共查询到12条相似文献,搜索用时 0 毫秒
1.
Summary Selenium deficiency produces no effect on either the total content of or the binding properties of rat liver -tocopherol binding protein. 相似文献
2.
Lamarine M Mornon JP Berezovsky N Chomilier J 《Cellular and molecular life sciences : CMLS》2001,58(3):492-498
Using a set of 372 proteins representative of a variety of 56 distinct globular folds, a statistical correlation was observed
between two recently revealed features of protein structures: tightened end fragments or 'closed loops', i. e. sequence fragments
that are able in three-dimensional (3D) space to nearly close their ends (a current parameter of polymer physics), and 'topohydrophobic
positions', i. e. positions always occupied in 3D space by strong hydrophobic amino acids for all members of a fold family.
Indeed, in sequence space, the distribution of preferred lengths for tightened end fragments and that for topohydrophobic
separation match. In addition to this statistically significant similarity, the extremities of these 'closed loops' may be
preferentially occupied by topohydrophobic positions, as observed on a random sample of various folds. This observation may
be of special interest for sequence comparison of distantly related proteins. It is also important for the ab initio prediction
of protein folds, considering the remarkable topological properties of topohydrophobic positions and their paramount importance
within folding nuclei. Consequently, topohydrophobic positions locking the 'closed loops' belong to the deep cores of protein
domains and might have a key role in the folding process.
Received 1 February 2001; accepted 7 February 2001 相似文献
3.
Linda Reinhard Henning Tidow Michael J. Clausen Poul Nissen 《Cellular and molecular life sciences : CMLS》2013,70(2):205-222
The Na+,K+-ATPase, or sodium pump, is well known for its role in ion transport across the plasma membrane of animal cells. It carries out the transport of Na+ ions out of the cell and of K+ ions into the cell and thus maintains electrolyte and fluid balance. In addition to the fundamental ion-pumping function of the Na+,K+-ATPase, recent work has suggested additional roles for Na+,K+-ATPase in signal transduction and biomembrane structure. Several signaling pathways have been found to involve Na+,K+-ATPase, which serves as a docking station for a fast-growing number of protein interaction partners. In this review, we focus on Na+,K+-ATPase as a signal transducer, but also briefly discuss other Na+,K+-ATPase protein–protein interactions, providing a comprehensive overview of the diverse signaling functions ascribed to this well-known enzyme. 相似文献
4.
Yasmina Manso Javier Carrasco Gemma Comes Paul A. Adlard Ashley I. Bush Juan Hidalgo 《Cellular and molecular life sciences : CMLS》2012,69(21):3665-3681
Alzheimer’s disease (AD) is by far the most commonly diagnosed dementia, and despite multiple efforts, there are still no effective drugs available for its treatment. One strategy that deserves to be pursued is to alter the expression and/or physiological action of endogenous proteins instead of administering exogenous factors. In this study, we intend to characterize the roles of the antioxidant, anti-inflammatory, and heavy-metal binding proteins, metallothionein-1?+?2 (MT1?+?2), in a mouse model of Alzheimer’s disease, Tg2576 mice. Contrary to expectations, MT1?+?2-deficiency rescued partially the human amyloid precursor protein-induced changes in mortality and body weight in a gender-dependent manner. On the other hand, amyloid plaque burden was decreased in the cortex and hippocampus in both sexes, while the amyloid cascade, neuroinflammation, and behavior were affected in the absence of MT1?+?2 in a complex manner. These results highlight that the control of the endogenous production and/or action of MT1?+?2 could represent a powerful therapeutic target in AD. 相似文献
5.
Summary Synthesis of blow fly calliphorin and other blood proteins by larval fat body in organ culture is inhibited by -ecdysone. The findings suggest a novel function for the hormone. 相似文献
6.
In 1837, Dirichlet proved that there are infinitely many primes in any arithmetic progression in which the terms do not all share a common factor. We survey implicit and explicit uses of Dirichlet characters in presentations of Dirichlet’s proof in the nineteenth and early twentieth centuries, with an eye toward understanding some of the pragmatic pressures that shaped the evolution of modern mathematical method. 相似文献
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8.
Tyler S. Smith Benjamin Spitzbarth Jian Li Donald R. Dugger Gabi Stern-Schneider Elisabeth Sehn Susan N. Bolch J. Hugh McDowell Jeremiah Tipton Uwe Wolfrum W. Clay Smith 《Cellular and molecular life sciences : CMLS》2013,70(23):4603-4616
Arrestins are dynamic proteins that move between cell compartments triggered by stimulation of G-protein-coupled receptors. Even more dynamically in vertebrate photoreceptors, arrestin1 (Arr1) moves between the inner and outer segments according to the light conditions. Previous studies have shown that the light-driven translocation of Arr1 in rod photoreceptors is initiated by rhodopsin through a phospholipase C/protein kinase C (PKC) signaling cascade. The purpose of this study is to identify the PKC substrate that regulates the translocation of Arr1. Mass spectrometry was used to identify the primary phosphorylated proteins in extracts prepared from PKC-stimulated mouse eye cups, confirming the finding with in vitro phosphorylation assays. Our results show that Bardet–Biedl syndrome 5 (BBS5) is the principal protein phosphorylated either by phorbol ester stimulation or by light stimulation of PKC. Via immunoprecipitation of BBS5 in rod outer segments, Arr1 was pulled down; phosphorylation of BBS5 reduced this co-precipitation of Arr1. Immunofluorescence and immunoelectron microscopy showed that BBS5 principally localizes along the axonemes of rods and cones, but also in photoreceptor inner segments, and synaptic regions. Our principal findings in this study are threefold. First, we demonstrate that BBS5 is post-translationally regulated by phosphorylation via PKC, an event that is triggered by light in photoreceptor cells. Second, we find a direct interaction between BBS5 and Arr1, an interaction that is modulated by phosphorylation of BBS5. Finally, we show that BBS5 is distributed along the photoreceptor axoneme, co-localizing with Arr1 in the dark. These findings suggest a role for BBS5 in regulating light-dependent translocation of Arr1 and a model describing its role in Arr1 translocation is proposed. 相似文献
9.
Summary 10–7 M 20-OH-ecdysone treatment of a diploidDrosophila clone results in an inhibition of 60% of the DNA synthesis from 18 h of treatment on. After 48 h of hormone treatment the thymidine kinase activity is 70% inhibited; concomitantly a 60–70% lowering of the acid-soluble specific activity is observed. In the meantime the DNA polymerase activity is reduced. 相似文献
10.
Wanfu Xu Fangyin Zeng Songyu Li Guihuan Li Xiaoju Lai Qiming Jane Wang Fan Deng 《Cellular and molecular life sciences : CMLS》2018,75(24):4583-4598
Protein kinase C ε (PKCε) has emerged as an oncogenic protein kinase and plays important roles in cancer cell survival, proliferation, and invasion. It is, however, still unknown whether PKCε affects cell proliferation via glucose metabolism in cancer cells. Here we report a novel function of PKCε that provides growth advantages for cancer cells by enhancing tumor cells glycolysis. We found that either PKCε or Smad2/3 promoted aerobic glycolysis, expression of the glycolytic genes encoding HIF-1α, HKII, PFKP and MCT4, and tumor cell proliferation, while overexpression of PKCε or Smad3 enhanced aerobic glycolysis and cell proliferation in a protein kinase D- or TGF-β-independent manner in PC-3M and DU145 prostate cancer cells. The effects of PKCε silencing were reversed by ectopic expression of Smad3. PKCε or Smad3 ectopic expression-induced increase in cell growth was antagonized by inhibition of lactate transportation. Furthermore, interaction of endogenous PKCε with Smad2/3 was primarily responsible for phosphorylation of Ser213 in the Samd3 linker region, and resulted in Smad3 binding to the promoter of the glycolytic genes, thereby promoting cell proliferation. Forced expression of mutant Smad3 (S213A) attenuated PKCε-stimulated protein overexpression of the glycolytic genes. Thus, our results demonstrate a novel PKCε function that promotes cell growth in prostate cancer cells by increasing aerobic glycolysis through crosstalk between PKCε and Smad2/3. 相似文献
11.
Véronique Pons Nizar Serhan Stéphanie Gayral Camille Malaval Michel Nauze Nicole Malet Muriel Laffargue Céline Galés Laurent O. Martinez 《Cellular and molecular life sciences : CMLS》2014,71(9):1775-1788
The protective effect of high density lipoproteins (HDL) against atherosclerosis is mainly attributed to their capacity to transport excess cholesterol from peripheral tissues back to the liver for further elimination into the bile, a process called reverse cholesterol transport (RCT). Recently, the importance of the P2Y13 receptor (P2Y13-R) was highlighted in HDL metabolism since HDL uptake by the liver was decreased in P2Y13-R deficient mice, which translated into impaired RCT. Here, we investigated for the first time the molecular mechanisms regulating cell surface expression of P2Y13-R. When transiently expressed, P2Y13-R was mainly detected in the endoplasmic reticulum (ER) and strongly subjected to proteasome degradation while its homologous P2Y12 receptor (P2Y12-R) was efficiently targeted to the plasma membrane. We observed an inverse correlation between cell surface expression and ubiquitination level of P2Y13-R in the ER, suggesting a close link between ubiquitination of P2Y13-R and its efficient targeting to the plasma membrane. The C-terminus tail exchange between P2Y13-R and P2Y12-R strongly restored plasma membrane expression of P2Y13-R, suggesting the involvement of the intra-cytoplasmic tail of P2Y13-R in expression defect. Accordingly, proteasomal inhibition increased plasma membrane expression of functionally active P2Y13-R in hepatocytes, and consequently stimulated P2Y13-R-mediated HDL endocytosis. Importantly, proteasomal inhibition strongly potentiated HDL hepatic uptake (>200 %) in wild-type but not in P2Y13-R-deficient mice, thus reinforcing the role of P2Y13-R expression in regulating HDL metabolism. Therefore, specific inhibition of the ubiquitin–proteasome system might be a novel powerful HDL therapy to enhance P2Y13-R expression and consequently promote the overall RCT. 相似文献
12.
Steffen Ducheyne 《Archive for History of Exact Sciences》2011,65(2):181-227
This article seeks to provide a historically well-informed analysis of an important post-Newtonian area of research in experimental
physics between 1798 and 1898, namely the determination of the mean density of the earth and, by the end of the nineteenth
century, the gravitational constant. Traditionally, research on these matters is seen as a case of “puzzle solving.” In this
article, the author shows that such focus does not do justice to the evidential significance of eighteenth- and nineteenth-century
experimental research on the mean density of the earth and the gravitational constant. As Newton’s theory of universal gravitation
was mainly based on astronomical observation, it remained to be shown that Newton’s law of universal gravitation did not break
down at terrestrial distances. In this context, Cavendish’ experiment and related nineteenth-century experiments played a
decisive role, for they provided converging and increasingly stronger evidence for the universality of Newton’s theory of
gravitation. More precisely, the author shall argue that, as the accuracy and precision of the experimental apparatuses and
the procedures to eliminate external disturbances involved increasingly improved, the empirical support for the universality
of Newton’s theory of gravitation improved correspondingly. 相似文献