Mammalian DNA (mammalian + dna)

Distribution by Scientific Domains


Selected Abstracts


IFN regulatory factor (IRF) 3/7-dependent and -independent gene induction by mammalian DNA that escapes degradation

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 11 2008
Yasutaka Okabe
Abstract DNase II in macrophages cleaves the DNA of engulfed apoptotic cells and of nuclei expelled from erythroid precursor cells. Macrophages in DNase II-deficient mice accumulate undigested DNA and constitutively produce IFN-, as well as TNF-,. The IFN-, causes severe anemia in the DNase II,/, embryos, which die prenatally. On the other hand, when the DNase II gene is inactivated postnatally, mice develop polyarthritis owing to the TNF-, produced by macrophages. Here, we showed that the IFN-, gene activation in DNase II,/, mice is dependent on IFN regulatory factor (IRF) 3 and 7. Accordingly, DNase II,/,IRF3,/,IRF7,/, mice do not suffer from anemia, but they still produce TNF-,, and age-dependently develop chronic polyarthritis. A microarray analysis of the gene expression in the fetal liver revealed a set of genes that is induced in DNase II,/, mice in an IRF3/IRF7-dependent manner, and another set that is induced independent of these factors. These results indicate that the mammalian chromosomal DNA that accumulates in macrophages due to inefficient degradation activates genes in both IRF3/IRF7-dependent and -independent manners. [source]


Effect of cytofectins on the immune response of murine macrophages to mammalian DNA

IMMUNOLOGY, Issue 2 2003
Fu-Gang Zhu
Summary DNA, depending on base sequence, can induce a wide range of immune responses. While bacterial DNA is stimulatory, mammalian DNA is inactive alone and can, moreover, inhibit the response to bacterial DNA. To determine whether the mode of cell entry affects the immune properties of mammalian DNA, we have investigated the effects of the cytofectin agents Fugene 6 (Roche Diagnostics Corp., Indianapolis, IN), Lipofectin and Lipofectamine (Life Technologies, Grand Island, NY) on the responses of murine macrophages to DNA from calf thymus and human placenta. Whereas calf thymus and human placenta DNA alone failed to stimulate J774 or RAW264·7 cell lines or bone marrow-derived macrophages, these DNAs in complexes with cytofectin agents stimulated macrophages to produce nitric oxide but not interleukin 12. Both single-stranded and double-stranded DNAs were active in the presence of cytofectins. Macrophage activation by the DNA,cytofectin complexes was reduced by chloroquine, suggesting a role of endosomal acidification in activation. As shown by flow cytometry and confocal microscopy, the cytofectins caused an increase in the uptake of DNA into cells. Our findings indicate that macrophages vary in their response to DNA depending on uptake pathway, suggesting that activation by DNA reflects not only sequence but also context or intracellular location. [source]


Developmental control via GATA factor interplay at chromatin domains

JOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2005
Emery H. Bresnick
Despite the extraordinary task of packaging mammalian DNA within the constraints of a cell nucleus, individual genes assemble into cell type-specific chromatin structures with high fidelity. This chromatin architecture is a crucial determinant of gene expression signatures that distinguish specific cell types. Whereas extensive progress has been made on defining biochemical and molecular mechanisms of chromatin modification and remodeling, many questions remain unanswered about how cell type-specific chromatin domains assemble and are regulated. This mini-review will discuss emerging studies on how interplay among members of the GATA family of transcription factors establishes and regulates chromatin domains. Dissecting mechanisms underlying the function of hematopoietic GATA factors has revealed fundamental insights into the control of blood cell development from hematopoietic stem cells and the etiology of pathological states in which hematopoiesis is perturbed. © 2005 Wiley-Liss, Inc. [source]