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71.
Chemokine Receptor Utilization by Human Immunodeficiency Virus Type 1 Isolates That Replicate in Microglia 总被引:2,自引:2,他引:0 下载免费PDF全文
Joseph T. C. Shieh Andrew V. Albright Matthew Sharron Suzanne Gartner Julie Strizki Robert W. Doms Francisco Gonzlez-Scarano 《Journal of virology》1998,72(5):4243-4249
The role of human immunodeficiency virus (HIV) strain variability remains a key unanswered question in HIV dementia, a condition affecting around 20% of infected individuals. Several groups have shown that viruses within the central nervous system (CNS) of infected patients constitute an independently evolving subset of HIV strains. A potential explanation for the replication and sequestration of viruses within the CNS is the preferential use of certain chemokine receptors present in microglia. To determine the role of specific chemokine coreceptors in infection of adult microglial cells, we obtained a small panel of HIV type 1 brain isolates, as well as other HIV strains that replicate well in cultured microglial cells. These viruses and molecular clones of their envelopes were used in infections, in cell-to-cell fusion assays, and in the construction of pseudotypes. The results demonstrate the predominant use of CCR5, at least among the major coreceptors, with minor use of CCR3 and CXCR4 by some of the isolates or their envelope clones. 相似文献
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Further studies on the oxidation of betaine by a marine bacterium, Achromobacter cholinophagum 总被引:2,自引:0,他引:2
H S Shieh 《Canadian journal of microbiology》1966,12(2):299-302
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Summary Addition of mercuric chloride at concentrations which resulted in an overall binding level of about 8 mmoles Hg/l packed cells and above caused a breakdown in the permeability of the cell membrane as indicated by a net efflux of internal K+. Below this level in region of 2 mmoles Hg/l packed cells the rate of K+ transfer across the cell surface was stimulated without affecting the internal K+ level. Maintainence of the stimulation was dependent both on time and dose. Enhancement of the rate of K+ turnover was associated with a fast component of the inorganic mercury uptake which could be removed by washing with cysteine. The mercury stimulated K+/K+ exchange was inhibited by low temperature, by the uncoupler CCCP and the energy transfer inhibitor DCCD. Overall binding concentrations of inorganic mercury below 0.5 mmoles/l packed cells had no effect on the K+ transport system. In contrast to mercuric chloride, methyl mercuric chloride over similar concentration ranges did not seem to induce a breakdown in the permeability barrier or directly interact with the K+/K+ exchange but more likely influenced the latter by inhibiting intracellular processes. 相似文献
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Jue‐Long Wang Chiang‐Ting Chou Kang Liu Wei‐Zhe Liang Jin‐Shiung Cheng Hong‐Tai Chang I‐Shu Chen Ti Lu Chun‐Chi Kuo Chia‐Cheng Yu Pochuen Shieh Daih‐Huang Kuo Fu‐An Chen Chung‐Ren Jan 《Journal of biochemical and molecular toxicology》2016,30(11):539-547
The effect of protriptyline on Ca2+ physiology in human hepatoma is unclear. This study explored the effect of protriptyline on [Ca2+]i and cytotoxicity in HepG2 human hepatoma cells. Protriptyline (50–150 μM) evoked [Ca2+]i rises. The Ca2+ entry was inhibited by removal of Ca2+. Protriptyline‐induced Ca2+ entry was confirmed by Mn2+‐induced quench of fura‐2 fluorescence. Except nifedipine, econazole, SKF96365, GF109203X, and phorbol 12‐myristate 13 acetate did not inhibit Ca2+ entry. Treatment with the endoplasmic reticulum Ca2+ pump inhibitor 2,5‐di‐tert‐butylhydroquinone (BHQ) inhibited 40% of protriptyline‐induced response. Treatment with protriptyline abolished BHQ‐induced response. Inhibition of phospholipase C (PLC) suppressed protriptyline‐evoked response by 70%. At 20–40 μM, protriptyline killed cells which was not reversed by the Ca2+ chelator 1,2‐bis(2‐aminophenoxy)ethane‐N,N,N′,N′‐tetraacetic acid‐acetoxymethyl ester (BAPTA/AM). Together, in HepG2 cells, protriptyline induced [Ca2+]i rises that involved Ca2+ entry through nifedipine‐sensitive Ca2+ channels and PLC‐dependent Ca2+ release from endoplasmic reticulum. Protriptyline induced Ca2+‐independent cell death. 相似文献
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Brugada syndrome is a life-threatening, inherited arrhythmia disorder associated with autosomal dominant mutations in SCN5A, the gene encoding the human cardiac Na+ channel α subunit (Nav1.5). Here, we characterized the biophysical properties of a novel Brugada syndrome-associated Nav1.5 mutation, A551T, identified in a proband who was successfully resuscitated from an episode of ventricular fibrillation with sudden collapse. Whole-cell currents through wild-type (WT) Nav1.5 and mutant (A551T) channels were recorded and compared in the human embryonic kidney cell line HEK293T transfected with SCN5A cDNA and SCN1B cDNA, using the patch-clamp technique. Current density was decreased in the A551T mutant compared to the WT. In addition, the A551T mutation reduced Nav1.5 activity by promoting entry of the channel into fast inactivation from the closed state, thereby shifting the steady-state inactivation curve by -5 mV. Furthermore, when evaluated at -90 mV, the resting membrane potential, but not at the conventionally used -120 mV, both the percentage, and rate, of channel recovery from inactivation were reduced in the mutant. These results suggest that the DI-DII linker may be involved in the stability of inactivation gating process. This study supports the notion that a reduction in Nav1.5 channel function is involved in the pathogenesis of Brugada syndrome. The structural-functional study of the Nav1.5 channel advances our understanding of its pathophysiolgocial function. 相似文献