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Dive into the research topics where Fazoil I. Ataullakhanov is active.

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Featured researches published by Fazoil I. Ataullakhanov.


Thrombosis and Haemostasis | 2007

Platelet microparticle membranes have 50- to 100-fold higher specific procoagulant activity than activated platelets.

Elena I. Sinauridze; Dmitry A. Kireev; Nadezhda Y. Popenko; Aleksei V. Pichugin; Mikhail A. Panteleev; Olga V. Krymskaya; Fazoil I. Ataullakhanov

Platelet microparticles (PMPs) are small vesicles released from blood platelets upon activation. The procoagulant activity of PMPs has been previously mainly characterized by their ability to bind coagulation factors VIII and Va in reconstructed systems. It can be supposed that PMPs can contribute to the development of thrombotic complications in the pathologic states associated with the increase of their blood concentration. In this study, we compared procoagulant properties of calcium ionophore A23187-activated platelets and PMPs using several in-vitro models of hemostasis. Surface densities of phosphatidylserine, CD61, CD62P and factor X bound per surface area unit were determined by flow cytometry. They were 2.7-, 8.4-, 4.3-, and 13-fold higher for PMPs than for activated platelets, respectively. Spatial clot growth rate (V(clot)) in the reaction-diffusion experimental model and endogenous thrombin potential (ETP) were determined in plasma, which was depleted of phospholipid cell surfaces by ultra-centrifugation and supplemented with activated platelets or PMPs at different concentrations. Both V(clot) and ETP rapidly increased with the increase of PMP or platelet concentration until saturation was reached. The plateau values of V(clot) and ETP for activated platelets and PMPs were similar. In both assays, the procoagulant activity of one PMP was almost equal to that of one activated platelet despite at least two-orders-of-magnitude difference in their surface areas. This suggests that the PMP surface is approximately 50- to 100-fold more procoagulant than the surface of activated platelets.


Journal of Microscopy | 2007

Cryo-fluorescence microscopy facilitates correlations between light and cryo-electron microscopy and reduces the rate of photobleaching

Cindi L. Schwartz; Vasily I. Sarbash; Fazoil I. Ataullakhanov; J. Richard McIntosh; Daniela Nicastro

Fluorescence light microscopy (LM) has many advantages for the study of cell organization. Specimen preparation is easy and relatively inexpensive, and the use of appropriate tags gives scientists the ability to visualize specific proteins of interest. LM is, however, limited in resolution, so when one is interested in ultrastructure, one must turn to electron microscopy (EM), even though this method presents problems of its own. The biggest difficulty with cellular EM is its limited utility in localizing macromolecules of interest while retaining good structural preservation. We have built a cryo‐light microscope stage that allows us to generate LM images of vitreous samples prepared for cryo‐EM. Correlative LM and EM allows one to find areas of particular interest by using fluorescent proteins or vital dyes as markers within vitrified samples. Once located, the sample can be placed in the EM for further study at higher resolution. An additional benefit of the cryo‐LM stage is that photobleaching is slower at cryogenic temperatures (−140°C) than at room temperature.


Bioscience Reports | 2002

What determines the intracellular ATP concentration.

Fazoil I. Ataullakhanov; Victor Vitvitsky

Analysis is made of the mechanisms that control the intracellular ATP level. The balance between energy production and expenditure determines the energy charge of the cell and the ratio of [ATP] to the adenylate pool. The absolute ATP concentration is determined by the adenylate pool, which, in its turn, depends on the balance between the rates of AMP synthesis and degradation. Experimental data are discussed that demonstrate an increase in the adenylate pool in response to activation of energy-consuming processes. A hypothesis is proposed according to which variation in the adenylate pool and absolute ATP concentration affords a cell the possibility of additional control over processes fulfilling useful work. A mechanism involved in this regulation is described using human erythrocytes as an example. The hypothesis explains why different metabolic pathways (protein and DNA syntheses, polysaccharide synthesis, and lipid synthesis) use different trinucleotides (GTP, UTP, and CTP, respectively) as an energy source. This allows the cell to independently control these metabolic processes by varying the individual nucleotide pools.


Redox Report | 2003

Redox regulation of homocysteine-dependent glutathione synthesis

Victor Vitvitsky; Eugene V Mosharov; Michael Tritt; Fazoil I. Ataullakhanov; Ruma Banerjee

Abstract In certain tissues, glutathione biosynthesis is connected to methionine metabolism via the trans-sulfuration pathway. The latter condenses homocysteine and serine to cystathionine in a reaction catalyzed by cystathionine β-synthase followed by cleavage of cystathionine to cysteine and α-ketoglutarate by γ-cystathionase. Cysteine is the limiting amino acid in glutathione biosynthesis, and studies in our laboratory have shown that approximately 50% of the cysteine in glutathione is derived from homocysteine in human liver cells. In this study, we have examined the effect of pro- and antioxidants on the flux of homocysteine through the trans-sulfuration pathway in the human hepatoma cell line, HepG2. Our studies reveal that pyrrolidine dithiocarbamate and butylated hydroxyanisole enhance the flux of homocysteine through the trans-sulfuration pathway as has been observed previously with the pro-oxidants, H2O2 and tertiary butyl hydroperoxide. In contrast, antioxidants such as catalase, superoxide dismutase and a water-soluble derivative of vitamin E elicit the opposite effect and result in diminished flux of homocysteine through the trans-sulfuration pathway. These studies provide the first evidence for the reciprocal sensitivity of the trans-sulfuration pathway to pro- and antioxidants, and demonstrate that the upstream half of the glutathione biosynthetic pathway (i.e. leading to cysteine biosynthesis) is redox sensitive as is the regulation of the well-studied enzymes in the downstream half (leading from cysteine to glutathione), namely, γ-glutamyl-cysteine ligase and glutathione synthetase.


Proceedings of the National Academy of Sciences of the United States of America | 2008

Different assemblies of the DAM1 complex follow shortening microtubules by distinct mechanisms

Ekaterina L. Grishchuk; Ilia S. Spiridonov; Vladimir A. Volkov; Artem K. Efremov; Stefan Westermann; David G. Drubin; Georjana Barnes; Fazoil I. Ataullakhanov; J. R. McIntosh

Mitotic chromosomes segregate at the ends of shortening spindle microtubules (MTs). In budding yeast, the Dam1 multiprotein complex supports this dynamic attachment, thereby contributing to accurate chromosome segregation. Purified Dam1 will track the end of a depolymerizing MT and can couple it to microbead transport in vitro. The processivity of such motions has been thought to depend on rings that the Dam1 complex can form around MTs, but the possibility that alternative coupling geometries contribute to these motilities has not been considered. Here, we demonstrate that both rings and nonencircling Dam1 oligomers can track MT ends and enable processive cargo movement in vitro. The coupling properties of these two assemblies are, however, quite different, so each may make a distinct contribution to chromosome motility.


Journal of Thrombosis and Haemostasis | 2005

Initiation and propagation of coagulation from tissue factor-bearing cell monolayers to plasma: initiator cells do not regulate spatial growth rate*

Mikhail V. Ovanesov; Natalya M. Ananyeva; Mikhail A. Panteleev; Fazoil I. Ataullakhanov; Evgueni L. Saenko

Summary.  Exposure of tissue factor (TF)‐bearing cells to blood is the initial event in coagulation and intravascular thrombus formation. However, the mechanisms which determine thrombus growth remain poorly understood. To explore whether the procoagulant activity of vessel wall‐bound cells regulates thrombus expansion, we studied in vitro spatial clot growth initiated by cultured human cells of different types in contact pathway‐inhibited, non‐flowing human plasma. Human aortic endothelial cells, smooth muscle cells, macrophages and lung fibroblasts differed in their ability to support thrombin generation in microplate assay with peaks of generated thrombin of 60 ± 53 nmol L−1, 135 ± 57 nmol L−1, 218 ± 55 nmol L−1 and 407 ± 59 nmol L−1 (mean ± SD), respectively. Real‐time videomicroscopy revealed the initiation and spatial growth phases of clot formation. Different procoagulant activity of cell monolayers was manifested as up to 4‐fold difference in the lag times of clot formation. In contrast, the clot growth rate, which characterized propagation of clotting from the cell surface to plasma, was largely independent of cell type (≤ 30% difference). Experiments with factor VII (FVII)‐, FVIII‐, FX‐ or FXI‐deficient plasmas and annexin V revealed that (i) cell surface‐associated extrinsic Xase was critical for initiation of clotting; (ii) intrinsic Xase regulated only the growth phase; and (iii) the contribution of plasma phospholipid surfaces in the growth phase was predominant. We conclude that the role of TF‐bearing initiator cells is limited to the initial stage of clot formation. The functioning of intrinsic Xase in plasma provides the primary mechanism of sustained and far‐ranging propagation of coagulation leading to the physical expansion of a fibrin clot.


Biophysical Journal | 2011

Platelet adhesion from shear blood flow is controlled by near-wall rebounding collisions with erythrocytes.

A.A. Tokarev; A.A. Butylin; Fazoil I. Ataullakhanov

The efficacy of platelet adhesion in shear flow is known to be substantially modulated by the physical presence of red blood cells (RBCs). The mechanisms of this regulation remain obscure due to the complicated character of platelet interactions with RBCs and vascular walls. To investigate this problem, we have created a mathematical model that takes into account shear-induced transport of platelets across the flow, platelet expulsion by the RBCs from the near-wall layer of the flow onto the wall, and reversible capture of platelets by the wall and their firm adhesion to it. This model analysis allowed us to obtain, for the first time to our knowledge, an analytical determination of the platelet adhesion rate constant as a function of the wall shear rate, hematocrit, and average sizes of platelets and RBCs. This formula provided a quantitative description of the results of previous in vitro adhesion experiments in perfusion chambers. The results of the simulations suggest that under a wide range of shear rates and hematocrit values, the rate of platelet adhesion from the blood flow is mainly limited by the frequency of their near-wall rebounding collisions with RBCs. This finding reveals the mechanism by which erythrocytes physically control platelet hemostasis.


Thrombosis Research | 1996

A MATHEMATICAL MODEL FOR THE SPATIO-TEMPORAL DYNAMICS OF INTRINSIC PATHWAY OF BLOOD COAGULATION. II. RESULTS

V.I. Zarnitsina; A.V. Pokhilko; Fazoil I. Ataullakhanov

This paper continues our study (see Part I) where we modeled the spatio-temporal dynamics of the intrinsic pathway of blood coagulation. Here, we analyzed this model and showed that it describes the threshold behavior of coagulation. When activation is subthreshold (which produces not more than 0.07 nM factor XIa at saturating free calcium concentrations of 2 mM or higher), the concentration of generated thrombin remains below 0.01 nM. At the abovethreshold activation corresponding to factor XIa exceeding 0.07 nM, the concentration of thrombin explosively increases and then abruptly decreases. The peak concentration of thrombin reaches hundreds nM. With respect to free calcium concentration, the system also behaves in a threshold manner. For activation corresponding to 0.3 nM factor XIa, the threshold concentration of free calcium where the outburst of explosive thrombin generation occur is equal to 0.21 mM. The model simulations are in a good agreement with the experimentally recorded kinetics of thrombin generation at different concentrations of free calcium (1). Analysis of the spatial dynamics of coagulation showed that if activation exceeded the threshold level at a certain point, the concentration wave of thrombin arises and propagates at a high speed from the activation zone. The parameters of this wave depends mainly on the efficiency of the feedback loops. The feedback loops through the backbone factors of the intrinsic pathway (autoactivation of factor X or activation of factor XI by thrombin) has a potential for the unlimited propagation of the thrombin wave. With increasing activity of activated protein C (the effect equivalent to that of thrombomodulin), oscillating regimes arise in the model. The first thrombin wave is followed by several secondary running waves. The amplitudes of secondary waves increases to the periphery of the clot consolidating its surface layer.


Thrombosis Research | 1996

A MATHEMATICAL MODEL FOR THE SPATIO-TEMPORAL DYNAMICS OF INTRINSIC PATHWAY OF BLOOD COAGULATION. I. THE MODEL DESCRIPTION

V.I. Zarnitsina; A.V. Pokhilko; Fazoil I. Ataullakhanov

We developed and analyzed the mathematical model of the intrinsic pathway based on the current biochemical data on the kinetics of blood coagulation individual stages. The model includes eight differential equations describing the spatio-temporal dynamics of activation of factors XI, IX, X, II, I, VIII, V, and protein C. The assembly of tenase and prothrombinase complexes is considered as a function of calcium concentration. The spatial dynamics of coagulation was analyzed for the one-dimensional case. We examined the formation of active factors, their spreading, and growth of the clot from the site of injury in the direction perpendicular to the vessel wall, into the blood thickness. We assumed that the site of injury (in the model one boundary of the space segment under examination) becomes a source of the continuous influx of factor XIa. In the first part, we described the model, selected the parameters, etc. In the second part, we compared the model with experimental data obtained in the homogeneous system and analyzed the spatial dynamics of the clot growth.


Thrombosis Research | 1994

Calcium threshold in human plasma clotting kinetics

Fazoil I. Ataullakhanov; A.V. Pohilko; Elena I. Sinauridze; Volkova Ri

In vitro clotting kinetics of citrate human blood plasma under its titration with calcium ions are studied. Contact activation (Factor XIa + plasma kallikrein) is shown to be independent of calcium while non-linear growth of thrombin concentration is demonstrated at calcium concentrations higher than 0.25 mM under conditions of contact activation caused by quartz walls of the measuring cell. Thrombin generation kinetics are well fitted with an exponential function. Power index of the exponential function steeply rises as calcium concentration increases from 0.25 to 0.5 mM and reaches plateau at higher concentrations. At free calcium concentrations under 0.25 mM thrombin level does not grow remaining lower than 30 pM. So, blood coagulation system behaves in a threshold manner under calcium concentration changes. The threshold concentration of free calcium is equal to 0.25 +/- 0.05 mM.

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Anna N. Balandina

Russian Academy of Sciences

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Natalya M. Ananyeva

Food and Drug Administration

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Elena N. Lipets

Russian Academy of Sciences

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Stepan S. Surov

Russian Academy of Sciences

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