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Lipocalin 2-Deficient Mice Exhibit Increased Sensitivity to Escherichia coli Infection but Not to Ischemia-Reperfusion Injury
by
You-Ten, Annick
, Togawa, Atsushi
, Wakeham, Andrew
, Cheung, Carol C.
, Mak, Tak W.
, Fong, Hannah E. H.
, Berger, Thorsten
, Elia, Andrew J.
, Duncan, Gordon S.
in
Acute-Phase Proteins - deficiency
/ Acute-Phase Proteins - genetics
/ Acute-Phase Proteins - metabolism
/ Animals
/ Apoptosis
/ Bacteria
/ Bacterial diseases
/ Bacterial infections
/ Biological Sciences
/ Bone marrow cells
/ Cells, Cultured
/ E coli
/ Embryonic growth stage
/ Escherichia coli
/ Escherichia coli - physiology
/ Escherichia coli Infections - genetics
/ Escherichia coli Infections - immunology
/ Escherichia coli Infections - metabolism
/ Escherichia coli Infections - microbiology
/ Immune response
/ Immunity, Innate - immunology
/ Immunology
/ Infections
/ Injuries
/ Innate immunity
/ Kidney - metabolism
/ Kidney - pathology
/ Kidneys
/ Lipocalin-2
/ Lipocalins
/ Mice
/ Mice, Knockout
/ Necrosis
/ Neutrophils
/ Oncogene Proteins - deficiency
/ Oncogene Proteins - genetics
/ Oncogene Proteins - metabolism
/ Reperfusion injury
/ Reperfusion Injury - immunology
/ Reperfusion Injury - metabolism
/ Rodents
/ Siderophores
2006
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Lipocalin 2-Deficient Mice Exhibit Increased Sensitivity to Escherichia coli Infection but Not to Ischemia-Reperfusion Injury
by
You-Ten, Annick
, Togawa, Atsushi
, Wakeham, Andrew
, Cheung, Carol C.
, Mak, Tak W.
, Fong, Hannah E. H.
, Berger, Thorsten
, Elia, Andrew J.
, Duncan, Gordon S.
in
Acute-Phase Proteins - deficiency
/ Acute-Phase Proteins - genetics
/ Acute-Phase Proteins - metabolism
/ Animals
/ Apoptosis
/ Bacteria
/ Bacterial diseases
/ Bacterial infections
/ Biological Sciences
/ Bone marrow cells
/ Cells, Cultured
/ E coli
/ Embryonic growth stage
/ Escherichia coli
/ Escherichia coli - physiology
/ Escherichia coli Infections - genetics
/ Escherichia coli Infections - immunology
/ Escherichia coli Infections - metabolism
/ Escherichia coli Infections - microbiology
/ Immune response
/ Immunity, Innate - immunology
/ Immunology
/ Infections
/ Injuries
/ Innate immunity
/ Kidney - metabolism
/ Kidney - pathology
/ Kidneys
/ Lipocalin-2
/ Lipocalins
/ Mice
/ Mice, Knockout
/ Necrosis
/ Neutrophils
/ Oncogene Proteins - deficiency
/ Oncogene Proteins - genetics
/ Oncogene Proteins - metabolism
/ Reperfusion injury
/ Reperfusion Injury - immunology
/ Reperfusion Injury - metabolism
/ Rodents
/ Siderophores
2006
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Lipocalin 2-Deficient Mice Exhibit Increased Sensitivity to Escherichia coli Infection but Not to Ischemia-Reperfusion Injury
by
You-Ten, Annick
, Togawa, Atsushi
, Wakeham, Andrew
, Cheung, Carol C.
, Mak, Tak W.
, Fong, Hannah E. H.
, Berger, Thorsten
, Elia, Andrew J.
, Duncan, Gordon S.
in
Acute-Phase Proteins - deficiency
/ Acute-Phase Proteins - genetics
/ Acute-Phase Proteins - metabolism
/ Animals
/ Apoptosis
/ Bacteria
/ Bacterial diseases
/ Bacterial infections
/ Biological Sciences
/ Bone marrow cells
/ Cells, Cultured
/ E coli
/ Embryonic growth stage
/ Escherichia coli
/ Escherichia coli - physiology
/ Escherichia coli Infections - genetics
/ Escherichia coli Infections - immunology
/ Escherichia coli Infections - metabolism
/ Escherichia coli Infections - microbiology
/ Immune response
/ Immunity, Innate - immunology
/ Immunology
/ Infections
/ Injuries
/ Innate immunity
/ Kidney - metabolism
/ Kidney - pathology
/ Kidneys
/ Lipocalin-2
/ Lipocalins
/ Mice
/ Mice, Knockout
/ Necrosis
/ Neutrophils
/ Oncogene Proteins - deficiency
/ Oncogene Proteins - genetics
/ Oncogene Proteins - metabolism
/ Reperfusion injury
/ Reperfusion Injury - immunology
/ Reperfusion Injury - metabolism
/ Rodents
/ Siderophores
2006
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Lipocalin 2-Deficient Mice Exhibit Increased Sensitivity to Escherichia coli Infection but Not to Ischemia-Reperfusion Injury
Journal Article
Lipocalin 2-Deficient Mice Exhibit Increased Sensitivity to Escherichia coli Infection but Not to Ischemia-Reperfusion Injury
2006
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Overview
Diverse functions have been reported for lipocalin 2. To investigate these functions in vivo, we generated gene-targeted lipocalin 2-deficient mice ($Lcn2^{-/-}$mice). In vitro studies have suggested that lipocalin 2 is important for cellular apoptosis induced by IL-3 withdrawal, and for the induction of kidney differentiation during embryogenesis. Analysis of$Lcn2^{-/-}$mice showed normal cell death upon IL-3 withdrawal and normal kidney development. However, we found that$Lcn2^{-/-}$mice exhibited an increased susceptibility to bacterial infections, in keeping with the proposed function of lipocalin 2 in iron sequestration. Neutrophils isolated from$Lcn2^{-/-}$mice showed significantly less bacteriostatic activity compared with WT controls. The bacteriostatic property of the WT neutrophils was abolished by the addition of exogenous iron, indicating that the main function of lipocalin 2 in the antibacterial innate immune response is to limit this essential element. Another important function ascribed to lipocalin 2 has been its protective role against kidney ischemia-reperfusion injury. We analyzed$Lcn2^{-/-}$mice using a mouse model for severe renal failure and could not detect any significant differences compared with their WT littermates.
Publisher
National Academy of Sciences,National Acad Sciences
Subject
Acute-Phase Proteins - deficiency
/ Acute-Phase Proteins - genetics
/ Acute-Phase Proteins - metabolism
/ Animals
/ Bacteria
/ E coli
/ Escherichia coli - physiology
/ Escherichia coli Infections - genetics
/ Escherichia coli Infections - immunology
/ Escherichia coli Infections - metabolism
/ Escherichia coli Infections - microbiology
/ Immunity, Innate - immunology
/ Injuries
/ Kidneys
/ Mice
/ Necrosis
/ Oncogene Proteins - deficiency
/ Oncogene Proteins - genetics
/ Oncogene Proteins - metabolism
/ Reperfusion Injury - immunology
/ Reperfusion Injury - metabolism
/ Rodents
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