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Article ; Online: ITK inhibitors in inflammation and immune-mediated disorders.

Sahu, Nisebita / August, Avery

2009 Volume 9, Issue 8, Page(s) 690–703

Abstract: Interleukin-2-inducible T cell kinase (ITK) is a non-receptor tyrosine kinase expressed in T cells, NKT cells and mast cells which plays a crucial role in regulating the T cell receptor (TCR), CD28, CD2, chemokine receptor CXCR4, and FcepsilonR-mediated ... ...

Abstract	Interleukin-2-inducible T cell kinase (ITK) is a non-receptor tyrosine kinase expressed in T cells, NKT cells and mast cells which plays a crucial role in regulating the T cell receptor (TCR), CD28, CD2, chemokine receptor CXCR4, and FcepsilonR-mediated signaling pathways. In T cells, ITK is an important mediator for actin reorganization, activation of PLCgamma, mobilization of calcium, and activation of the NFAT transcription factor. ITK plays an important role in the secretion of IL-2, but more critically, also has a pivotal role in the secretion of Th2 cytokines, IL-4, IL-5 and IL-13. As such, ITK has been shown to regulate the development of effective Th2 response during allergic asthma as well as infections of parasitic worms. This ability of ITK to regulate Th2 responses, along with its pattern of expression, has led to the proposal that it would represent an excellent target for Th2-mediated inflammation. We discuss here the possibilities and pitfalls of targeting ITK for inflammatory disorders.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Cell Differentiation/drug effects ; Humans ; Inflammation/drug therapy ; Inflammation/pathology ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Protein-Tyrosine Kinases/chemistry ; Signal Transduction/drug effects ; T-Lymphocytes/drug effects
Chemical Substances	Anti-Inflammatory Agents ; Protein Kinase Inhibitors ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; emt protein-tyrosine kinase (EC 2.7.10.2)
Language	English
Publishing date	2009-08-18
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2064823-6
ISSN	1873-4294 ; 1568-0266
ISSN (online)	1873-4294
ISSN	1568-0266
DOI	10.2174/156802609789044443
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Article ; Online: Functional screening implicates miR-371-3p and peroxiredoxin 6 in reversible tolerance to cancer drugs

Nisebita Sahu / Jean-Philippe Stephan / Darlene Dela Cruz / Mark Merchant / Benjamin Haley / Richard Bourgon / Marie Classon / Jeff Settleman

Nature Communications, Vol 7, Iss 1, Pp 1-

2016 Volume 10

Abstract: Acquired resistance significantly limits the efficacy of cancer drug therapies. Here, the authors identify miR-371-3p as a suppressor of drug tolerance in cancer cell lines by its target gene PRDX6, which in turn regulates PLA2/PKCα signalling and ROS ... ...

Abstract	Acquired resistance significantly limits the efficacy of cancer drug therapies. Here, the authors identify miR-371-3p as a suppressor of drug tolerance in cancer cell lines by its target gene PRDX6, which in turn regulates PLA2/PKCα signalling and ROS levels.
Keywords	Science ; Q
Language	English
Publishing date	2016-08-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cotargeting of MEK and PDGFR/STAT3 Pathways to Treat Pancreatic Ductal Adenocarcinoma.

Sahu, Nisebita / Chan, Emily / Chu, Felix / Pham, Thinh / Koeppen, Hartmut / Forrest, William / Merchant, Mark / Settleman, Jeff

Molecular cancer therapeutics

2017 Volume 16, Issue 9, Page(s) 1729–1738

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal human diseases and remains largely refractory to available drug treatments. Insufficient targeting of the known oncogenic drivers and activation of compensatory feedback loops and inability ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal human diseases and remains largely refractory to available drug treatments. Insufficient targeting of the known oncogenic drivers and activation of compensatory feedback loops and inability to prevent metastatic spread contribute to poor prognosis for this disease. The
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Apoptosis ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Carcinoma, Pancreatic Ductal/pathology ; Cell Line, Tumor ; Disease Models, Animal ; Drug Synergism ; Female ; Gene Knockdown Techniques ; Humans ; MAP Kinase Signaling System/drug effects ; Mice ; Molecular Targeted Therapy ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; RNA Interference ; Receptors, Platelet-Derived Growth Factor/metabolism ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Signal Transduction/drug effects ; Spheroids, Cellular ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; Protein Kinase Inhibitors ; STAT3 Transcription Factor ; Receptors, Platelet-Derived Growth Factor (EC 2.7.10.1)
Language	English
Publishing date	2017-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-17-0009
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Article ; Online: Functional screening implicates miR-371-3p and peroxiredoxin 6 in reversible tolerance to cancer drugs.

Sahu, Nisebita / Stephan, Jean-Philippe / Cruz, Darlene Dela / Merchant, Mark / Haley, Benjamin / Bourgon, Richard / Classon, Marie / Settleman, Jeff

Nature communications

2016 Volume 7, Page(s) 12351

Abstract: Acquired resistance to cancer drug therapies almost always occurs in advanced-stage patients even following a significant response to treatment. In addition to mutational mechanisms, various non-mutational resistance mechanisms have now been recognized. ... ...

Abstract	Acquired resistance to cancer drug therapies almost always occurs in advanced-stage patients even following a significant response to treatment. In addition to mutational mechanisms, various non-mutational resistance mechanisms have now been recognized. We previously described a chromatin-mediated subpopulation of reversibly drug-tolerant persisters that is dynamically maintained within a wide variety of tumour cell populations. Here we explore a potential role for microRNAs in such transient drug tolerance. Functional screening of 879 human microRNAs reveals miR-371-3p as a potent suppressor of drug tolerance. We identify PRDX6 (peroxiredoxin 6) as a key target of miR-371-3p in establishing drug tolerance by regulating PLA2/PKCα activity and reactive oxygen species. PRDX6 expression is associated with poor prognosis in cancers of multiple tissue origins. These findings implicate miR-371-3p as a suppressor of PRDX6 and suggest that co-targeting of peroxiredoxin 6 or modulating miR-371-3p expression together with targeted cancer therapies may delay or prevent acquired drug resistance.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Base Sequence ; Cell Line, Tumor ; Down-Regulation/drug effects ; Drug Resistance, Neoplasm/drug effects ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Peroxiredoxin VI/metabolism ; Phospholipase C beta/metabolism ; Phospholipases A2/metabolism ; Protein Kinase C-alpha/metabolism
Chemical Substances	Antineoplastic Agents ; MIRN371 microRNA, human ; MicroRNAs ; Peroxiredoxin VI (EC 1.11.1.15) ; Protein Kinase C-alpha (EC 2.7.11.13) ; Phospholipases A2 (EC 3.1.1.4) ; Phospholipase C beta (EC 3.1.4.11)
Language	English
Publishing date	2016-08-03
Publishing country	England
Document type	Journal Article
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/ncomms12351
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: IL-2-inducible T-cell kinase modulates TH2-mediated allergic airway inflammation by suppressing IFN-γ in naive CD4+ T cells.

Kannan, Arun K / Sahu, Nisebita / Mohanan, Sunish / Mohinta, Sonia / August, Avery

The Journal of allergy and clinical immunology

2013 Volume 132, Issue 4, Page(s) 811–20.e1–5

Abstract: Background: Asthma is a predominantly TH2 cell-dominated inflammatory disease characterized by airway inflammation and a major public health concern affecting millions of persons. The Tec family tyrosine kinase IL-2-inducible T-cell kinase (Itk) is ... ...

Abstract	Background: Asthma is a predominantly TH2 cell-dominated inflammatory disease characterized by airway inflammation and a major public health concern affecting millions of persons. The Tec family tyrosine kinase IL-2-inducible T-cell kinase (Itk) is primarily expressed in T cells and critical for the function and differentiation of TH cells. Itk(-/-) mice have a defective TH2 response and are not susceptible to allergic asthma. Objective: We sought to better understand the role of Itk signaling in TH differentiation programs and in the development and molecular pathology of allergic asthma. Methods: Using a murine model of allergic airway inflammation, we dissected the role of Itk in regulating TH cell differentiation through genetic ablation of critical genes, chromatin immunoprecipitation assays, and house dust mite-driven allergic airway inflammation. Results: Peripheral naive Itk(-/-) CD4(+) T cells have substantially increased transcripts and expression of the prototypic TH1 genes Eomesodermin, IFN-γ, T-box transcription factor (T-bet), and IL-12Rβ1. Removal of IFN-γ on the Itk(-/-) background rescues expression of TH2-related genes in TH cells and allergic airway inflammation in Itk(-/-) mice. Furthermore, small hairpin RNA-mediated knockdown of Itk in human peripheral blood T cells results in increased expression of mRNA for IFN-γ and T-bet and reduction in expression of IL-4. Conclusion: Our results indicate that Itk signals suppress the expression of IFN-γ in naive CD4(+) T cells, which in a positive feed-forward loop regulates the expression of TH1 factors, such as T-bet and Eomesodermin, and suppress development of TH2 cells and allergic airway inflammation.
MeSH term(s)	Animals ; Asthma/etiology ; Asthma/immunology ; CD4-Positive T-Lymphocytes/cytology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Cell Differentiation ; Chromatin Immunoprecipitation ; Female ; Humans ; Hypersensitivity/etiology ; Hypersensitivity/immunology ; Inflammation/etiology ; Inflammation/immunology ; Interferon-gamma/drug effects ; Interferon-gamma/metabolism ; Male ; Mice ; Protein-Tyrosine Kinases/immunology ; Protein-Tyrosine Kinases/metabolism ; Pyroglyphidae/immunology ; Th1 Cells/cytology ; Th1 Cells/immunology ; Th2 Cells/cytology ; Th2 Cells/immunology
Chemical Substances	Interferon-gamma (82115-62-6) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; emt protein-tyrosine kinase (EC 2.7.10.2)
Language	English
Publishing date	2013-06-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2013.04.033
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Article ; Online: Modeling susceptibility versus resistance in allergic airway disease reveals regulation by Tec kinase Itk.

Nisebita Sahu / J Luis Morales / Deborah Fowell / Avery August

PLoS ONE, Vol 5, Iss 6, p e

2010 Volume 11348

Abstract: Murine models of allergic asthma have been used to understand the mechanisms of development and pathology in this disease. In addition, knockout mice have contributed significantly to our understanding of the roles of specific molecules and cytokines in ... ...

Abstract	Murine models of allergic asthma have been used to understand the mechanisms of development and pathology in this disease. In addition, knockout mice have contributed significantly to our understanding of the roles of specific molecules and cytokines in these models. However, results can vary significantly depending on the mouse strain used in the model, and in particularly in understanding the effect of specific knockouts. For example, it can be equivocal as to whether specific gene knockouts affect the susceptibility of the mice to developing the disease, or lead to resistance. Here we used a house dust mite model of allergic airway inflammation to examine the response of two strains of mice (C57BL/6 and BALB/c) which differ in their responses in allergic airway inflammation. We demonstrate an algorithm that can facilitate the understanding of the behavior of these models with regards to susceptibility (to allergic airway inflammation) (S(aai)) or resistance (R(aai)) in this model. We verify that both C57BL/6 and BALB/c develop disease, but BALB/c mice have higher S(aai) for development. We then use this approach to show that the absence of the Tec family kinase Itk, which regulates the production of Th2 cytokines, leads to R(aai) in the C57BL/6 background, but decreases S(aai) on the BALB/c background. We suggest that the use of such approaches could clarify the behavior of various knockout mice in modeling allergic asthma.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2010-06-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Modeling susceptibility versus resistance in allergic airway disease reveals regulation by Tec kinase Itk.

Sahu, Nisebita / Morales, J Luis / Fowell, Deborah / August, Avery

PloS one

2010 Volume 5, Issue 6, Page(s) e11348

Abstract	Murine models of allergic asthma have been used to understand the mechanisms of development and pathology in this disease. In addition, knockout mice have contributed significantly to our understanding of the roles of specific molecules and cytokines in these models. However, results can vary significantly depending on the mouse strain used in the model, and in particularly in understanding the effect of specific knockouts. For example, it can be equivocal as to whether specific gene knockouts affect the susceptibility of the mice to developing the disease, or lead to resistance. Here we used a house dust mite model of allergic airway inflammation to examine the response of two strains of mice (C57BL/6 and BALB/c) which differ in their responses in allergic airway inflammation. We demonstrate an algorithm that can facilitate the understanding of the behavior of these models with regards to susceptibility (to allergic airway inflammation) (S(aai)) or resistance (R(aai)) in this model. We verify that both C57BL/6 and BALB/c develop disease, but BALB/c mice have higher S(aai) for development. We then use this approach to show that the absence of the Tec family kinase Itk, which regulates the production of Th2 cytokines, leads to R(aai) in the C57BL/6 background, but decreases S(aai) on the BALB/c background. We suggest that the use of such approaches could clarify the behavior of various knockout mice in modeling allergic asthma.
MeSH term(s)	Algorithms ; Animals ; Bronchial Hyperreactivity ; Disease Susceptibility ; Hypersensitivity/enzymology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Protein-Tyrosine Kinases/metabolism
Chemical Substances	Tec protein-tyrosine kinase (EC 2.7.1.-) ; Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2010-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0011348
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Differential sensitivity to Itk kinase signals for T helper 2 cytokine production and chemokine-mediated migration.

Sahu, Nisebita / Mueller, Cynthia / Fischer, Angela / August, Avery

Journal of immunology (Baltimore, Md. : 1950)

2008 Volume 180, Issue 6, Page(s) 3833–3838

Abstract: Allergic asthma is dependent on chemokine-mediated Th2 cell migration and Th2 cytokine secretion into the lungs. The inducible T cell tyrosine kinase Itk regulates the production of Th2 cytokines as well as migration in response to chemokine gradients. ... ...

Abstract	Allergic asthma is dependent on chemokine-mediated Th2 cell migration and Th2 cytokine secretion into the lungs. The inducible T cell tyrosine kinase Itk regulates the production of Th2 cytokines as well as migration in response to chemokine gradients. Mice lacking Itk are resistant to developing allergic asthma. However, the role of kinase activity of Itk in the development of this disease is unclear. In addition, whether distinct Itk-derived signals lead to T cell migration and secretion of Th2 cytokines is also unknown. Using transgenic mice specifically lacking Itk kinase activity, we show that active kinase signaling is required for control of Th2 responses and development of allergic asthma. Moreover, dominant suppression of kinase Itk activity led to normal Th2 responses, but significantly reduced chemokine-mediated migration, resulting in prevention of allergic asthma. These observations indicate that signals required for Th2 responses and migration are differentially sensitive to Itk activity. Manipulation of Itk's activity can thus provide a new strategy to treat allergic asthma by differentially affecting migration of T cells into the lungs, leaving Th2 responses intact.
MeSH term(s)	Allergens/administration & dosage ; Animals ; Asthma/enzymology ; Asthma/immunology ; Asthma/pathology ; Bronchial Hyperreactivity/enzymology ; Bronchial Hyperreactivity/immunology ; Bronchial Hyperreactivity/pathology ; Chemokines/physiology ; Chemotaxis, Leukocyte/genetics ; Chemotaxis, Leukocyte/immunology ; Cytokines/biosynthesis ; Inflammation Mediators/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Ovalbumin/administration & dosage ; Ovalbumin/immunology ; Protein Structure, Tertiary/genetics ; Protein Structure, Tertiary/physiology ; Protein-Tyrosine Kinases/deficiency ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/physiology ; Signal Transduction/genetics ; Signal Transduction/immunology ; Th2 Cells/enzymology ; Th2 Cells/immunology ; Th2 Cells/metabolism ; Th2 Cells/pathology
Chemical Substances	Allergens ; Chemokines ; Cytokines ; Inflammation Mediators ; Ovalbumin (9006-59-1) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; emt protein-tyrosine kinase (EC 2.7.10.2)
Language	English
Publishing date	2008-03-05
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; 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.180.6.3833
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Article: IL-2–inducible T-cell kinase modulates TH2-mediated allergic airway inflammation by suppressing IFN-γ in naive CD4+ T cells

Kannan, Arun K / Sahu, Nisebita / Mohanan, Sunish / Mohinta, Sonia / August, Avery

The Journal of Allergy and Clinical Immunology. 2013 Oct., v. 132, no. 4

2013

Abstract: BACKGROUND: Asthma is a predominantly TH2 cell–dominated inflammatory disease characterized by airway inflammation and a major public health concern affecting millions of persons. The Tec family tyrosine kinase IL-2–inducible T-cell kinase (Itk) is ... ...

Abstract	BACKGROUND: Asthma is a predominantly TH2 cell–dominated inflammatory disease characterized by airway inflammation and a major public health concern affecting millions of persons. The Tec family tyrosine kinase IL-2–inducible T-cell kinase (Itk) is primarily expressed in T cells and critical for the function and differentiation of TH cells. Itk−/− mice have a defective TH2 response and are not susceptible to allergic asthma. OBJECTIVE: We sought to better understand the role of Itk signaling in TH differentiation programs and in the development and molecular pathology of allergic asthma. METHODS: Using a murine model of allergic airway inflammation, we dissected the role of Itk in regulating TH cell differentiation through genetic ablation of critical genes, chromatin immunoprecipitation assays, and house dust mite–driven allergic airway inflammation. RESULTS: Peripheral naive Itk−/− CD4+ T cells have substantially increased transcripts and expression of the prototypic TH1 genes Eomesodermin, IFN-γ, T-box transcription factor (T-bet), and IL-12Rβ1. Removal of IFN-γ on the Itk−/− background rescues expression of TH2-related genes in TH cells and allergic airway inflammation in Itk−/− mice. Furthermore, small hairpin RNA–mediated knockdown of Itk in human peripheral blood T cells results in increased expression of mRNA for IFN-γ and T-bet and reduction in expression of IL-4. CONCLUSION: Our results indicate that Itk signals suppress the expression of IFN-γ in naive CD4+ T cells, which in a positive feed-forward loop regulates the expression of TH1 factors, such as T-bet and Eomesodermin, and suppress development of TH2 cells and allergic airway inflammation.
Keywords	CD4-positive T-lymphocytes ; animal models ; asthma ; cell differentiation ; chromatin ; dust ; gene expression ; genes ; humans ; inflammation ; interferon-gamma ; interleukin-4 ; messenger RNA ; mice ; people ; precipitin tests ; public health ; transcription factors ; tyrosine
Language	English
Dates of publication	2013-10
Size	p. 811-820.e5.
Publishing place	Mosby, Inc.
Document type	Article
ZDB-ID	121011-7
ISSN	1085-8725 ; 1097-6825 ; 0091-6749
ISSN (online)	1085-8725 ; 1097-6825
ISSN	0091-6749
DOI	10.1016/j.jaci.2013.04.033
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Article: Memory phenotype CD8+ T cells with innate function selectively develop in the absence of active Itk.

Hu, Jianfang / Sahu, Nisebita / Walsh, Elizabeth / August, Avery

European journal of immunology

2007 Volume 37, Issue 10, Page(s) 2892–2899

Abstract: T cells with a memory-like phenotype and possessing innate immune function have been previously identified as CD8(+)CD44(hi) cells. These cells rapidly secrete IFN-gamma upon stimulation with IL-12/IL-18 and are involved in innate responses to infection ... ...

Abstract	T cells with a memory-like phenotype and possessing innate immune function have been previously identified as CD8(+)CD44(hi) cells. These cells rapidly secrete IFN-gamma upon stimulation with IL-12/IL-18 and are involved in innate responses to infection with Listeria monocytogenes. The signals regulating these cells are unclear. The Tec kinase Itk regulates T cell activation and we report here that a majority of the CD8(+) T cells in Itk null mice have a phenotype of CD44(hi) similar to memory-like innate T cells. These cells are observed in mice carrying an Itk mutant lacking the kinase domain, indicating that active Tec kinase signaling suppresses their presence. These cells carry preformed message for and are able to rapidly produce IFN-gamma upon stimulation in vitro with IL-12/IL-18, and endow Itk null mice the ability to effectively respond to infection with L. monocytogenes or exposure to lipopolysaccharides by secretion of IFN-gamma. Transfer of these cells rescues the ability of IFN-gamma null mice to reduce bacterial burden following L. monocytogenes infection, indicating that these cells are functional CD8(+)CD44(hi) T cells previously detected in vivo. These results indicate that active signals from Tec kinases regulate the development of memory-like CD8(+) T cells with innate function.
MeSH term(s)	Animals ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/enzymology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/microbiology ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Immunity, Innate/genetics ; Immunologic Memory/genetics ; Immunophenotyping ; Interferon-gamma/biosynthesis ; Interferon-gamma/deficiency ; Interferon-gamma/genetics ; Listeriosis/enzymology ; Listeriosis/genetics ; Listeriosis/immunology ; Listeriosis/prevention & control ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Protein-Tyrosine Kinases/deficiency ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/physiology ; RNA, Messenger/biosynthesis ; Signal Transduction/genetics ; Signal Transduction/immunology
Chemical Substances	RNA, Messenger ; Interferon-gamma (82115-62-6) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; emt protein-tyrosine kinase (EC 2.7.10.2)
Language	English
Publishing date	2007-07-27
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.200737311
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