• HET3 mice used in this program are (F2) offspring of CByB6F1/J and C3D2F1/J (combining BALB/cBy, C57BL/6, C3H, and DBA/2) strains. (jax.org)
  • J:235854 lists J:27148 as the reference for these mice but then describes them as "B6C3F1" when the mice in the given reference were C57BL/6J mice fostered on C3Hf/Nctr mice. (jax.org)
  • Pathobiology of aging mice and GEM: background strains and experimental design. (jax.org)
  • C57BL6, 129, and FVB/N strains are emphasized because of their widespread use in the generation of knockout, transgenic, and conditional mutant GEM. (jax.org)
  • Transplantation between genetically identical individuals, i.e., members of the same species with identical histocompatibility antigens, such as monozygotic twins, members of the same inbred strain, or members of a hybrid population produced by crossing certain inbred strains. (lookformedical.com)
  • By employing a conditional knock-in approach using the human EGFR cDNA mice humanised for EGFR ( hEGFR KI/KI )were generated. (silverchair.com)
  • The use of induced and spontaneous mutant mice and genetically engineered mice (and combinations thereof) to study cancers and other aging phenotypes to advance improved functional human life spans will involve studies of aging mice. (jax.org)
  • Increased recognition of expected phenotypes, experimental variables that influence phenotypes and research outcomes, and experimental design options and rationales can maximize the utility of genetically engineered mice (GEM) models to translational research on aging. (jax.org)
  • Mice lacking the epidermal growth factor receptor (EGFR) develop epithelial defects and a neurodegenerative disease and die within the first month of birth. (silverchair.com)
  • However, these mice are growth retarded and show skin and hair defects similar to Egfr -/- mutants. (silverchair.com)
  • LPS administration to C3H/HeOuJ mice resulted in a rapid induction of TREM-1 and TREM-3, but a decrease in TREM-2 in liver macrophages and endothelial cells. (nih.gov)
  • Using neuron-glia and microglia-enriched cultures from mice deficient in the MAC1 receptor (MAC1-/-), we demonstrate that lipopolysaccharide (LPS) treatment results in lower TNFalpha response, attenuated loss of DA neurons, and absence of extracellular superoxide production in MAC1-/- cultures. (nih.gov)
  • However, microglia derived from Toll-like receptor 4 deficient mice and MAC1-/- mice failed to show a significant decrease in intracellular accumulation of labeled LPS, when compared with controls. (nih.gov)
  • It binds to a specific high affinity receptor ( RECEPTOR, MACROPHAGE COLONY-STIMULATING FACTOR ). (lookformedical.com)
  • Complement receptor 3 (CR3, CD11b/CD18) is a major macrophage phagocytic receptor. (bvsalud.org)
  • Mice deficient in TLR4 or TLR4 signaling are protected from intestinal and systemic immune responses upon oral challenge with ATIs. (nih.gov)
  • Tlr4 normal) mice were exposed continuously to 0.3 ppm O 3 or filtered air for 6, 24, 48, or 72 hr. (nih.gov)
  • Results: O 3 -induced TLR4 signaling occurred through myeloid differentiation protein 88 (MyD88)-dependent and -independent pathways in OuJ mice and involved multiple downstream pathways. (nih.gov)
  • These results suggest that TREM proteins are important in the inflammatory response of hepatic macrophages and endothelial cells to acute endotoxemia. (nih.gov)
  • Proteins released by sensitized LYMPHOCYTES and possibly other cells that inhibit the migration of MACROPHAGES away from the release site. (lookformedical.com)
  • BALB/C is a commonly used strain of inbred mice in medical research, known for their genetic uniformity and susceptibility to various diseases. (lookformedical.com)
  • Furthermore, because of the highly significant homologies in gene order and chromosomal structure that exist between mouse and man, identification of the chromosomal location of a susceptibility gene in the mouse provides the basis for potentially localizing a homologous human gene. (medscape.com)
  • Positional cloning strategy using inbred mice to identify candidate susceptibility genes that may be tested for association with disease in human populations. (medscape.com)
  • It is initiated by lymphokines , such as the macrophage activation factor (MAF) and the macrophage migration-inhibitory factor (MMIF), immune complexes, C3b, and various peptides, polysaccharides, and immunologic adjuvants. (lookformedical.com)
  • LPS-induced alterations in TREM expression were not evident in cells from C3H/HeJ TLR-4 mutant mice, indicating that the response is dependent on TLR-4. (nih.gov)
  • To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. (lookformedical.com)
  • The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. (lookformedical.com)
  • Hsp70+/+ wild-type control) mice were used for candidate gene validation studies. (nih.gov)
  • Regulation of TREM expression in hepatic macrophages and endothelial cells during acute endotoxemia. (nih.gov)
  • In these studies, we analyzed the expression of TREM in hepatic macrophages and endothelial cells which play a central role in LPS clearance. (nih.gov)
  • IL-1beta and TNFalpha upregulated TREM-1 and TREM-3 expression and suppressed TREM-2 expression in macrophages and endothelial cells. (nih.gov)
  • Treatment of macrophages and endothelial cells with LPS upregulated expression of nitric oxide synthase-2 (NOS-2). (nih.gov)
  • The compound stimulates the survival, proliferation, and differentiation of hematopoietic cells of the monocyte-macrophage series. (lookformedical.com)
  • Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. (lookformedical.com)
  • Interestingly, no significant differences were noted in TREM expression between wild-type and TNFR1-/- mice treated with LPS. (nih.gov)
  • However, linkage analyses are ideally suited for genetically well-controlled models, particularly inbred mice. (medscape.com)
  • A number of laboratories have used various exogenous and endogenous stimuli (e.g., hyperoxia, metals and endotoxin) to develop genetic models of ALI in mice. (medscape.com)