Production of a p65 fl/fl /LysMCre mouse model with dysfunctional NF-κB signaling in bone marrow-derived macrophages
Here, we describe the production and characterization of a novel p65 /LysMCre mouse model, which lacks canonical nuclear factor-kappaB member RelA/p65 (indicated as p65 hereafter) in bone marrow-derived macrophages. Cultured bone marrow-derived macrophages that lack p65 protein reveal NF-κB signalin...
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| Veröffentlicht in: | Innate immunity (London, England) England), 2023-11, Vol.29 (8), p.171-185 |
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| container_title | Innate immunity (London, England) |
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| creator | Korkaya, Ahmet K Fischer, Jeffrey Peppers, Anthony Crosson, Sean M Rayamajhi, Manira Miao, Edward A Baldwin, Jr, Albert S Bradford, Jennifer W |
| description | Here, we describe the production and characterization of a novel p65
/LysMCre mouse model, which lacks canonical nuclear factor-kappaB member RelA/p65 (indicated as p65 hereafter) in bone marrow-derived macrophages. Cultured bone marrow-derived macrophages that lack p65 protein reveal NF-κB signaling deficiencies, a reduction in phagocytic ability, and reduced ability to produce nitrites. Despite abnormal bone marrow-derived macrophage function, p65
/LysMCre mice do not exhibit differences in naïve systemic immune profiles or colony forming units and time to death following
infection as compared to controls. Additionally, p65
/LysMCre mice, especially females, display splenomegaly, but no other obvious physical or behavioral differences as compared to control animals. As bone marrow-derived macrophages from this transgenic model are almost completely devoid of canonical nuclear factor-kappaB pathway member p65, this model has the potential for being very useful in investigating bone marrow-derived macrophage NF-kappaB signaling in diverse biological and biomedical studies. |
| doi_str_mv | 10.1177/17534259231205993 |
| format | Article |
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/LysMCre mouse model, which lacks canonical nuclear factor-kappaB member RelA/p65 (indicated as p65 hereafter) in bone marrow-derived macrophages. Cultured bone marrow-derived macrophages that lack p65 protein reveal NF-κB signaling deficiencies, a reduction in phagocytic ability, and reduced ability to produce nitrites. Despite abnormal bone marrow-derived macrophage function, p65
/LysMCre mice do not exhibit differences in naïve systemic immune profiles or colony forming units and time to death following
infection as compared to controls. Additionally, p65
/LysMCre mice, especially females, display splenomegaly, but no other obvious physical or behavioral differences as compared to control animals. As bone marrow-derived macrophages from this transgenic model are almost completely devoid of canonical nuclear factor-kappaB pathway member p65, this model has the potential for being very useful in investigating bone marrow-derived macrophage NF-kappaB signaling in diverse biological and biomedical studies.</description><identifier>ISSN: 1753-4259</identifier><identifier>EISSN: 1753-4267</identifier><identifier>DOI: 10.1177/17534259231205993</identifier><identifier>PMID: 37828842</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Disease Models, Animal ; Female ; Macrophages ; Mice ; NF-kappa B - metabolism ; Signal Transduction ; Transcription Factor RelA</subject><ispartof>Innate immunity (London, England), 2023-11, Vol.29 (8), p.171-185</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c652-4192481517255be629f9e99b838149b33b867e481e02dace333ec9cd367dc97f3</cites><orcidid>0000-0002-1337-8382</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37828842$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Korkaya, Ahmet K</creatorcontrib><creatorcontrib>Fischer, Jeffrey</creatorcontrib><creatorcontrib>Peppers, Anthony</creatorcontrib><creatorcontrib>Crosson, Sean M</creatorcontrib><creatorcontrib>Rayamajhi, Manira</creatorcontrib><creatorcontrib>Miao, Edward A</creatorcontrib><creatorcontrib>Baldwin, Jr, Albert S</creatorcontrib><creatorcontrib>Bradford, Jennifer W</creatorcontrib><title>Production of a p65 fl/fl /LysMCre mouse model with dysfunctional NF-κB signaling in bone marrow-derived macrophages</title><title>Innate immunity (London, England)</title><addtitle>Innate Immun</addtitle><description>Here, we describe the production and characterization of a novel p65
/LysMCre mouse model, which lacks canonical nuclear factor-kappaB member RelA/p65 (indicated as p65 hereafter) in bone marrow-derived macrophages. Cultured bone marrow-derived macrophages that lack p65 protein reveal NF-κB signaling deficiencies, a reduction in phagocytic ability, and reduced ability to produce nitrites. Despite abnormal bone marrow-derived macrophage function, p65
/LysMCre mice do not exhibit differences in naïve systemic immune profiles or colony forming units and time to death following
infection as compared to controls. Additionally, p65
/LysMCre mice, especially females, display splenomegaly, but no other obvious physical or behavioral differences as compared to control animals. As bone marrow-derived macrophages from this transgenic model are almost completely devoid of canonical nuclear factor-kappaB pathway member p65, this model has the potential for being very useful in investigating bone marrow-derived macrophage NF-kappaB signaling in diverse biological and biomedical studies.</description><subject>Animals</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Macrophages</subject><subject>Mice</subject><subject>NF-kappa B - metabolism</subject><subject>Signal Transduction</subject><subject>Transcription Factor RelA</subject><issn>1753-4259</issn><issn>1753-4267</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNplkEtOwzAQhi0EoqVwADbIFwiN7fi1hIoCUnksuo8SP1qjNI7shqpX6yE4Ey6FbtjMzD-ab2b0A3CN8luEOB8jTkmBqcQE4ZxKSU7AcN_LCsz46bGmcgAuYvzIc5bG-DkYEC6wEAUegv49eN2rtfMt9BZWsGMU2mZsGziebePLJBi48n3cR20auHHrJdTbaPv2B6oa-DrNvnb3MLpFUq5dQNfC2reJqELwm0yb4D6NTlIF3y2rhYmX4MxWTTRXv3kE5tOH-eQpm709Pk_uZpliFGcFkrgQiCKOKa0Nw9JKI2UtiECFrAmpBeMmTZgc60oZQohRUmnCuFaSWzIC6LA2HY4xGFt2waWvtiXKy72D5T8HE3NzYLq-Xhl9JP4sI98rjGwL</recordid><startdate>202311</startdate><enddate>202311</enddate><creator>Korkaya, Ahmet K</creator><creator>Fischer, Jeffrey</creator><creator>Peppers, Anthony</creator><creator>Crosson, Sean M</creator><creator>Rayamajhi, Manira</creator><creator>Miao, Edward A</creator><creator>Baldwin, Jr, Albert S</creator><creator>Bradford, Jennifer W</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><orcidid>https://orcid.org/0000-0002-1337-8382</orcidid></search><sort><creationdate>202311</creationdate><title>Production of a p65 fl/fl /LysMCre mouse model with dysfunctional NF-κB signaling in bone marrow-derived macrophages</title><author>Korkaya, Ahmet K ; Fischer, Jeffrey ; Peppers, Anthony ; Crosson, Sean M ; Rayamajhi, Manira ; Miao, Edward A ; Baldwin, Jr, Albert S ; Bradford, Jennifer W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c652-4192481517255be629f9e99b838149b33b867e481e02dace333ec9cd367dc97f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Macrophages</topic><topic>Mice</topic><topic>NF-kappa B - metabolism</topic><topic>Signal Transduction</topic><topic>Transcription Factor RelA</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Korkaya, Ahmet K</creatorcontrib><creatorcontrib>Fischer, Jeffrey</creatorcontrib><creatorcontrib>Peppers, Anthony</creatorcontrib><creatorcontrib>Crosson, Sean M</creatorcontrib><creatorcontrib>Rayamajhi, Manira</creatorcontrib><creatorcontrib>Miao, Edward A</creatorcontrib><creatorcontrib>Baldwin, Jr, Albert S</creatorcontrib><creatorcontrib>Bradford, Jennifer W</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Innate immunity (London, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Korkaya, Ahmet K</au><au>Fischer, Jeffrey</au><au>Peppers, Anthony</au><au>Crosson, Sean M</au><au>Rayamajhi, Manira</au><au>Miao, Edward A</au><au>Baldwin, Jr, Albert S</au><au>Bradford, Jennifer W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Production of a p65 fl/fl /LysMCre mouse model with dysfunctional NF-κB signaling in bone marrow-derived macrophages</atitle><jtitle>Innate immunity (London, England)</jtitle><addtitle>Innate Immun</addtitle><date>2023-11</date><risdate>2023</risdate><volume>29</volume><issue>8</issue><spage>171</spage><epage>185</epage><pages>171-185</pages><issn>1753-4259</issn><eissn>1753-4267</eissn><abstract>Here, we describe the production and characterization of a novel p65
/LysMCre mouse model, which lacks canonical nuclear factor-kappaB member RelA/p65 (indicated as p65 hereafter) in bone marrow-derived macrophages. Cultured bone marrow-derived macrophages that lack p65 protein reveal NF-κB signaling deficiencies, a reduction in phagocytic ability, and reduced ability to produce nitrites. Despite abnormal bone marrow-derived macrophage function, p65
/LysMCre mice do not exhibit differences in naïve systemic immune profiles or colony forming units and time to death following
infection as compared to controls. Additionally, p65
/LysMCre mice, especially females, display splenomegaly, but no other obvious physical or behavioral differences as compared to control animals. As bone marrow-derived macrophages from this transgenic model are almost completely devoid of canonical nuclear factor-kappaB pathway member p65, this model has the potential for being very useful in investigating bone marrow-derived macrophage NF-kappaB signaling in diverse biological and biomedical studies.</abstract><cop>United States</cop><pmid>37828842</pmid><doi>10.1177/17534259231205993</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-1337-8382</orcidid></addata></record> |
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| language | eng |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Sage Journals GOLD Open Access 2024; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Disease Models, Animal Female Macrophages Mice NF-kappa B - metabolism Signal Transduction Transcription Factor RelA |
| title | Production of a p65 fl/fl /LysMCre mouse model with dysfunctional NF-κB signaling in bone marrow-derived macrophages |
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