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31.
Although the amino acid glutamate is used as an intercellular signaling molecule for normal bone homeostasis, little is known regarding its possible role in the metabolic disruption characteristic of bone metastasis. We have previously shown in vitro that cancer cell lines relevant to bone metastasis release glutamate into the extracellular environment. This study demonstrates the expression of multiple glutamate transporters in cancer cell lines of non-central nervous system origin. Furthermore, we identify the molecular mechanism responsible for glutamate export and show that this system can be inhibited pharmacologically. By highlighting that glutamate secretion is a common biological feature of cancer cells, this study suggests that tumor-derived glutamate could interfere with glutamate-dependent intercellular signaling in normal bone. Pharmacological interference with cancer cell glutamate release may be a viable option for limiting host bone response to invading tumor cells in bone metastasis. 相似文献
32.
Makio Kitada Shinya Morotomi Koki Horikoshi Toshiaki Kudo 《Extremophiles : life under extreme conditions》1997,1(3):135-141
A K+/H+ antiport system was detected for the first time in right-side-out membrane vesicles prepared from alkaliphilic Bacillus sp. no. 66 (JCM 9763). An outwardly directed K+ gradient (intravesicular K+ concentration, Kin, 100 mM; extravesicular K+ concentration, Kout, 0.25 mM) stimulated uphill H+ influx into right-side-out vesicles and created the inside-acidic pH gradient (ΔpH). This H+ influx was pH-dependent and increased as the pH increased from 6.8 to 8.4. Addition of 100 μM quinine inhibited the H+ influx by 75%. This exchange process was electroneutral, and the H+ influx was not stimulated by the imposition of the membrane potential (interior negative). Addition of K+ at the point of maximum ΔpH caused a rapid K+-dependent H+ eflux consistent with the inward exchange of external K+ for internal H+ by a K+/H+ antiporter. Rb+ and Cs+ could replace K+ but Na+ and Li+ could not. The H+ efflux rate was a hyperbolic function of K+ and increased with increasing extravesicular pH (pHout) from 7.5 to 8.5. These findings were consistent with the presence of K+/H+ antiport activity in these membrane vesicles.
Received: March 20, 1997 / Accepted: May 22, 1997 相似文献
33.
Fine‐tuned regulation of the K+/H+ antiporter KEA3 is required to optimize photosynthesis during induction 下载免费PDF全文
Caijuan Wang Hiroshi Yamamoto Fumika Narumiya Yuri Nakajima Munekage Giovanni Finazzi Ildiko Szabo Toshiharu Shikanai 《The Plant journal : for cell and molecular biology》2017,89(3):540-553
KEA3 is a thylakoid membrane localized K+/H+ antiporter that regulates photosynthesis by modulating two components of proton motive force (pmf), the proton gradient (?pH) and the electric potential (?ψ). We identified a mutant allele of KEA3, disturbed proton gradient regulation (dpgr) based on its reduced non‐photochemical quenching (NPQ) in artificial (CO2‐free with low O2) air. This phenotype was enhanced in the mutant backgrounds of PSI cyclic electron transport (pgr5 and crr2‐1). In ambient air, reduced NPQ was observed during induction of photosynthesis in dpgr, the phenotype that was enhanced after overnight dark adaptation. In contrast, the knockout allele of kea3‐1 exhibited a high‐NPQ phenotype during steady state in ambient air. Consistent with this kea3‐1 phenotype in ambient air, the membrane topology of KEA3 indicated a proton efflux from the thylakoid lumen to the stroma. The dpgr heterozygotes showed a semidominant and dominant phenotype in artificial and ambient air, respectively. In dpgr, the protein level of KEA3 was unaffected but the downregulation of its activity was probably disturbed. Our findings suggest that fine regulation of KEA3 activity is necessary for optimizing photosynthesis. 相似文献
34.
Chunxia Wu Xiuhua Gao Xiangqiang Kong Yanxiu Zhao Hui Zhang 《Plant Molecular Biology Reporter》2009,27(1):1-12
Na+/H+ exchanger catalyzes the countertransport of Na+ and H+ across membranes. Using the rapid amplification of cDNA ends method, a Na+/H+ antiporter gene (ThNHX1) was isolated from a halophytic plant, salt cress (Thellungiella halophila). The deduced amino acid sequence contained 545 amino acid residues with a conserved amiloride-binding domain (87LFFIYLLPPI96) and shared more than 94% identity with that of AtNHX1 from Arabidopsis thaliana. The ThNHX1 mRNA level was upregulated by salt and other stresses (abscisic acid, polyethylene glycol, and high temperature). This gene
partially complemented the Na+/Li+-sensitive phenotype of a yeast mutant that was deficient in the endosomal–vacuolar Na+/H+ antiporter ScNHX1. Overexpression of ThNHX1 in Arabidopsis increased salt tolerance of transgenic plants compared with the wild-type plants. In addition, the silencing of ThNHX1 gene in T. halophila caused the transgenic plants to be more salt and osmotic sensitive than wild-type plant. Together, these results suggest
that ThNHX1 may function as a tonoplast Na+/H+ antiporter and play an important role in salt tolerance of T. halophila.
Chunxia Wu, Xiuhua Gao, and Xiangqiang Kong contributed equally to this work. 相似文献
35.
Oxidative glutamate toxicity in the neuronal cell line HT22 is a model for cell death by oxidative stress. In this paradigm, an excess of extracellular glutamate blocks the glutamate/cystine-antiporter system Xc-, depleting the cell of cysteine, a building block of the antioxidant glutathione. Loss of glutathione leads to the accumulation of reactive oxygen species and eventually cell death. We selected cells resistant to oxidative stress, which exhibit reduced glutamate-induced glutathione depletion mediated by an increase in the antiporter subunit xCT and system Xc- activity. Cystine uptake was less sensitive to inhibition by glutamate and we hypothesized that glutamate import via excitatory amino acid transporters and immediate re-export via system Xc- underlies this phenomenon. Inhibition of glutamate transporters by l-trans-pyrrolidine-2,4-dicarboxylic acid (PDC) and DL-threo-beta-benzyloxyaspartic acid (TBOA) exacerbated glutamate-induced cell death. PDC decreased intracellular glutamate accumulation and exacerbated glutathione depletion in the presence of glutamate. Transient overexpression of xCT and the glutamate transporter EAAT3 cooperatively protected against glutamate. We conclude that EAATs support system Xc- to prevent glutathione depletion caused by high extracellular glutamate. This knowledge could be of use for the development of novel therapeutics aimed at diseases associated with depletion of glutathione like Parkinson's disease. 相似文献
36.
37.
Yusuf Muhammad Noor Nurul Hidayah Samsulrizal Noor Azah Jema'on Kheng Oon Low Aizi Nor Mazila Ramli Noor Izawati Alias Siti Intan Rosdianah Damis Siti Fatimah Zaharah Mohd Fuzi Mohd Noor Mat Isa Abdul Munir Abdul Murad Mohd Firdaus Mohd Raih Farah Diba Abu Bakar Nazalan Najimudin Nor Muhammad Mahadi Rosli Md. Illias 《Gene》2014
Bacillus lehensis G1 is a Gram-positive, moderately alkalitolerant bacterium isolated from soil samples. B. lehensis produces cyclodextrin glucanotransferase (CGTase), an enzyme that has enabled the extensive use of cyclodextrin in foodstuffs, chemicals, and pharmaceuticals. The genome sequence of B. lehensis G1 consists of a single circular 3.99 Mb chromosome containing 4017 protein-coding sequences (CDSs), of which 2818 (70.15%) have assigned biological roles, 936 (23.30%) have conserved domains with unknown functions, and 263 (6.55%) have no match with any protein database. Bacillus clausii KSM-K16 was established as the closest relative to B. lehensis G1 based on gene content similarity and 16S rRNA phylogenetic analysis. A total of 2820 proteins from B. lehensis G1 were found to have orthologues in B. clausii, including sodium–proton antiporters, transport proteins, and proteins involved in ATP synthesis. A comparative analysis of these proteins and those in B. clausii and other alkaliphilic Bacillus species was carried out to investigate their contributions towards the alkalitolerance of the microorganism. The similarities and differences in alkalitolerance-related genes among alkalitolerant/alkaliphilic Bacillus species highlight the complex mechanism of pH homeostasis. The B. lehensis G1 genome was also mined for proteins and enzymes with potential viability for industrial and commercial purposes. 相似文献
38.
F.I. Wolf V. Covacci N. Bruzzese A. Di Francesco A. Sacchetti D. Corda A. Cittadini 《Journal of cellular biochemistry》1998,71(3):441-448
Magnesium homeostasis in HL-60 promyelocytic leukemia cells was compared to that in neutrophyl-like HL-60 cells obtained by 1.3% DMSO treatment. Magnesium homeostasis was studied by the characterization of magnesium efflux, the identification of intracellular magnesium pools, and the regulation of intracellular ionized Mg2+. In both undifferentiated and neutrophyl-like HL-60 cells, magnesium efflux occurred via the Na-Mg antiporter which was inhibited by imipramine and stimulated by db cAMP and forskolin. Receptor-mediated signals such as ATP, IFN-α, or PGE1, which can trigger cAMP-dependent magnesium efflux, were ineffective in undifferentiated HL-60 cells but induced 60–70% increase of magnesium efflux in neutrophyl-like HL-60 cells. Selective membrane permeabilization by the cation ionophore A23187 induced a large magnesium release when cells were treated with rotenone. In both cell populations, the addition of glucose to rotenone-treated cells restored magnesium release to the control level. Permeabilization by 0.005% digitonin provoked the release of 90% cell total magnesium in both cell types. Intracellular [Mg2+]i was 0.15 and 0.26 mM in undifferentiated and neutrophyl-like HL-60 cells, respectively. Stimuli that triggered magnesium efflux, such as db cAMP in undifferentiated and IFN-α in neutrophyl-like HL-60 cells, induced a slow but consistent increase of [Mg2+]i which was independent from Ca2+movements. Overall, these data indicate that magnesium homeostasis is regulated by receptor-mediated magnesium efflux which was modified during differentiation of HL-60 cells. Stimulation of magnesium efflux is paralleled by an increase of [Mg2+]i which reflects a release of magnesium from the bound cation pool. J. Cell. Biochem. 71:441–448, 1998. © 1998 Wiley-Liss, Inc. 相似文献
39.
Like other alkaliphiles, the cyanobacterium Spirulina platensis (Norst.) Geitler requires sodium to function properly at elevated pH values. At pH 10.0, 150–250 mM Na+ were required for optimal growth, whereas 2.5 mM were sufficient for short-term photosynthetic oxygen evolution. The complete absence of sodium, however, caused S. platensis to deteriorate. O2 evolution stopped, the absorbance at 620 nm corresponding to phycocyanin decreased, and the cells lysed within 1 h, a process accelerated by light. The activity of photosystem II, but not that of photosystem I, was affected in the process, which was irreversible unless sodium was readded within 15 minfrom the onset of the deprivation. The effect was mimicked, even in the presence of sodium, by the ionophore nigericin. We suggest that the cascade of events leading to cell lysis is primarily due to the inability of S. platensis to maintain a proton gradient (acid inside), possibly due to inactivity of a sodium/proton antiporter, as demonstrated for other alkaliphiles. 相似文献
40.
Sodium-transloating ATPase in the fermentative bacteriumStreptococcus faecalis exchanges sodium for potassium ions. Sodium ions stimulate its activity, but K+ ions have no significant effect at present. Although the molecular nature of the sodium ATPase is not clear, the enzyme is distinct from other ion-motive ATPases (E1E2 type and F1F0 type) as judged by its resistance to vanadate as well as dicyclohexylcarbodiimde. The sodium ATPase is induced when cells are grown on media rich in sodium, particularly under conditions that limit the generation of a proton potential or block the constitutive sodium/proton antiporter, indicating that an increase in the cytoplasmic sodium level serves as the signal. The enzyme is not induced in response to K+ deprivation. The sodium ATPase may have evolved to cope with a sodium-rich environment under conditions that limit the magnitude of the proton potential. 相似文献