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1.
Summary Adenylate kinase activity of intact mitochondria is strongly inhibited by Ap5A, i.e.p
1,p
5-Di (adenosine-5-) pentaphosphate, whereas oxidative phosphorylation is not affected. Therefore, Ap5A is a useful tool to distinguish between oxidative and non oxidative ATP generating reactions.Acknowledgment. The generous support of Prof. Dr.Walther Lamprecht is gratefully acknowledged. J. L. thanks the Stipendienfonds des Verbandes der Chemische Industrie for a scholarship. 相似文献
2.
Summary Two possible mechanisms for oxidative phosphorylation are suggested, based on participation of quinones in the process.Both of them postulate the 1–4 addition of inorganic phosphate on a reactive quinone isomer (the quinone-methide II) without exchange of the quinone oxygen atoms. They also account for the P1-18OH2 exchange observed during oxidative phosphorylation.
Communication présentée au Symposium International de Chimie organique des Produits Naturels, Bruxelles (12–15 juin 1962). Résumé dans: Industrie Chimique Belge27, 558 (1962). 相似文献
Communication présentée au Symposium International de Chimie organique des Produits Naturels, Bruxelles (12–15 juin 1962). Résumé dans: Industrie Chimique Belge27, 558 (1962). 相似文献
3.
M. Renucci A. Tirard L. Sreng J. Khlat J. L. Clément 《Cellular and molecular life sciences : CMLS》1996,52(8):762-768
In insect antennal extracts, Schleicher et al.1 showed that protein kinase C (PKC) inhibitors abolish the transience of pheromone-induced rapid inositol trisphosphate responses, which suggests that pheromonal signals act on phosphorylation of specific proteins. To confirm this hypothesis, we studied the effects of second messengers and a pheromonal blend on phosphorylation of antennal proteins in the cockroachPeriplaneta americana. Proteins from adult male antennae were phosphorylated in vitro in the presence of [32P] triphosphate, then separated by SDS-polyacrylamide gel electrophoresis. Numerous phosphopolypeptides were visualized. The presence of Ca++/calmodulin in the incubation medium resulted in increased phosphorylation of polypeptides with molecular weights of 38, 48, 51, 54 and 58 kDa. Stimulation of PKC by addition of Ca++ phosphatidylserine (PS)/phorbol myristate acetate (PMA) resulted in the appearance of three phosphopolypeptides of 36, 70 and 120 kDa. In the presence of cyclic adenosine monophosphate, two new major polypeptides of 46 and 42 kDa appeared; the latter polypeptide also appeared in the presence of cyclic guanosine monophosphate. Comparison with polypeptide composition of tissue from the cerci, leg, brain and fat body showed that the 36 and 48 kDa polypeptides were specific to antennae, whereas the 120 kDa polypeptide was also present in the adult brain. When antennae are subjected to pheromonal stimulation for 16 seconds prior to homogenization, in vitro phosphorylation of the 120, 70, 64 and 38 kDa polypeptides was inhibited, whereas phosphorylation of the 58, 54, 51 and 48 kDa polypeptides was strongly stimulated. It is noteworthy that a 107 kDa polypeptide was observed only after pheromonal stimulation by Ca++/PS/PMA. Our findings suggest that Ca++-and PKC-dependent protein phosphorylation systems play an important role in the transduction of pheromonal signals in antennae of male cockroachP. americana. We speculate that specific phosphoproteins may modulate sensitivity and signal amplification during the olfactory transduction process. 相似文献
4.
Gineitis A Treigyte G Savickiene J Shanbhag VP Stigbrand T 《Cellular and molecular life sciences : CMLS》1999,55(2):317-326
The two-dimensional electrophoretic patterns of nuclear proteins and their tyrosine phosphorylation were compared for HL-60
cells before and after differentiation induction to granulocytes by dimethyl sulfoxide, all-trans retinoic acid and N
6,O
2-dibutyryl adenosine 3′5′-cyclic monophosphate. Regardless of the inducer used, some nuclear proteins, which are tyrosine-phosphorylated
in proliferating HL-60 cells, undergo gradual dephosphorylation 12–72 h after induction of differentiation, followed by drastic
dephosphorylation during maturation to granulocytes. At least 13 nuclear proteins with a molecular mass of 35–110 kDa are
dephosphorylated, and 6 nuclear proteins undergo tyrosine phosphorylation. Analysis of the nuclear proteins differentially
extracted by salt and detergents indicates that changes in their tyrosine phosphorylation during the maturation stage of differentiating
granulocytes occur mainly in proteins which are abundant in nucleoplasm, chromatin and residual nuclear structures. The abundance
of these proteins, residing in the nuclear structures, and their long-term modification in phosphorylation during the maturation
stages of differentiation strongly suggest that tyrosine phosphorylation of these proteins is involved in reorganization of
the differentiating cell nucleus.
Received 21 September 1998; received after revision 24 November 1998; accepted 3 December 1998 相似文献
5.
Cancer cell metabolism is characterized by limited oxidative phosphorylation in order to minimize oxidative stress. We have
previously shown that the flavonoid flavone in HT-29 colon cancer cells increases the uptake of pyruvate or lactate into mitochondria,
which is followed by an increase in O2−.. production that finally leads to apoptosis. Similarly, a supply of palmitoylcarnitine in combination with carnitine induces
apoptosis in HT-29 cells by increasing the mitochondrial respiration rate. Here we show that flavone-induced apoptosis is
increased more than twofold in the presence of palmitoylcarnitine due to increased mitochondrial fatty acid transport and
the subsequent metabolic generation of O2−. in mitochondria is the initiating factor for the execution of apoptosis.
Received 12 August 2005; received after revision 12 October 2005; accepted 14 October 2005 相似文献
6.
According to the widely acknowledged mitochondrial free radical theory of aging (MFRTA), the macromolecular damage that results
from the production of toxic reactive oxygen species (ROS) during cellular respiration is the cause of aging. However, although
it is clear that oxidative damage increases during aging, the fundamental question regarding whether mitochondrial oxidative
stress is in any way causal to the aging process remains unresolved. An increasing number of studies on long-lived vertebrate
species, mutants and transgenic animals have seriously challenged the pervasive MFRTA. Here, we describe some of these new
results, including those pertaining to the phenotype of the long-lived Mclk1
+/−
mice, which appear irreconcilable with the MFRTA. Thus, we believe that it is reasonable to now consider the MFRTA as refuted
and that it is time to use the insight gained by many years of testing this theory to develop new views as to the physiological
causes of aging. 相似文献
7.
Identification of tyrosine-phosphorylated proteins of the mitochondrial oxidative phosphorylation machinery 总被引:1,自引:1,他引:0
Augereau O Claverol S Boudes N Basurko MJ Bonneu M Rossignol R Mazat JP Letellier T Dachary-Prigent J 《Cellular and molecular life sciences : CMLS》2005,62(13):1478-1488
The role of some serine/threonine kinases in the regulation of mitochondrial physiology is now well established, but little is known about mitochondrial tyrosine kinases. We showed that tyrosine phosphorylation of rat brain mitochondrial proteins was increased by in vitro addition of ATP and H2O2, and also during in situ ATP production at state 3, and maximal reactive oxygen species production. The Src kinase inhibitor PP2 decreased tyrosine phosphorylation and respiratory rates at state 3. We found that the 39-kDa subunit of complex I was tyrosine phosphorylated, and we identified putative tyrosine-phosphorylated subunits for the other complexes. We also have strong evidence that the FoF1-ATP synthase α chain is probably tyrosine-phosphorylated, but demonstrated that the β chain is not. The tyrosine phosphatase PTP 1B was found in brain but not in muscle, heart or liver mitochondria. Our results suggest that tyrosine kinases and phosphatases are involved in the regulation of oxidative phosphorylation.Received 7 January 2005; received after revision 19 April 2005; accepted 22 April 2005 相似文献
8.
T. Nakaki B. C. Wise D. M. Chuang R. Kato 《Cellular and molecular life sciences : CMLS》1989,45(9):879-881
Summary The effects of serotonin on the formation of inositol phosphates and protein phosphorylation were examined in cultured smooth muscle cells. Serotonin stimulated the formation of [3H]inositol monophosphate, [3H]inositol bisphosphate and [3H]inositol trisphosphate. This effect was prevented by 5-HT2 specific antagonist, 6-methyl-1-(1-methylethyl)ergoline-8-carboxylic acid, 2-hydroxy-1-methylpropyl ester [Z]-2-butenedioate (LY53857). Serotonin stimulated the phosphorylation of many polypeptides, among which a 20 kDa polypeptide was the most prominent. The phosphorylation was also inhibited by LY53857. LY53857 alone produced no effects on protein phosphorylation. The 20 kDa polypeptides were also phosphorylated by the addition of 12-O-tetradecanoylphorbol-13-acetate. These results suggest that serotonin stimulates protein phosphorylation through 5-HT2 receptors and possibly activates protein kinase C in intact vascular smooth muscle cells.Part of the data contained in this paper was presented at the 74th local meeting of the Japanese Society of Pharmacology at Kanagawa. 相似文献
9.
Summary During oxidative phosphorylation with cell-free extracts ofMycobacterium phlei, carried out in the presence of tritiated water, only negligible incorporation of tritium has been found either into endogenous MK-9(H2) or into phylloquinone added to the irradiated extract. These results rule out previously postulated mechanisms involving the enzymatic isomerization of menaquinones into quinone-methides 2. 相似文献
10.
Despite the absence of classical tyrosine kinases encrypted in the kinome of Plasmodium falciparum, biochemical analyses have detected significant tyrosine phosphorylation in its cell lysates. Supporting such phosphorylation
is critical for parasite development. These observations have thus raised queries regarding the plasmodial enzymes accountable
for tyrosine kinase activities in vivo. In the current investigation, immunoblot analysis intriguingly demonstrated that Pfnek3,
a plasmodial mitogen-activated protein kinase kinase (MAPKK), displayed both serine/threonine and tyrosine kinase activities
in autophosphorylation reactions as well as in phosphorylation of the exogenous myelin basic protein substrate. The results
obtained strongly support Pfnek3 as a novel dual-specificity kinase of the malarial parasite, even though it displays a HGDLKSTN
motif in the catalytic loop that resembles the consensus HRDLKxxN signature found in the serine/threonine kinases. Notably,
its serine/threonine and tyrosine kinase activities were found to be distinctly influenced by Mg2+ and Mn2+ cofactors. Further probing into the regulatory mechanism of Pfnek3 also revealed tyrosine phosphorylation to be a crucial
factor that stimulates its kinase activity. Through biocomputational analyses and functional assays, tyrosine residues Y117,
Y122, Y172, and Y238 were proposed as phosphorylation sites essential for mediating the catalytic activities of Pfnek3. The
discovery of Pfnek3’s dual role in phosphorylation marks its importance in closing the loop for cellular regulation in P. falciparum, which remains elusive to date. 相似文献
11.
Summary Incubation ofM. phlei washed cells with [14C3H3]-l-methionine led to [2-14C3H3] dihydromena-quinone-9 with an isotope ratio identical to that of methionine. Chromatography of the doubly labelled quinone indicated, despite a pronounced isotope effect, that bothcis andtrans isomers had the same isotope ratio. This result eliminates any possibility of hydrogen exchange in the 2-methyl group of menaquinones during oxydative phosphorylation, even in thecis isomer. Furthermore, it is confirmed that this compound is certainly formed from natural or synthetic menaquinones during isolation or incubation periods by the effect of daylight irradiation. 相似文献
12.
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
13.
Summary In the experimental B1-avitaminosis a decrease of oxidative ATP-resynthesis in liver homogenates, and a significant diminution of the optical density of mitochondrial suspension were simultaneously observed: in other words a probable parallelism in the alteration of function and structure. In ariboflavinosis neither oxidative phosphorylation nor optical density seems to be notably impaired, but the nitrogen content of mitochondrial suspensions decreases significantly. Therefore this second type of avitaminosis would appear to affect the mitochondrial population rather than energetic metabolism or structural integrity of the protoplasmic granules.
Communication présentée au 3e Congrès International de Biochimie, Bruxelles 1955. 相似文献
Communication présentée au 3e Congrès International de Biochimie, Bruxelles 1955. 相似文献
14.
Alexander V. Zhdanov Ruslan I. Dmitriev Dmitri B. Papkovsky 《Cellular and molecular life sciences : CMLS》2011,68(5):903-917
Bafilomycin A1 (Baf) induces an elevation of cytosolic Ca2+ and acidification in neuronal cells via inhibition of the V-ATPase. Also, Baf uncouples mitochondria in differentiated PC12
(dPC12), dSH-SY5Y cells and cerebellar granule neurons, and markedly elevates their respiration. This respiratory response in dPC12 is accompanied by morphological changes in the mitochondria and decreases the mitochondrial pH, Ca2+ and ΔΨm. The response to Baf is regulated by cytosolic Ca2+ fluxes from the endoplasmic reticulum. Inhibition of permeability transition pore opening increases the depolarizing effect
of Baf on the ΔΨm. Baf induces stochastic flickering of the ΔΨm with a period of 20 ± 10 s. Under conditions of suppressed
ATP production by glycolysis, oxidative phosphorylation impaired by Baf does not provide cells with sufficient ATP levels.
Cells treated with Baf become more susceptible to excitation with KCl. Such mitochondrial uncoupling may play a role in a
number of (patho)physiological conditions induced by Baf. 相似文献
15.
Andrea Venerando Oriano Marin Giorgio Cozza Victor H. Bustos Stefania Sarno Lorenzo Alberto Pinna 《Cellular and molecular life sciences : CMLS》2010,67(7):1105-1118
The ability of three isoforms of protein kinase CK1 (α, γ1, and δ) to phosphorylate the N-terminal region of p53 has been assessed using either recombinant p53 or a synthetic peptide
reproducing its 1–28 sequence. Both substrates are readily phosphoylated by CK1δ and CK1α, but not by the γ isoform. Affinity
of full size p53 for CK1 is 3 orders of magnitude higher than that of its N-terminal peptide (K
m 0.82 μM vs 1.51 mM). The preferred target is S20, whose phosphorylation critically relies on E17, while S6 is unaffected
despite displaying the same consensus (E-x-x-S). Our data support the concept that non-primed phosphorylation of p53 by CK1
is an isoform-specific reaction preferentially affecting S20 by a mechanism which is grounded both on a local consensus and
on a remote docking site mapped to the K221RQK224 loop according to modeling and mutational analysis. 相似文献
16.
S. Ishibashi K. Kawasaki Y. Tate T. Ihara K. Shimada 《Cellular and molecular life sciences : CMLS》1995,51(9-10):980-985
The smooth muscle relaxation induced by nitroglycerin is hypothesized to be mediated by an increase in the cytoplasmic concentration of guanosine 3′,5′-monophosphate (cGMP) and subsequent dephosphorylation of the 20-kilodalton myosin light chain (MLC). We investigated this hypothesis in procine coronary arterial smooth muscle stimulated with histamine (3 μM) or K+ (30 mM). Stimulation of [32P]Pi-labeled muscle with histamine or K+ for 2 min resulted in a four- or 6.2-fold increase, respectively, in the incorporation of32P into MLC. After 48 min of exposure to histamine. MLC phosphorylation decreased to the basal level and the phosphorylation of desmin, synemin, and of three unidentified cytosolic proteins was increased. K+ stimulation resulted in a sustained increase of MLC phosphorylation but had no effect on the phosphorylation of desmin, synemin, or the three unidentified cytosolic proteins. Application of nitroglycerin (1 μM) 48 min after histamine stimulation inhibited the phosphorylation of desmin, synemin, and the three cytosolic proteins. The sustained phase of histamine-induced contraction was also inhibited to a greater extent then the acute phase of histamine-induced contraction and both the acute and sustained phases of K+-induced contraction. These results suggest that MLC phosphorylation is required for both phases of K+-induced contraction, whereas phosphorylation of intermediate filament proteins is required for the sustained phase of histamine-induced contraction. Intermediate filament proteins, rather than MLC, may also be the target for the relaxant action of nitroglycerin during histamine-induced sustained contraction. 相似文献
17.
The in vitro characterization of the inhibition of mouse brain protein kinase-C by retinoids and their receptors 总被引:1,自引:0,他引:1
Dr F. O. Cope Mr B. D. Howard Dr R. K. Boutwell 《Cellular and molecular life sciences : CMLS》1986,42(9):1023-1027
Summary The mechanism of the in vitro inhibition of Ca2+-, phosphatidylserine-dependent protein kinase C (PK-C)2 by the purifiedholo (ligand-saturated) forms of cellular retinol-binding protein (cRBP) and cellular retinoic acid-binding protein (cRABP) was studied. We report here that i) the PK-C-inhibitory action ofholo-cRBP andholo-cRABP is due to their respective ligands, all-trans-retinol and all-trans-retinoic acid; ii) the reduced phosphorylation of theholo-retinoid-binding proteins and brain cytosolic proteins is not the result of a retinoid-induced soluble phosphatase or protease activity; iii) retinoids reduce PK-C affinity for calcium and phosphatidylserine in vitro; and iv) the structure-function activity of the retinoids and the specific interaction of these effect of retinoids on plasma membrane-associated PK-C activity pays a significant role in defining the early epigenetic aspects of PK-C-dependent tumor promotion and may be a physiological mechanism by which retinoids induce terminal differentiation in cell types that do not express soluble retinoid-binding proteins.We would like to thank Dr L.M. De Luca (NIH, USA) for his contribution of retinylphosphate, Dr H.N. Bhagavan (Hoffmann-La Roche) for his contribution of the arotinoids, and Merrill-Dow Corp. for their contribution of difluoromethylornithine. This work was supported by NIH Grants CA-34968, CA-07175, CA-22484, and CA-09020. 相似文献
18.
A. Viarengo L. Canesi M. Pertica D. R. Livingstone M. Orunesu 《Cellular and molecular life sciences : CMLS》1991,47(5):454-457
Summary The main cellular defence systems against free radical-mediated oxidative stress are significantly reduced in the dige+ive gland of aged (>10 years old) compared to younger (2–4 years old) mussels (Mytilus edulis L.). Moreover, the concentration of lipid peroxidation products (malondialdehyde) is increased in the same age group with respect to younger animals. The obtained data indicate that an impairment of the antioxidant defence systems would render the older animals more susceptible to peroxidative stress, thus supporting the general significance of the free radical theory of aging. 相似文献
19.
Summary Mg2+-ATPase deficient mutant ofEscherichia coli showed an evident dependency of thiamine uptake on the oxidative metabolism of glucose, whereas the parent strain did not. In both cells, this uptake was completely inhibited by H+ conductors.Acknowledgment. We are indebted to Miss M. Abe for her excellent technical assistance. 相似文献
20.
Dhar-Chowdhury P Malester B Rajacic P Coetzee WA 《Cellular and molecular life sciences : CMLS》2007,64(23):3069-3083
Glycolysis is an evolutionary conserved metabolic pathway that provides small amounts of energy in the form of ATP when compared
to other pathways such as oxidative phosphorylation or fatty acid oxidation. The ATP levels inside metabolically active cells
are not constant and the local ATP level will depend on the site of production as well as the respective rates of ATP production,
diffusion and consumption. Membrane ion transporters (pumps, exchangers and channels) are located at sites distal to the major
sources of ATP formation (the mitochondria). We review evidence that the glycolytic complex is associated with membranes;
both at the plasmalemma and with membranes of the endo/sarcoplasmic reticular network. We examine the evidence for the concept
that many of the ion transporters are regulated preferentially by the glycolytic process. These include the Na+/K+-ATPase, the H+-ATPase, various types of Ca2+-ATPases, the Na+/H+ exchanger, the ATP-sensitive K+ channel, cation channels, Na+ channels, Ca2+ channels and other channels involved in intracellular Ca2+ homeostasis. Regulation of these pumps, exchangers and ion channels by the glycolytic process has important consequences
in a variety of physiological and pathophysiological processes, and a better understanding of this mode of regulation may
have important consequences for developing future strategies in combating disease and developing novel therapeutic approaches.
Received 20 July 2007; received after revision 30 July 2007; accepted 17 August 2007 相似文献