LIVIVO - Search results -

Search results

Result 1 - 10 of total 13

Search options

Article ; Online: Assessing Changes in Human Natural Killer Cell Metabolism Using the Seahorse Extracellular Flux Analyzer.

Traba, Javier / Antón, Olga M

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2463, Page(s) 165–180

Abstract: Natural killer (NK) cells are cytotoxic cells that mediate anti-tumor and anti-viral immunity. The response of NK cells to different cytokines and stimuli may involve cell survival, proliferation, and changes in their cytotoxic function. These responses ... ...

Abstract	Natural killer (NK) cells are cytotoxic cells that mediate anti-tumor and anti-viral immunity. The response of NK cells to different cytokines and stimuli may involve cell survival, proliferation, and changes in their cytotoxic function. These responses will be supported by changes in cellular metabolism. Therefore, changes in NK metabolic parameters could somehow predict changes in NK cell function and cytotoxicity. In this chapter, we describe a protocol to measure NK cell metabolism in primary human NK cells by using an extracellular flux analyzer. This machine measures pH and oxygen changes in the medium and allows the study of NK cell glycolysis and mitochondrial respiration in real time with a small number of cells.
MeSH term(s)	Animals ; Energy Metabolism ; Glycolysis ; Humans ; Killer Cells, Natural ; Oxidative Phosphorylation ; Smegmamorpha
Language	English
Publishing date	2022-03-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2160-8_12
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Measurement of Cytosolic Mitochondrial DNA After NLRP3 Inflammasome Activation.

Antón, Olga M / Traba, Javier

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2459, Page(s) 117–129

Abstract: The NLRP3 inflammasome, a key component of the innate immune system that mediates caspase-1 activation, which in turn induces cleavage of the pyroptosis executioner gasdermin D and the proinflammatory cytokines IL-1β and IL-18, requires two signals to be ...

Abstract	The NLRP3 inflammasome, a key component of the innate immune system that mediates caspase-1 activation, which in turn induces cleavage of the pyroptosis executioner gasdermin D and the proinflammatory cytokines IL-1β and IL-18, requires two signals to be activated. First, inflammasome priming is achieved after activation of Toll-like receptors, which leads to NF-κB signaling and transcriptional activation of the genes for NLRP3 and IL-1β. Next, the inflammasome complex is activated by a second signal that induces extrusion of mitochondrial DNA to the cytosol of the cell, which leads to its oligomerization by a not fully understood mechanism. Here we describe a simple method that employs quantitative polymerase chain reaction (qPCR) using SYBR green to measure the presence of mitochondrial DNA (mtDNA) in the cytosol, which can be used to measure cytosolic mtDNA levels after inflammasome activation.
MeSH term(s)	Caspase 1 ; Cytosol ; DNA, Mitochondrial/genetics ; Inflammasomes ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Pyroptosis
Chemical Substances	DNA, Mitochondrial ; Inflammasomes ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein ; Caspase 1 (EC 3.4.22.36)
Language	English
Publishing date	2022-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2144-8_12
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article: Analysis of human natural killer cell metabolism

Traba, Javier / Waldmann, Thomas A / Anton, Olga M

Journal of visualized experiments. 2020 June 22, , no. 160

2020

Abstract: Natural Killer (NK) cells mediate mainly innate anti-tumor and anti-viral immune responses and respond to a variety of cytokines and other stimuli to promote survival, cellular proliferation, production of cytokines such as interferon gamma (IFNγ) and/or ...

Abstract	Natural Killer (NK) cells mediate mainly innate anti-tumor and anti-viral immune responses and respond to a variety of cytokines and other stimuli to promote survival, cellular proliferation, production of cytokines such as interferon gamma (IFNγ) and/or cytotoxicity programs. NK cell activation by cytokine stimulation requires a substantial remodeling of metabolic pathways to support their bioenergetic and biosynthetic requirements. There is a large body of evidence that suggests that impaired NK cell metabolism is associated with a number of chronic diseases including obesity and cancer, which highlights the clinical importance of the availability of a method to determine NK cell metabolism. Here we describe the use of an extracellular flux analyzer, a platform that allows real-time measurements of glycolysis and mitochondrial oxygen consumption, as a tool to monitor changes in the energy metabolism of human NK cells. The method described here also allows for the monitoring of metabolic changes after stimulation of NK cells with cytokines such as IL-15, a system that is currently being investigated in a wide range of clinical trials.
Keywords	biosynthesis ; cell proliferation ; cytotoxicity ; energy metabolism ; glycolysis ; humans ; interferon-gamma ; interleukin-15 ; mitochondria ; natural killer cells ; obesity ; oxygen consumption
Language	English
Dates of publication	2020-0622
Size	p. e61466.
Publishing place	Journal of Visualized Experiments
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/61466
Database	NAL-Catalogue (AGRICOLA)

Order via subito

Article ; Online: Analysis of Human Natural Killer Cell Metabolism.

Traba, Javier / Waldmann, Thomas A / Anton, Olga M

Journal of visualized experiments : JoVE

2020 , Issue 160

Abstract	Natural Killer (NK) cells mediate mainly innate anti-tumor and anti-viral immune responses and respond to a variety of cytokines and other stimuli to promote survival, cellular proliferation, production of cytokines such as interferon gamma (IFNγ) and/or cytotoxicity programs. NK cell activation by cytokine stimulation requires a substantial remodeling of metabolic pathways to support their bioenergetic and biosynthetic requirements. There is a large body of evidence that suggests that impaired NK cell metabolism is associated with a number of chronic diseases including obesity and cancer, which highlights the clinical importance of the availability of a method to determine NK cell metabolism. Here we describe the use of an extracellular flux analyzer, a platform that allows real-time measurements of glycolysis and mitochondrial oxygen consumption, as a tool to monitor changes in the energy metabolism of human NK cells. The method described here also allows for the monitoring of metabolic changes after stimulation of NK cells with cytokines such as IL-15, a system that is currently being investigated in a wide range of clinical trials.
MeSH term(s)	Cell Proliferation ; Cells, Cultured ; Cytokines/metabolism ; Humans ; Interferon-gamma/biosynthesis ; Interleukin-15/metabolism ; Killer Cells, Natural/cytology ; Killer Cells, Natural/immunology ; Killer Cells, Natural/physiology ; Lymphocyte Activation/immunology
Chemical Substances	Cytokines ; IL15 protein, human ; Interleukin-15 ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2020-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/61466
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Immunometabolism at the Nexus of Cancer Therapeutic Efficacy and Resistance.

Traba, Javier / Sack, Michael N / Waldmann, Thomas A / Anton, Olga M

Frontiers in immunology

2021 Volume 12, Page(s) 657293

Abstract: Constitutive activity of the immune surveillance system detects and kills cancerous cells, although many cancers have developed strategies to avoid detection and to resist their destruction. Cancer immunotherapy entails the manipulation of components of ... ...

Abstract	Constitutive activity of the immune surveillance system detects and kills cancerous cells, although many cancers have developed strategies to avoid detection and to resist their destruction. Cancer immunotherapy entails the manipulation of components of the endogenous immune system as targeted approaches to control and destroy cancer cells. Since one of the major limitations for the antitumor activity of immune cells is the immunosuppressive tumor microenvironment (TME), boosting the immune system to overcome the inhibition provided by the TME is a critical component of oncotherapeutics. In this article, we discuss the main effects of the TME on the metabolism and function of immune cells, and review emerging strategies to potentiate immune cell metabolism to promote antitumor effects either as monotherapeutics or in combination with conventional chemotherapy to optimize cancer management.
MeSH term(s)	Adaptive Immunity ; Animals ; Cell Communication/immunology ; Cell Transformation, Neoplastic/immunology ; Cell Transformation, Neoplastic/metabolism ; Cytokines/metabolism ; Disease Management ; Disease Susceptibility/immunology ; Disease Susceptibility/metabolism ; Energy Metabolism ; Humans ; Immunity, Innate ; Immunomodulation ; Immunotherapy ; Molecular Targeted Therapy ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Tumor Escape/genetics ; Tumor Escape/immunology ; Tumor Microenvironment/immunology
Chemical Substances	Cytokines
Language	English
Publishing date	2021-05-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.657293
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Centrosome polarization in T cells: a task for formins.

Andrés-Delgado, Laura / Antón, Olga M / Alonso, Miguel Angel

Frontiers in immunology

2013 Volume 4, Page(s) 191

Abstract: T-cell antigen receptor (TCR) engagement triggers the rapid reorientation of the centrosome, which is associated with the secretory machinery, toward the immunological synapse (IS) for polarized protein trafficking. Recent evidence indicates that upon ... ...

Abstract	T-cell antigen receptor (TCR) engagement triggers the rapid reorientation of the centrosome, which is associated with the secretory machinery, toward the immunological synapse (IS) for polarized protein trafficking. Recent evidence indicates that upon TCR triggering the INF2 formin, together with the formins DIA1 and FMNL1, promotes the formation of a specialized array of stable detyrosinated MTs that breaks the symmetrical organization of the T-cell microtubule (MT) cytoskeleton. The detyrosinated MT array and TCR-induced tyrosine phosphorylation should coincide for centrosome polarization. We propose that the pushing forces produced by the detyrosinated MT array, which modify the position of the centrosome, in concert with Src kinase dependent TCR signaling, which provide the reference frame with respect to which the centrosome reorients, result in the repositioning of the centrosome to the IS.
Language	English
Publishing date	2013-07-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2013.00191
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: NK Cell Proliferation Induced by IL-15 Transpresentation Is Negatively Regulated by Inhibitory Receptors.

Anton, Olga M / Vielkind, Susina / Peterson, Mary E / Tagaya, Yutaka / Long, Eric O

Journal of immunology (Baltimore, Md. : 1950)

2015 Volume 195, Issue 10, Page(s) 4810–4821

Abstract: IL-15 bound to the IL-15Rα-chain (IL-15Rα) is presented in trans to cells bearing the IL-2Rβ-chain and common γ-chain. As IL-15 transpresentation occurs in the context of cell-to-cell contacts, it has the potential for regulation by and of other receptor- ...

Abstract	IL-15 bound to the IL-15Rα-chain (IL-15Rα) is presented in trans to cells bearing the IL-2Rβ-chain and common γ-chain. As IL-15 transpresentation occurs in the context of cell-to-cell contacts, it has the potential for regulation by and of other receptor-ligand interactions. In this study, human NK cells were tested for the sensitivity of IL-15 transpresentation to inhibitory receptors. Human cells expressing HLA class I ligands for inhibitory receptors KIR2DL1, KIR2DL2/3, or CD94-NKG2A were transfected with IL-15Rα. Proliferation of primary NK cells in response to transpresented IL-15 was reduced by engagement of either KIR2DL1 or KIR2DL2/3 by cognate HLA-C ligands. Inhibitory KIR-HLA-C interactions did not reduce the proliferation induced by soluble IL-15. Therefore, transpresentation of IL-15 is subject to downregulation by MHC class I-specific inhibitory receptors. Similarly, proliferation of the NKG2A(+) cell line NKL induced by IL-15 transpresentation was inhibited by HLA-E. Coengagement of inhibitory receptors, either KIR2DL1 or CD94-NKG2A, did not inhibit phosphorylation of Stat5 but inhibited selectively phosphorylation of Akt and S6 ribosomal protein. IL-15Rα was not excluded from, but was evenly distributed across, inhibitory synapses. These findings demonstrate a novel mechanism to attenuate IL-15-dependent NK cell proliferation and suggest that inhibitory NK cell receptors contribute to NK cell homeostasis.
MeSH term(s)	Cell Proliferation/physiology ; Female ; HLA-C Antigens/immunology ; Humans ; Interleukin-15/immunology ; Interleukin-2 Receptor beta Subunit/immunology ; Killer Cells, Natural/cytology ; Killer Cells, Natural/immunology ; Male ; NK Cell Lectin-Like Receptor Subfamily C/immunology ; NK Cell Lectin-Like Receptor Subfamily D/immunology ; Phosphorylation/immunology ; Proto-Oncogene Proteins c-akt/immunology ; Receptors, Interleukin-15/immunology ; Receptors, KIR2DL1/immunology ; Receptors, KIR2DL2/immunology ; Receptors, KIR2DL3/immunology
Chemical Substances	HLA-C Antigens ; IL15 protein, human ; IL15RA protein, human ; IL2RB protein, human ; Interleukin-15 ; Interleukin-2 Receptor beta Subunit ; KIR2DL1 protein, human ; KIR2DL2 protein, human ; KIR2DL3 protein, human ; KLRD1 protein, human ; NK Cell Lectin-Like Receptor Subfamily C ; NK Cell Lectin-Like Receptor Subfamily D ; Receptors, Interleukin-15 ; Receptors, KIR2DL1 ; Receptors, KIR2DL2 ; Receptors, KIR2DL3 ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2015-10-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1500414
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 28: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Trans

Anton, Olga M / Peterson, Mary E / Hollander, Michael J / Dorward, David W / Arora, Gunjan / Traba, Javier / Rajagopalan, Sumati / Snapp, Erik L / Garcia, K Christopher / Waldmann, Thomas A / Long, Eric O

Proceedings of the National Academy of Sciences of the United States of America

2019 Volume 117, Issue 1, Page(s) 522–531

Abstract: Interleukin 15 (IL-15) is an essential cytokine for the survival and proliferation of natural killer (NK) cells. IL-15 activates signaling by the β and common γ ( ... ...

Abstract	Interleukin 15 (IL-15) is an essential cytokine for the survival and proliferation of natural killer (NK) cells. IL-15 activates signaling by the β and common γ (γ
MeSH term(s)	Cell Communication/physiology ; Cell Line ; Cell Proliferation ; Dendritic Cells/metabolism ; Endocytosis/physiology ; Healthy Volunteers ; Humans ; Interleukin-15/metabolism ; Interleukin-15 Receptor alpha Subunit/metabolism ; Killer Cells, Natural/physiology ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Monomeric GTP-Binding Proteins/genetics ; Monomeric GTP-Binding Proteins/metabolism ; Phosphorylation/physiology ; Primary Cell Culture ; Ribosomal Protein S6/metabolism
Chemical Substances	IL15 protein, human ; Interleukin-15 ; Interleukin-15 Receptor alpha Subunit ; Membrane Proteins ; Ribosomal Protein S6 ; RRAS2 protein, human (EC 3.6.1) ; Monomeric GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2019-12-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1911678117
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1148: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: IL-15 enhanced antibody-dependent cellular cytotoxicity mediated by NK cells and macrophages.

Zhang, Meili / Wen, Bernard / Anton, Olga M / Yao, Zhengsheng / Dubois, Sigrid / Ju, Wei / Sato, Noriko / DiLillo, David J / Bamford, Richard N / Ravetch, Jeffrey V / Waldmann, Thomas A

Proceedings of the National Academy of Sciences of the United States of America

2018 Volume 115, Issue 46, Page(s) E10915–E10924

Abstract: The goal of cancer immunotherapy is to stimulate the host immune system to attack malignant cells. Antibody-dependent cellular cytotoxicity (ADCC) is a pivotal mechanism of antitumor action of clinically employed antitumor antibodies. IL-15 administered ... ...

Abstract	The goal of cancer immunotherapy is to stimulate the host immune system to attack malignant cells. Antibody-dependent cellular cytotoxicity (ADCC) is a pivotal mechanism of antitumor action of clinically employed antitumor antibodies. IL-15 administered to patients with metastatic malignancy by continuous i.v. infusion at 2 μg/kg/d for 10 days was associated with a 38-fold increase in the number and activation status of circulating natural killer (NK) cells and activation of macrophages which together are ADCC effectors. We investigated combination therapy of IL-15 with rituximab in a syngeneic mouse model of lymphoma transfected with human CD20 and with alemtuzumab (Campath-1H) in a xenograft model of human adult T cell leukemia (ATL). IL-15 greatly enhanced the therapeutic efficacy of both rituximab and alemtuzumab in tumor models. The additivity/synergy was shown to be associated with augmented ADCC. Both NK cells and macrophages were critical elements in the chain of interacting effectors involved in optimal therapeutic responses mediated by rituximab with IL-15. We provide evidence supporting the hypothesis that NK cells interact with macrophages to augment the NK-cell activation and expression of FcγRIV and the capacity of these cells to become effectors of ADCC. The present study supports clinical trials of IL-15 combined with tumor-directed monoclonal antibodies.
MeSH term(s)	Alemtuzumab/administration & dosage ; Animals ; Antibodies, Monoclonal/immunology ; Antibody-Dependent Cell Cytotoxicity/drug effects ; Antibody-Dependent Cell Cytotoxicity/immunology ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Cell Line, Tumor ; Female ; Humans ; Interleukin-15/administration & dosage ; Interleukin-15/immunology ; Killer Cells, Natural/drug effects ; Killer Cells, Natural/immunology ; Macrophages/drug effects ; Macrophages/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, SCID ; Rituximab/administration & dosage
Chemical Substances	Antibodies, Monoclonal ; IL15 protein, human ; Interleukin-15 ; Alemtuzumab (3A189DH42V) ; Rituximab (4F4X42SYQ6)
Language	English
Publishing date	2018-10-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1811615115
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1148: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: MAL protein controls protein sorting at the supramolecular activation cluster of human T lymphocytes.

Antón, Olga M / Andrés-Delgado, Laura / Reglero-Real, Natalia / Batista, Alicia / Alonso, Miguel A

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 186, Issue 11, Page(s) 6345–6356

Abstract: T cell membrane receptors and signaling molecules assemble at the immunological synapse (IS) in a supramolecular activation cluster (SMAC), organized into two differentiated subdomains: the central SMAC (cSMAC), with the TCR, Lck, and linker for ... ...

Abstract	T cell membrane receptors and signaling molecules assemble at the immunological synapse (IS) in a supramolecular activation cluster (SMAC), organized into two differentiated subdomains: the central SMAC (cSMAC), with the TCR, Lck, and linker for activation of T cells (LAT), and the peripheral SMAC (pSMAC), with adhesion molecules. The mechanism of protein sorting to the SMAC subdomains is still unknown. MAL forms part of the machinery for protein targeting to the plasma membrane by specialized mechanisms involving condensed membranes or rafts. In this article, we report our investigation of the dynamics of MAL during the formation of the IS and its role in SMAC assembly in the Jurkat T cell line and human primary T cells. We observed that under normal conditions, a pool of MAL rapidly accumulates at the cSMAC, where it colocalized with condensed membranes, as visualized with the membrane fluorescent probe Laurdan. Mislocalization of MAL to the pSMAC greatly reduced membrane condensation at the cSMAC and redistributed machinery involved in docking microtubules or transport vesicles from the cSMAC to the pSMAC. As a consequence of these alterations, the raft-associated molecules Lck and LAT, but not the TCR, were missorted to the pSMAC. MAL, therefore, regulates membrane order and the distribution of microtubule and transport vesicle docking machinery at the IS and, by doing so, ensures correct protein sorting of Lck and LAT to the cSMAC.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/immunology ; Adaptor Proteins, Signal Transducing/metabolism ; Amino Acid Sequence ; Cell Line, Tumor ; Cells, Cultured ; Endosomes/immunology ; Endosomes/metabolism ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Humans ; Immunological Synapses/immunology ; Jurkat Cells ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/genetics ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/immunology ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/metabolism ; Membrane Microdomains/immunology ; Membrane Microdomains/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/immunology ; Membrane Proteins/metabolism ; Membrane Transport Proteins/genetics ; Membrane Transport Proteins/immunology ; Membrane Transport Proteins/metabolism ; Microscopy, Confocal ; Microtubules/immunology ; Microtubules/metabolism ; Models, Immunological ; Myelin Proteins/genetics ; Myelin Proteins/immunology ; Myelin Proteins/metabolism ; Myelin and Lymphocyte-Associated Proteolipid Proteins ; Protein Binding ; Protein Transport ; Proteolipids/genetics ; Proteolipids/immunology ; Proteolipids/metabolism ; RNA Interference ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; LAT protein, human ; MAL protein, human ; Membrane Proteins ; Membrane Transport Proteins ; Myelin Proteins ; Myelin and Lymphocyte-Associated Proteolipid Proteins ; Proteolipids ; Green Fluorescent Proteins (147336-22-9) ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck) (EC 2.7.10.2)
Language	English
Publishing date	2011-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1003771
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 28: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito