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771.
Apolipoprotein M (apoM) is a novel apolipoprotein found mainly in high-density lipoproteins (HDL). Its function is yet to
be defined. ApoM (25 kDa) has a typical lipocalin ?-barrel fold and a hydrophobic pocket. Retinoids bind apoM but with low
affinity and may not be the natural ligands. ApoM retains its signal peptide, which serves as a hydrophobic anchor to the
lipoproteins. This prevents apoM from being lost in the urine. Approximately 5% of HDL carries an apoM molecule. ApoM in plasma
(1 μM) correlates strongly with both low-density lipoprotein (LDL) and HDL cholesterol, suggesting a link to cholesterol metabolism.
However, in casecontrol studies, apoM levels in patients with coronary heart disease (CHD) and controls were similar, suggesting
apoM levels not to affect the risk for CHD in humans. Experiments in transgenic mice suggested apoM to have antiatherogenic
properties; possible mechanisms include increased formation of pre-? HDL, enhanced cholesterol mobilization from foam cells,
and increased antioxidant properties.
Received 28 November 2008; received after revision 15 December 2008; accepted 16 December 2008 相似文献
772.
Reticulons (RTNs) are membrane-spanning proteins sharing a typical domain named reticulon homology domain (RHD). RTN genes
have been identified in all eukaryotic organisms examined so far, and the corresponding proteins have been found predominantly
associated to the endoplasmic reticulum membranes. In animal and yeast, in which knowledge of the protein family is more advanced,
RTNs are involved in numerous cellular processes such as apoptosis, cell division and intracellular trafficking. Up to now,
a little attention has been paid to their plant counterparts, i.e., RTNLBs. In this review, we summarize the data available for RTNLB proteins and, using the data obtained with animal and
yeast models, several functions for RTNLBs in plant cells are proposed and discussed.
Received 01 July 2008; received after revision 08 September 2008; accepted 30 September 2008 相似文献
773.
G. M. C. Janssen P. Schwertman T. A. T. Wanga R. S. Jahangir Tafrechi P. J. A. van den Broek A. K. Raap 《Cellular and molecular life sciences : CMLS》2009,66(4):721-730
Cytoplasmic translation is under sophisticated control but how cells adapt its rate to constitutive loss of mitochondrial
oxidative phosphorylation is unknown. Here we show that translation is repressed in cells with the pathogenic A3243G mtDNA
mutation or in mtDNA-less ρ0 cells by at least two distinct pathways, one transiently targeting elongation factor eEF-2 and the other initiation factor
eIF-2α constitutively. Under conditions of exponential cell growth and mammalian target of rapamycin (mTOR) activation, eEF-2
becomes transiently phosphorylated by an AMP-activated protein kinase (AMPK)-dependent pathway, especially high in mutant
cells. Independent of AMPK and mTOR, eIF-2α is constitutively phosphorylated in mutant cells, likely a signature of endoplasmic
reticulum (ER)-stress response induced by the loss of oxidative phosphorylation. While the AMPK/eEF-2K/eEF-2 pathway appears
to function in adaptation to physiological fluctuations in ATP levels in the mutant cells, the ER stress signified by constitutive
protein synthesis inhibition through eIF-2α-mediated repression of translation initiation may have pathobiochemical consequences.
Received 29 October 2008; received after revision 11 December 2008; accepted 16 December 2008 相似文献
774.
V. Le Fourn K. Gaplovska-Kysela B. Guhl R. Santimaria C. Zuber J. Roth 《Cellular and molecular life sciences : CMLS》2009,66(8):1434-1445
Little is known about the fate of machinery proteins of the protein quality control and endoplasmic reticulum(ER)-associated
degradation (ERAD). We investigated the degradation of the ERAD component EDEM1, which directs overexpressed misfolded glycoproteins
to degradation. Endogenous EDEM1 was studied since EDEM1 overexpression not only resulted in inappropriate occurrence throughout
the ER but also caused cytotoxic effects. Proteasome inhibitors had no effect on the clearance of endogenous EDEM1 in non-starved
cells. However, EDEM1 could be detected by immunocytochemistry in autophagosomes and biochemically in LC3 immuno-purified
autophagosomes. Furthermore, influencing the lysosome-autophagy pathway by vinblastine or pepstatin A/E64d and inhibiting
autophagosome formation by 3-methyladenine or ATGs short interfering RNA knockdown stabilized EDEM1. Autophagic degradation
involved removal of cytosolic Triton X-100-insoluble deglycosylated EDEM1, but not of EDEM1-containing ER cisternae. Our studies
demonstrate that endogenous EDEM1 in cells not stressed by the expression of a transgenic misfolded protein reaches the cytosol
and is degraded by basal autophagy.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.
Received 15 January 2009; received after revision 16 February 2009; accepted 17 February 2009
V. Le Fourn, K. Gaplovska-Kysela: These authors equally contributed to this work. 相似文献
775.
R. P. Massengo-Tiassé J. E. Cronan 《Cellular and molecular life sciences : CMLS》2009,66(9):1507-1517
The enoyl-acyl carrier protein reductase (ENR) is the last enzyme in the fatty acid elongation cycle. Unlike most enzymes
in this essential pathway, ENR displays an unusual diversity among organisms. The growing interest in ENRs is mainly due to
the fact that a variety of both synthetic and natural antibacterial compounds are shown to specifically target their activity.
The primary anti-tuberculosis drug, isoniazid, and the broadly used antibacterial compound, triclosan, both target this enzyme.
In this review, we discuss the diversity of ENRs, and their inhibitors in the light of current research progress.
Received 3 November 2008; received after revision 5 December 2008; accepted 8 December 2008 相似文献
776.
Functions and pathologies of BiP and its interaction partners 总被引:1,自引:1,他引:0
J. Dudek J. Benedix S. Cappel M. Greiner C. Jalal L. Müller R. Zimmermann 《Cellular and molecular life sciences : CMLS》2009,66(9):1556-1569
The endoplasmic reticulum (ER) is involved in a variety of essential and interconnected processes in human cells, including
protein biogenesis, signal transduction, and calcium homeostasis. The central player in all these processes is the ER-lumenal
polypeptide chain binding protein BiP that acts as a molecular chaperone. BiP belongs to the heat shock protein 70 (Hsp70)
family and crucially depends on a number of interaction partners, including co-chaperones, nucleotide exchange factors, and
signaling molecules. In the course of the last five years, several diseases have been linked to BiP and its interaction partners,
such as a group of infectious diseases that are caused by Shigella toxin producing E. coli. Furthermore, the inherited diseases Marinesco-Sj?gren syndrome, autosomal dominant polycystic liver disease, Wolcott-Rallison
syndrome, and several cancer types can be considered BiP-related diseases. This review summarizes the physiological and pathophysiological
characteristics of BiP and its interaction partners.
Received 20 November 2008; received after revision 09 December 2008; accepted 12 December 2008 相似文献
777.
The elucidation of assembly pathways of multi-subunit membrane proteins is of growing interest in structural biology. In this
study, we provide an analysis of the assembly of the asymmetrically oriented PsaC subunit on the pseudo C2-symmetric Photosystem I core. Based on a comparison of the differences in the NMR solution structure of unbound PsaC with
that of the X-ray crystal structure of bound PsaC, and on a detailed analysis of the PsaC binding site surrounding the FX iron-sulfur cluster, two models can be envisioned for what are likely the last steps in the assembly of Photosystem I. Here,
we dissect both models and attempt to address heretofore unrecognized issues by proposing a mechanism that includes a thermodynamic
perspective. Experimental strategies to verify the models are proposed. In closing, the evolutionary aspects of the assembly
process will be considered, with special reference to the structural arrangement of the PsaC binding surface.
Received 22 October 2008; received after revision 17 November 2008; accepted 05 December 2008 相似文献
778.
卫星低频电磁辐射在轨探测研究 总被引:2,自引:0,他引:2
利用地球空间探测双星计划探测一号卫星上的磁场波动分析仪的原始数据, 分析了探测一号卫星在轨电磁辐射的特性. 结果显示卫星的电磁辐射主要集中在30 Hz以下. 在30 Hz以上, 卫星的电磁辐射最多延伸到 190 Hz左右, 而且强度明显减弱. 在 190 Hz以下的卫星电磁辐射具有与卫星姿态相关的长周期变化. 在 190~830 Hz的范围的电磁辐射有不明显的长周期变化特征. 830~3990 Hz范围的电磁辐射没有长周期变化特征. 卫星电磁辐射的长周期变化是由卫星姿态变化造成的. 卫星姿态变化引起卫星太阳方位角变化. 卫星太阳方位角越大, 卫星电磁辐射越大. 卫星太阳方位角从90.6增加到93.6, 低于10 Hz以下的电磁辐射约增大为原来的9倍, 10~190 Hz范围的电磁辐射大约增加到原来的1.6倍. 卫星在<10和10~190 Hz范围内的电磁辐射强度与卫星太阳方位角的相关系数分别达到0.90和0.91. 卫星在光照情况下的电磁辐射要比卫星在阴影情况下大. 卫星太阳能帆板电流产生的电磁辐射是卫星电磁辐射主要来源, 约占整个卫星电磁辐射的87%(低频段<150 Hz)和94%(高频段>150 Hz). 这些中国首次对卫星电磁辐射的在轨探测结果对于我国未来相关科学和应用卫星的设计方案的优化具有重要的参考价值. 相似文献
779.
借鉴经典动力学中约束力的思想,提出了一种编队卫星构形精确保持的非线性控制方法.该方法首先将非线性和摄动条件下编队卫星构形保持问题转换为带有完整约束的拉格朗日动力学系统,然后将问题转换为一组微分代数方程,通过求解微分代数方程,确定编队卫星构形保持的非线性控制律.由于借鉴了约束力的思想,该方法自然地利用了编队卫星动力学系统的力学特性,具有节省能量和高精度的特点.通过对线性和非线性条件下空间圆编队卫星构形保持问题的仿真,验证了提出的非线性控制方法的这些特性. 相似文献
780.
Wolfs JL Comfurius P Bekers O Zwaal RF Balasubramanian K Schroit AJ Lindhout T Bevers EM 《Cellular and molecular life sciences : CMLS》2009,66(2):314-323
The exposure of phosphatidylserine (PS) at the cell surface plays a critical role in blood coagulation and serves as a macrophage
recognition moiety for the engulfment of apoptotic cells. Previous observations have shown that a high extracellular [K+] and selective K+ channel blockers inhibit PS exposure in platelets and erythrocytes. Here we show that the rate of PS exposure in erythrocytes
decreases by ~50% when the intracellular [K+] increases from 0 to physiological concentrations. Using resealed erythrocyte membranes, we further show that lipid scrambling
is inducible by raising the intracellular [Ca2+] and that K+ ions have a direct inhibitory effect on this process. Lipid scrambling in resealed ghosts occurs in the absence of cell shrinkage
and microvesicle formation, processes that are generally attributed to Ca2+-induced lipid scrambling in intact erythrocytes. Thus, opening of Ca2+-sensitive K+ channels causes loss of intracellular K+ that results in reduced intrinsic inhibitory effect of these ions on scramblase activity.
Received 11 September 2008; received after revision 17 October 2008; accepted 27 October 2008 相似文献