Knockout Mouse Models of Iron Homeostasis
Murine models have made valuable contributions to our understanding of iron metabolism. Investigation of mice with inherited forms of anemia has led to the discovery of novel proteins involved in iron homeostasis. A growing number of murine models are being developed to investigate mitochondrial iro...
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| Veröffentlicht in: | Annual review of nutrition 2011-08, Vol.31 (1), p.117-137 |
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| container_title | Annual review of nutrition |
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| creator | Fleming, Robert E Feng, Qi Britton, Robert S |
| description | Murine models have made valuable contributions to our understanding of iron metabolism. Investigation of mice with inherited forms of anemia has led to the discovery of novel proteins involved in iron homeostasis. A growing number of murine models are being developed to investigate mitochondrial iron metabolism. Mouse strains are available for the major forms of hereditary hemochromatosis. Findings in murine models support the concept that the pathogenesis of nearly all forms of hereditary hemochromatosis involves inappropriately low expression of hepcidin. The availability of mice with floxed iron-related genes allows the study of the in vivo consequences of cell-selective deletion of these genes. |
| doi_str_mv | 10.1146/annurev-nutr-072610-145117 |
| format | Article |
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Investigation of mice with inherited forms of anemia has led to the discovery of novel proteins involved in iron homeostasis. A growing number of murine models are being developed to investigate mitochondrial iron metabolism. Mouse strains are available for the major forms of hereditary hemochromatosis. Findings in murine models support the concept that the pathogenesis of nearly all forms of hereditary hemochromatosis involves inappropriately low expression of hepcidin. 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Investigation of mice with inherited forms of anemia has led to the discovery of novel proteins involved in iron homeostasis. A growing number of murine models are being developed to investigate mitochondrial iron metabolism. Mouse strains are available for the major forms of hereditary hemochromatosis. Findings in murine models support the concept that the pathogenesis of nearly all forms of hereditary hemochromatosis involves inappropriately low expression of hepcidin. The availability of mice with floxed iron-related genes allows the study of the in vivo consequences of cell-selective deletion of these genes.</description><subject>anemia</subject><subject>Anemia - genetics</subject><subject>Anemia - metabolism</subject><subject>animal models</subject><subject>Animals</subject><subject>Disease Models, Animal</subject><subject>genes</subject><subject>hemochromatosis</subject><subject>Hemochromatosis - genetics</subject><subject>Hemochromatosis - metabolism</subject><subject>hepcidin</subject><subject>Homeostasis</subject><subject>in vivo studies</subject><subject>Iron - metabolism</subject><subject>metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mitochondria - metabolism</subject><subject>Models, Animal</subject><subject>pathogenesis</subject><subject>proteins</subject><subject>Signal Transduction</subject><issn>0199-9885</issn><issn>1545-4312</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kDtPwzAQgC0EoqXwFyBiQQwBX-zEDhuqeFQUMUBny3XOKJDExU6Q-Pe4SmG4u-W710fIOdArAF5c664bPH6n3dD7lIqsAJoCzwHEHplCzvOUM8j2yZRCWaallPmEHIXwQSktGWOHZJJFSgpRTMnlU-fMpxv65NkNAWOusAmJs8nCuy55dC260OtQh2NyYHUT8GRXZ2R1f_c2f0yXLw-L-e0yNZzKPrVgwHCxZmCsrgDKCqVGIXRlBAVujIAcbWnyYm0ZKzmCRlYUlbEyQwmGzcjFOHfj3deAoVdtHQw2je4wnqji3RxoIbJI3oyk8S4Ej1ZtfN1q_6OAqq0ptTOltqbUaEqNpmLz6W7NsG6x-m_9UxOBsxGw2in97uugVq9ZfIHGACmB_QLK6nHC</recordid><startdate>20110821</startdate><enddate>20110821</enddate><creator>Fleming, Robert E</creator><creator>Feng, Qi</creator><creator>Britton, Robert S</creator><general>Annual Reviews</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20110821</creationdate><title>Knockout Mouse Models of Iron Homeostasis</title><author>Fleming, Robert E ; Feng, Qi ; Britton, Robert S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-f1c1c47b31cfad119de8ae77adc7014cc715ef9c56bf3394e1ae366dcf82e81c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>anemia</topic><topic>Anemia - genetics</topic><topic>Anemia - metabolism</topic><topic>animal models</topic><topic>Animals</topic><topic>Disease Models, Animal</topic><topic>genes</topic><topic>hemochromatosis</topic><topic>Hemochromatosis - genetics</topic><topic>Hemochromatosis - metabolism</topic><topic>hepcidin</topic><topic>Homeostasis</topic><topic>in vivo studies</topic><topic>Iron - metabolism</topic><topic>metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mitochondria - metabolism</topic><topic>Models, Animal</topic><topic>pathogenesis</topic><topic>proteins</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fleming, Robert E</creatorcontrib><creatorcontrib>Feng, Qi</creatorcontrib><creatorcontrib>Britton, Robert S</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Annual review of nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fleming, Robert E</au><au>Feng, Qi</au><au>Britton, Robert S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Knockout Mouse Models of Iron Homeostasis</atitle><jtitle>Annual review of nutrition</jtitle><addtitle>Annu Rev Nutr</addtitle><date>2011-08-21</date><risdate>2011</risdate><volume>31</volume><issue>1</issue><spage>117</spage><epage>137</epage><pages>117-137</pages><issn>0199-9885</issn><eissn>1545-4312</eissn><abstract>Murine models have made valuable contributions to our understanding of iron metabolism. 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| fulltext | fulltext |
| identifier | ISSN: 0199-9885 |
| ispartof | Annual review of nutrition, 2011-08, Vol.31 (1), p.117-137 |
| issn | 0199-9885 1545-4312 |
| language | eng |
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| source | Annual Reviews; MEDLINE |
| subjects | anemia Anemia - genetics Anemia - metabolism animal models Animals Disease Models, Animal genes hemochromatosis Hemochromatosis - genetics Hemochromatosis - metabolism hepcidin Homeostasis in vivo studies Iron - metabolism metabolism Mice Mice, Knockout Mitochondria - metabolism Models, Animal pathogenesis proteins Signal Transduction |
| title | Knockout Mouse Models of Iron Homeostasis |
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