2. All four cell lines promoted the generation of large amounts of thrombin in platelet-free plasma in glass tubes; the peak thrombin concentration of 25 iu/ml was equivalent to that generated by a procoagulant phospholipid reagent. This activity was dependent on the presence of plasma Factor VIII, and was shown to be due to phospholipids in the cell membranes by its inhibition with phospholipase A2 and C and its activity in a purified system with Factors VIII, IXa and X. Normal T lynphocytes generated similar thromboplastin PCA to JURKAT after PHA stimulation, but their intrinsic PCA in the thrombin generation test was only 15% of that of the lymphoma cells.These results show that some T lymphocytes can develop PCA in both intrinsic and extrinsic systems and this should be taken into account in studies of the PCA of mixed leucocyte populations. The difference in intrinsic PCA between normal and lymphoma cells could be an interesting marker for malignant transformation.
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Kolb, Juergen F., Jody A. White, Uwe Pliquett, Richard Nuccitelli, Karl H. Schoenbach, Stephen J. Beebe, Ravindra P. Joshi, and Wolfgang Frey. "Plasma Membrane Charging of Jurkat Cells by Nanosecond Pulsed Electric Fields." In 2007 IEEE Pulsed Power Plasma Science Conference. IEEE, 2007. http://dx.doi.org/10.1109/ppps.2007.4345783.

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Fabi, Gianluca, C. H. Joseph, Xin Jin, Xiaopeng Wang, Tiziana Pietrangelo, Xuanhong Cheng, James C. M. Hwang, and Marco Farina. "Electrical properties of Jurkat cells: an inverted scanning microwave microscope study." In 2020 IEEE/MTT-S International Microwave Symposium (IMS). IEEE, 2020. http://dx.doi.org/10.1109/ims30576.2020.9223785.

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Perisic Nanut, MM, S. Žurga, Š. Konjar, M. Prunk, J. Kos, and J. Sabotič. "P01.02 Selective induction of cell death in Jurkat cells with recombinant fungal lectin CNL." In iTOC9 – 9th Immunotherapy of Cancer Conference, September 22–24, 2022 – Munich, Germany. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-itoc9.14.

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Lauria, Michael V., Payson Dieffenbach, Anand Vadlamani, Jennifer Firehammer, Alexey Shashurin, and Allen L. Garner. "Synergistic Effects of Cold Atmospheric Plasma and Electric Pulses on Jurkat Cells*." In 2017 IEEE International Conference on Plasma Science (ICOPS). IEEE, 2017. http://dx.doi.org/10.1109/plasma.2017.8495983.

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Vasil’eva, O. A., A. V. Isaeva, T. S. Prokhorenko, A. P. Zima, and V. V. Novitsky. "Galectin-1 and Galectin-3 induce mitochondrial apoptotic pathway in Jurkat cells." In PHYSICS OF CANCER: INTERDISCIPLINARY PROBLEMS AND CLINICAL APPLICATIONS (PC’16): Proceedings of the International Conference on Physics of Cancer: Interdisciplinary Problems and Clinical Applications 2016. Author(s), 2016. http://dx.doi.org/10.1063/1.4960287.

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