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10.1016/j.immuni.2016.10.011 http://scihub22266oqcxt.onion/10.1016/j.immuni.2016.10.011 C5694686!5694686 !27814941     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27814941 &cmd=llinks): Failed to open stream: HTTP request failed! 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Deleting an Nr4a1 Super-Enhancer Subdomain Ablates Ly6C(low) Monocytes while Preserving Macrophage Gene Function |pdf=|usr=}}{{27814941 }} gab.com Text Deleting an Nr4a1 Super-Enhancer Subdomain Ablates Ly6C(low) Monocytes while Preserving Macrophage Gene Function JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=27814941 #FOAvip Mononuclear phagocytes are a heterogeneous family that occupy all tissues and assume numerous roles to support tissue function and systemic homeostasis. Our ability to dissect the roles of individual subsets is limited by a lack of technologies that ablate gene function within specific mononuclear phagocyte sub-populations. Using Nr4a1-dependent Ly6C(low) monocytes, we present a proof-of-principle approach that addresses these limitations. Combining ChIP-seq and molecular approaches we identified a single, conserved, sub-domain within the Nr4a1 enhancer that was essential for Ly6C(low) monocyte development. Mice lacking this enhancer lacked Ly6C(low) monocytes but retained Nr4a1 gene expression in macrophages during steady state and in response to LPS. Because Nr4a1 regulates inflammatory gene expression and differentiation of Ly6C(low) monocytes, decoupling these processes allows Ly6C(low) monocytes to be studied independently. Twit Text FOAVip Deleting an Nr4a1 Super-Enhancer Subdomain Ablates Ly6C(low) Monocytes while Preserving Macrophage Gene Function ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=27814941 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27814941 #FOAvip English Wikipedia <ref>{{Cite pmid|27814941 }}</ref> Deleting an Nr4a1 Super-Enhancer Subdomain Ablates Ly6C(low) Monocytes while Preserving Macrophage Gene Function #MMPMID27814941 Thomas GD ; Hanna RN ; Vasudevan NT ; Hamers AA ; Romanoski CE ; McArdle S ; Ross KD ; Blatchley A ; Yoakum D ; Hamilton BA ; Mikulski Z ; Jain MK ; Glass CK ; Hedrick CC Immunity 2016[Nov]; 45 (5 ): 975-987 PMID27814941 show ga Mononuclear phagocytes are a heterogeneous family that occupy all tissues and assume numerous roles to support tissue function and systemic homeostasis. Our ability to dissect the roles of individual subsets is limited by a lack of technologies that ablate gene function within specific mononuclear phagocyte sub-populations. Using Nr4a1-dependent Ly6C(low) monocytes, we present a proof-of-principle approach that addresses these limitations. Combining ChIP-seq and molecular approaches we identified a single, conserved, sub-domain within the Nr4a1 enhancer that was essential for Ly6C(low) monocyte development. Mice lacking this enhancer lacked Ly6C(low) monocytes but retained Nr4a1 gene expression in macrophages during steady state and in response to LPS. Because Nr4a1 regulates inflammatory gene expression and differentiation of Ly6C(low) monocytes, decoupling these processes allows Ly6C(low) monocytes to be studied independently. |Animals [MESH] |Antigens, Ly/immunology [MESH] |Cell Differentiation/*immunology [MESH] |Cell Separation [MESH] |Chromatin Immunoprecipitation [MESH] |Macrophages/cytology/*immunology [MESH] |Melanoma, Experimental/*immunology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Monocytes/cytology/*immunology [MESH] |Nuclear Receptor Subfamily 4, Group A, Member 1/deficiency/*immunology [MESH]Deleting an Nr4a1 Super-Enhancer Subdomain Ablates Ly6C(low) Monocytes(epmc).pdf DeepDyve Pubget Overpricing