Adiponectin Enhances Antibacterial Activity of Hematopoietic Cells by Suppressing Bone Marrow Inflammation.
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A. Yoshimura | T. Kadowaki | N. Kubota | I. Takamoto | Y. Iwakura | M. Kurokawa | S. Arai | Tomohiko Sato | A. Yoshimi | Y. Masamoto | Iseki Takamoto | Yosuke Masamoto
[1] S. Wirtz,et al. Microbiota from Obese Mice Regulate Hematopoietic Stem Cell Differentiation by Altering the Bone Niche. , 2015, Cell metabolism.
[2] Danielle E. Green,et al. High Fat Diet Rapidly Suppresses B Lymphopoiesis by Disrupting the Supportive Capacity of the Bone Marrow Niche , 2014, PloS one.
[3] Markus G. Manz,et al. Emergency granulopoiesis , 2014, Nature Reviews Immunology.
[4] K. Matsuda,et al. A small-molecule AdipoR agonist for type 2 diabetes and short life in obesity , 2013, Nature.
[5] J. Lord,et al. Adiponectin Inhibits Neutrophil Phagocytosis of Escherichia coli by Inhibition of PKB and ERK 1/2 MAPK Signalling and Mac-1 Activation , 2013, PloS one.
[6] Chao-ke Tang,et al. Enhanced adiponectin actions by overexpression of adiponectin receptor 1 in macrophages. , 2013, Atherosclerosis.
[7] J. Syrjänen,et al. Obesity and the risk and outcome of infection , 2013, International Journal of Obesity.
[8] M. Heikenwalder,et al. Cutting Edge: LPS-Induced Emergency Myelopoiesis Depends on TLR4-Expressing Nonhematopoietic Cells , 2012, The Journal of Immunology.
[9] P. Fraker,et al. Enhancement of hematopoiesis and lymphopoiesis in diet-induced obese mice , 2012 .
[10] K. Ley,et al. NR4A1 (Nur77) Deletion Polarizes Macrophages Toward an Inflammatory Phenotype and Increases Atherosclerosis , 2012, Circulation research.
[11] Carolyn M. Gray,et al. A critical role for SOCS3 in innate resistance to Toxoplasma gondii. , 2011, Cell host & microbe.
[12] F. Geissmann,et al. The transcription factor NR4A1 (Nur77) controls bone marrow differentiation and the survival of Ly6C− monocytes , 2011, Nature Immunology.
[13] R. DePinho,et al. IL-7 Engages Multiple Mechanisms to Overcome Chronic Viral Infection and Limit Organ Pathology , 2011, Cell.
[14] A. D. Panopoulos,et al. STAT3 controls myeloid progenitor growth during emergency granulopoiesis. , 2010, Blood.
[15] S. Price,et al. Adiponectin is produced by lymphocytes and is a negative regulator of granulopoiesis , 2010, Journal of leukocyte biology.
[16] N. Van Rooijen,et al. Liposomes for specific depletion of macrophages from organs and tissues. , 2010, Methods in molecular biology.
[17] K. Walsh,et al. Adiponectin Promotes Macrophage Polarization toward an Anti-inflammatory Phenotype* , 2009, The Journal of Biological Chemistry.
[18] A. Matsuda,et al. Preoperative plasma adiponectin level is a risk factor for postoperative infection following colorectal cancer surgery. , 2009, The Journal of surgical research.
[19] G. Daley,et al. Bone marrow adipocytes as negative regulators of the hematopoietic microenvironment , 2009, Nature.
[20] B. Weimer,et al. Cytosporone B is an agonist for nuclear orphan receptor Nur77. , 2008, Nature chemical biology.
[21] P. Libby,et al. The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions , 2007, The Journal of experimental medicine.
[22] C. Voermans,et al. Identification of Adiponectin as a Novel Hemopoietic Stem Cell Growth Factor1 , 2007, The Journal of Immunology.
[23] P. Blackshear,et al. Regulation of Suppressor of Cytokine Signaling 3 (SOCS3) mRNA Stability by TNF-α Involves Activation of the MKK6/p38MAPK/MK2 Cascade1 , 2007, The Journal of Immunology.
[24] Bianca Sperl,et al. Stattic: a small-molecule inhibitor of STAT3 activation and dimerization. , 2006, Chemistry & biology.
[25] M. Falagas,et al. Obesity and infection. , 2006, The Lancet. Infectious diseases.
[26] K. Akashi,et al. C/EBPbeta is required for 'emergency' granulopoiesis. , 2006, Nature immunology.
[27] Yoshinao Abe,et al. Impairment of host resistance to Listeria monocytogenes infection in liver of db/db and ob/ob mice. , 2005, Diabetes.
[28] C. Kahn,et al. Suppressor of Cytokine Signaling 1 (SOCS-1) and SOCS-3 Cause Insulin Resistance through Inhibition of Tyrosine Phosphorylation of Insulin Receptor Substrate Proteins by Discrete Mechanisms , 2004, Molecular and Cellular Biology.
[29] W. Alexander,et al. SOCS3 is a critical physiological negative regulator of G-CSF signaling and emergency granulopoiesis. , 2004, Immunity.
[30] W. Reith,et al. Conditional gene targeting in macrophages and granulocytes using LysMcre mice , 1999, Transgenic Research.
[31] M. Desai,et al. Obesity is associated with macrophage accumulation in adipose tissue. , 2003, The Journal of clinical investigation.
[32] S. Akira,et al. IL-6 induces an anti-inflammatory response in the absence of SOCS3 in macrophages , 2003, Nature Immunology.
[33] D. Charnock-Jones,et al. vavCre Transgenic mice: A tool for mutagenesis in hematopoietic and endothelial lineages , 2002, Genesis.
[34] Philippe Froguel,et al. Disruption of Adiponectin Causes Insulin Resistance and Neointimal Formation* , 2002, The Journal of Biological Chemistry.
[35] R. DePinho,et al. STAT3 is a negative regulator of granulopoiesis but is not required for G-CSF-dependent differentiation. , 2002, Immunity.
[36] M. Matsuda,et al. Diet-induced insulin resistance in mice lacking adiponectin/ACRP30 , 2002, Nature Medicine.
[37] Y. Terauchi,et al. The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity , 2001, Nature Medicine.
[38] S. Kihara,et al. Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages. , 2000, Blood.
[39] Dieter Häussinger,et al. LPS and TNFα induce SOCS3 mRNA and inhibit IL‐6‐induced activation of STAT3 in macrophages , 1999, FEBS letters.
[40] C. Cheers,et al. Essential Roles for Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) and G-CSF in the Sustained Hematopoietic Response ofListeria monocytogenes–Infected Mice , 1998 .
[41] C. Cheers,et al. Essential roles for granulocyte-macrophage colony-stimulating factor (GM-CSF) and G-CSF in the sustained hematopoietic response of Listeria monocytogenes-infected mice. , 1998, Blood.
[42] E. Momotani,et al. Failure of germinal center formation and impairment of response to endotoxin in tumor necrosis factor alpha-deficient mice. , 1997, Laboratory investigation; a journal of technical methods and pathology.
[43] A. Nakane,et al. Endogenous tumor necrosis factor (cachectin) is essential to host resistance against Listeria monocytogenes infection , 1988, Infection and immunity.