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Chromatin-binding in vivo of the erythroid kruppel-like factor,EKLF,in the murine globin loci 被引量:2
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作者 Yu-Chiau Shyu Shau-Ching Wen +6 位作者 Tung-Liang Lee Xin Chen Chia-Tse Hsu Hsin Chen Ruei-Lin Chen Jau-Lang Hwang Che-Kun James Shen 《Cell Research》 SCIE CAS CSCD 2006年第4期347-355,共9页
EKLF is an erythroid-specific, zinc finger-containing transcription factor essential for the activation of the mammalian beta globin gene in erythroid cells of definitive lineage. We have prepared a polyclonal anti-mo... EKLF is an erythroid-specific, zinc finger-containing transcription factor essential for the activation of the mammalian beta globin gene in erythroid cells of definitive lineage. We have prepared a polyclonal anti-mouse EKLF antibody suitable for Western blotting and immunoprecipitation (IP) qualities, and used it to define the expression patterns of the EKLF protein during mouse erythroid development. We have also used this antibody for the chromatin-immunoprecipitation (CHIP) assay. EKLF was found to bind in vivo at both the mouse beta-major-globin promoter and the HS2 site of beta-LCR in the mouse erythroleukemia cells (MEL) in a DMSO-inducible manner. The DMSO-induced bindings of EKLF as well as three other proteins, namely, RNA polymerase Ⅱ, acetylated histone H3, and methylated histone H3, were not abolished but significantly lowered in CB3, a MEL-derived cell line with null-expression of p45/NF-E2, an erythroid-enriched factor needed for activation of the mammalian globin loci. Interestingly, binding of EKLF in vivo was also detected in the mouse alpha-like globin locus, at the adult alpha globin promoter and its far upstream regulatory element alpha-MRE (HS26). This study provides direct evidence for EKLF-binding in vivo at the major regulatory elements of the mouse beta-like globin gene clusters the data also have interesting implications with respect to the role of EKLF-chromatin interaction in mammalian globin gene regulation. 展开更多
关键词 EKLF murine globin gene clusters chromatin-immunoprecipitation (CHIP) chromosome structure
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"APONEUROTIC SYSTEM" IN MEDICAL CLASSIC THE YELLOW EMPEROR'S CANON OF INTERN AL MEDICINE IS THE EARLIEST DESCRIPTION ON NERVOUS SYSTEM IN HUMAN HI STORY
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作者 王峥 马雯 宋永霞 《World Journal of Acupuncture-Moxibustion》 2005年第4期49-53,57,共6页
The description of “Jingjin” ( 经筋 aponeurotic system or muscles or tendinomuscular structures of the 12 regular meridians) in Chapter Jingjin of book Huangdi Neijing (《黄帝内经》 the Yellow Emperor' s Conon o... The description of “Jingjin” ( 经筋 aponeurotic system or muscles or tendinomuscular structures of the 12 regular meridians) in Chapter Jingjin of book Huangdi Neijing (《黄帝内经》 the Yellow Emperor' s Conon of Internal Medicine ) is the earliest record on nervous system. The Jingjin and channels are interdependent, and together they form the major parts of the channel-collateral system in the theory of traditional Chinese medicine (TCM). The integration of their own functions contributes to the “Qiji” (气机 functional activities) of the channel-collateral system. The Jingjin distributes in the human body regularly like channels, with starting and ending points (which goes up and down), main streams and branches, converging and connecting spots, and specific manifestations for a certain disease. Observation by modern anatomy shows that blood vessels, nerves, and lymphatic vessels accompany closely with each other to run in the human body and work together to maintain human's life activities. 展开更多
关键词 Aponeurotic system Channel-collateral system Nervous system
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Innate immune responses regulate morphogenesis and degeneration:roles of Toll-like receptors and Sarm1 in neurons 被引量:9
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作者 Hsin-Yu Liu Chiung-Ya Chen Yi-Ping Hsueh 《Neuroscience Bulletin》 SCIE CAS CSCD 2014年第4期645-654,共10页
The central nervous system is recognized as an immunoprivileged site because peripheral immune cells do not typically enter it. Microglial cells are thought to be the main immune cells in brain. However, recent report... The central nervous system is recognized as an immunoprivileged site because peripheral immune cells do not typically enter it. Microglial cells are thought to be the main immune cells in brain. However, recent reports have indicated that neurons express the key players of innate immunity, including Toll-like receptors (TLRs) and their adaptor proteins (Sarml, Myd88, and Trif), and may produce cytokines in response to pathogen infection. In the absence of an immune challenge, neuronal TLRs can detect intrinsic danger signals and modulate neuronal morphology and function. In this article, we review the recent findings on the involvement of TLRs and Sarml in controlling neuronal morphogenesis and neurodegeneration. Abnormal behaviors in TLR- and Sarml-deficient mice are also discussed. 展开更多
关键词 AXON cytokines DENDRITE innate immunity INTERLEUKIN-6 Sarml toll-like receptor
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