Gotowe bibliografie tematyczne / Adenosine kinase

Gotowa bibliografia na temat „Adenosine kinase”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "Adenosine kinase"

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Park, Jae, Bhag Singh i Radhey S. Gupta. "Mycobacterial adenosine kinase is not a typical adenosine kinase". FEBS Letters 583, nr 13 (8.06.2009): 2231–36. http://dx.doi.org/10.1016/j.febslet.2009.06.002.

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Kowaluk, Elizabeth A., Shripad S. Bhagwatt i Michael F. Jarvis. "Adenosine Kinase Inhibitors". Current Pharmaceutical Design 4, nr 5 (październik 1998): 403–16. http://dx.doi.org/10.2174/138161280405221010163056.

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Abstract: Adenosine (ADO) is an endogenous modulator of intercellular signaling that provides homeostatic reductions in cell excitability during tissue stress and trauma. The inhibitory actions of ADO are mediated by interactions with specific cell-surface G­ protein coupled receptors regulating membrane cation flux, polarization, and the release of excitatory neurotransmitters. ADO kinase (AK; EC 2.7.1.20) is the key intracellular enzyme regulating intra- and extracellular ADO concentrations. Inhibition of AK produces marked increases in extracellular ADO levels that are localized to cells and tissues undergoing accelerated ADO release. Thus AK inhibiton represents a mechanism to selectively enhance the protective actions of ADO during tissue trauma without producing the nonspecific effects associated with the systemic administration of ADO receptor agonists. During the last 10 years, specific inhibitors of AK based on the endogenous purine nucleoside substrate, ADO, have been developed. Potent AK inhibitors have recently been synthesized that demonstrate high specificity for this enzyme as compared to other ADO metabolic enzymes, transporters, and receptors. In both in vitro and in vivo models, AK inhibitors have been shown to potently increase ADO concentrations in a tissue and event specific fashion and to demonstrate potential clinical utility in animal models of epilepsy, ischemia, pain, and inflammation. AK inhibitors have demonstrated superior efficacy in these models as compared to other mechanisms of modulating ADO availability, and these agents exhibit reduced side-effect liabilities compared to direct acting ADO receptor agonists. The preclinical profile of AK inhibitors indicate that these agents may have therapeutic utility in a variety of central and peripheral diseases associated with cellular trauma and inflammation. Clinical trials are currently underway to evaluate the efficacy of AK inhibitors in seizure disorders and pain.
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Boison, Detlev. "Adenosine Dysfunction and Adenosine Kinase in Epileptogenesis". Open Neuroscience Journal 4, nr 1 (1.01.2010): 93–101. http://dx.doi.org/10.2174/1874082001004010093.

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Ratcliffe, Steven J., Tracey Yi i Sanjay S. Khandekar. "Synthesis and Characterization of 5′-p-fluorosulfonylbenzoyl-2′ (or 3′)-(biotinyl)adenosine as an Activity-Based Probe for Protein Kinases". Journal of Biomolecular Screening 12, nr 1 (12.11.2006): 126–32. http://dx.doi.org/10.1177/1087057106296685.

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Most of the kinase inhibitors that are approved for therapeutic uses or that are undergoing clinical trials are directed toward the adenosine triphosphate (ATP) binding site of protein kinases. 5'-Fluorosulfonylbenzoyl 5′-adenosine (FSBA) is an activitybased probe (ABP) that covalently modifies a conserved lysine present in the nucleotide binding site of most kinases. Here the authors describe synthesis of FSBA derivatives, 2′-biotinyl-FSBA and 3′-biotinyl-FSBA as kinase ABPs, and delineate a Western blot method to screen and validate ATP competitive protein kinase inhibitors using biotinyl-FSBA as a nonselective activity-based probe for protein kinases.
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Zhulai, Galina, Eugenia Oleinik, Mikhail Shibaev i Kirill Ignatev. "Adenosine-Metabolizing Enzymes, Adenosine Kinase and Adenosine Deaminase, in Cancer". Biomolecules 12, nr 3 (8.03.2022): 418. http://dx.doi.org/10.3390/biom12030418.

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The immunosuppressive effect of adenosine in the microenvironment of a tumor is well established. Presently, researchers are developing approaches in immune therapy that target inhibition of adenosine or its signaling such as CD39 or CD73 inhibiting antibodies or adenosine A2A receptor antagonists. However, numerous enzymatic pathways that control ATP-adenosine balance, as well as understudied intracellular adenosine regulation, can prevent successful immunotherapy. This review contains the latest data on two adenosine-lowering enzymes: adenosine kinase (ADK) and adenosine deaminase (ADA). ADK deletes adenosine by its phosphorylation into 5′-adenosine monophosphate. Recent studies have revealed an association between a long nuclear ADK isoform and an increase in global DNA methylation, which explains epigenetic receptor-independent role of adenosine. ADA regulates the level of adenosine by converting it to inosine. The changes in the activity of ADA are detected in patients with various cancer types. The article focuses on the biological significance of these enzymes and their roles in the development of cancer. Perspectives of future studies on these enzymes in therapy for cancer are discussed.
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Khandekar, Sanjay S., Bingbing Feng, Tracey Yi, Susan Chen, Nicholas Laping i Neal Bramson. "A Liquid Chromatography/Mass Spectrometry-Based Method for the Selection of ATP Competitive Kinase Inhibitors". Journal of Biomolecular Screening 10, nr 5 (sierpień 2005): 447–55. http://dx.doi.org/10.1177/1087057105274846.

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The currently approved kinase inhibitors for therapeutic uses and a number of kinase inhibitors that are undergoing clinical trials are directed toward the adenosine triphosphate (ATP) binding site of protein kinases. The 5β-fluorosulfonylbenzoyl 5'-adenosine (FSBA) is an ATP-affinity reagent that covalently modifies a conserved lysine present in the nucleotide-binding site of most kinases. The authors have developed a liquid chromatography/mass spectrometry-basedmethod tomonitor binding ofATP competitive protein kinase inhibitors using FSBAas a nonselective activity-based probe for protein kinases. Their method provides a general, rapid, and reproducible means to screen and validate selective ATP competitive inhibitors of protein kinases.
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Drabikowska, Alicja K., Lidia Halec i David Shugar. "Purification and Properties of Adenosine Kinase from Rat Liver: Separation from Deoxyadenosine Kinase Activity". Zeitschrift für Naturforschung C 40, nr 1-2 (1.02.1985): 34–41. http://dx.doi.org/10.1515/znc-1985-1-209.

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Ion exchange and affinity chromatography techniques, similar to those previously reported for purification of adenosine kinase from human placenta, were applied to purification of rat liver adenosine kinase. The enzyme, purified 400-fold in 41% yield, was homogeneous on SDS- polyacrylamide gel electrophoresis, with a molecular weight of 52000. It specific activity, 18 μmol/min/mg protein, is the highest hitherto reported for this enzyme from mammalian sources. Chromatography on DEAE-cellulose removed about 98% of the phosphorylating activity towards 2′-deoxyadenosine present in the initial pH-treated liver extract. The final preparation exhibited only minimal activity (~ 1.5%) under optimal conditions (pH 7.5) vs- 2′-deoxy- adenosine, the lowest yet reported for such a preparation, with a Km of 670 μᴍ, as compared to 0.3 μᴍ for adenosine. The residual activity towards deoxyadenosine is considered an intrinsic property of the purified adenosine kinase and, in fact, phosphorylation of adenosine was inhibited competitively by deoxyadenosine, with a of 70 μᴍ. Competitive inhibition was also exhibited by cordycepin (3′-deoxyadenosine) with a Ki of 150 μᴍ. A more potent competitive inhibitor was tubercidin, the Ki for which was 1.9 μᴍ.
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Fassett, John T., Xinli Hu, Xin Xu, Zhongbing Lu, Ping Zhang, Yingjie Chen i Robert J. Bache. "Adenosine kinase regulation of cardiomyocyte hypertrophy". American Journal of Physiology-Heart and Circulatory Physiology 300, nr 5 (maj 2011): H1722—H1732. http://dx.doi.org/10.1152/ajpheart.00684.2010.

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There is evidence that extracellular adenosine can attenuate cardiac hypertrophy, but the mechanism by which this occurs is not clear. Here we investigated the role of adenosine receptors and adenosine metabolism in attenuation of cardiomyocyte hypertrophy. Phenylephrine (PE) caused hypertrophy of neonatal rat cardiomyocytes with increases of cell surface area, protein synthesis, and atrial natriuretic peptide (ANP) expression. These responses were attenuated by 5 μM 2-chloroadenosine (CADO; adenosine deaminase resistant adenosine analog) or 10 μM adenosine. While antagonism of adenosine receptors partially blocked the reduction of ANP expression produced by CADO, it did not restore cell size or protein synthesis. In support of a role for intracellular adenosine metabolism in regulating hypertrophy, the adenosine kinase (AK) inhibitors iodotubercidin and ABT-702 completely reversed the attenuation of cell size, protein synthesis, and expression of ANP by CADO or ADO. Examination of PE-induced phosphosignaling pathways revealed that CADO treatment did not reduce AKTSer473 phosphorylation but did attenuate sustained phosphorylation of RafSer338 (24–48 h), mTORSer2448 (24–48 h), p70S6kThr389 (2.5–48 h), and ERKThr202/Tyr204 (48 h). Inhibition of AK restored activation of these enzymes in the presence of CADO. Using dominant negative and constitutively active Raf adenoviruses, we found that Raf activation is necessary and sufficient for PE-induced mTORC1 signaling and cardiomyocyte hypertrophy. CADO treatment still blocked p70S6kThr389 phosphorylation and hypertrophy downstream of constitutively active Raf, however, despite a high level phosphorylation of ERKThr202/Tyr204 and AKTSer473. Reduction of Raf-induced p70S6kThr389 phosphorylation and hypertrophy by CADO was reversed by inhibiting AK. Together, these results identify AK as an important mediator of adenosine attenuation of cardiomyocyte hypertrophy, which acts, at least in part, through inhibition of Raf signaling to mTOR/p70S6k.
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Gomtsyan, Arthur, i Chih-Hung Lee. "Nonnucleoside Inhibitors of Adenosine Kinase". Current Pharmaceutical Design 10, nr 10 (1.04.2004): 1093–103. http://dx.doi.org/10.2174/1381612043452703.

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Galazka, Jon, Boris Striepen i Buddy Ullman. "Adenosine kinase from Cryptosporidium parvum". Molecular and Biochemical Parasitology 149, nr 2 (październik 2006): 223–30. http://dx.doi.org/10.1016/j.molbiopara.2006.06.001.

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Rozprawy doktorskie na temat "Adenosine kinase"

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Davis, Alison Jane. "Kinase-anchoring proteins and the intracellular targeting of cyclic adenosine monophosphate (cAMP)-dependent protein kinase". Thesis, University of Leicester, 2007. http://hdl.handle.net/2381/29960.

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Kinase anchoring proteins (AKAPs) are a family of structurally diverse multidomain proteins classified solely by their ability to bind cAMP-dependent protein kinase/protein kinase A (PKA). We show that the prototypic AKAP, AKAP79, targets PKA to the plasma membrane. This subcellular localisation is mediated via interactions between basic regions on AKAP79 and acidic phospholipids in the plasma membrane. We show that while PKA and protein kinase C (PKC)-dependent phosphorylation of AKAP79 targeting residues has no effect on its subcellular localization, Gq-coupled receptor-driven depletion of the lipid anchor PtdIns(4,5)P2 causes release of AKAP79 from the membrane. Receptor-mediated regulation of AKAP membrane binding may be an important feedback mechanism controlling the degree of access that AKAP-bound enzymes have to membrane-associated substrates. Real-time confocal imaging failed to show significant redistribution of AKAP79 following Gq-coupled receptor activation, which may reflect only limited short-range movements.;In addition to regulated association with membrane, we also show through co-immunoprecipitation studies a direct interaction between AKAP79 and all three members of the inwardly rectifying potassium channel Kir2 family. Using a combination of deletion analysis and structural modelling we show that AKAP79 binds the Kir2 family via a novel binding motif located on the C terminus of the ion channel and not via a leucine zipper as has been reported for other AKAP-channel interactions. Interestingly, we also show using a PKA regulatory subunit overlay assays that this region of Kir2.1 is capable of isolating other, potentially novel, AKAPs from rat brain and heart homogenates.;Finally, we use whole-cell patch clamp analysis to demonstrate that cAMP-dependent modulation of Kir2.1 channel activity is significantly enhanced in the presence of AKAP79, thus confirming an important role for AKAP79 in targeting PKA to key channel phosphorylation sites.
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Yang, Zhaogang. "ADENOSINE RECEPTOR MEDIATED PROTEIN KINASE C ACTIVATION IN THE HEART". The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1338320892.

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Kong, Cheng-Te. "Mechanism of the Adenosine 3',5'-Monophosphate Dependent Protein Kinase". Thesis, North Texas State University, 1988. https://digital.library.unt.edu/ark:/67531/metadc330934/.

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Isotope partitioning experiments were carried out with the adenosine 3',5'-monophosphate-dependent protein kinase catalytic subunit (cAPK) from bovine hearts to obtain information on the order of addition of reactants and the relative rates of reactant release from enzyme compared to the catalytic step(s). A value of 100% trapping for both ErMgATP-[γ-32P] and E:3H-Serpeptide at low Mgf indicates that MgATP and Serpeptide dissociate slowly from the enzyme compared to the catalytic step(s). The K_Serpeptide for MgATP trapping is 17 μM, while the K_MgATP for Serpeptide trapping is 0.58 mM. The latter data indicate that the off-rate for MgATP from the E:MgATP complex is 14 s^-1 while that for Serpeptide from the E: Serpeptide complex is 64 s^-1. At high Mg^, 100% trapping is obtained for the E:MgATP-[γ-32P] complex but only 40% is obtained for the E:Serpeptide complex. Thus, the off-rate for Serpeptide from the E:MgATP:Serpeptide complex becomes significant at high Mg_f. Data suggest a random mechanism in which MgATP is sticky. The V for the cAPK reaction increases 1.5-1.7 fold in the presence of the R_II in the presence of saturating cAMP at a stoichiometry of R:C of 1:1. No change is obtained with the type-I complex under these conditions. At higher ratio of R:C (up to 100) no further change is observed with the type-II complex but inhibition by the type-I R_2(cAMP)_4 complex competitive vs. Serpeptide is observed. The activiation observed in the presence type-II R_2(cAMP)_4 effects neither the K_m for Serpeptide nor the K_m for MgATP. Both the activating affect of the type-II complex and the inhibitory effect of the type-I complex are dependent on the Mg_f with more type-II activation obtained the higher the Mg_f and more type-I complex required for inhibition the higher the Mg_f. The activation and inhibition are discussed in terms of the mechanism of the protein kinase.
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Dahlstedt, Anders. "Intracellular mechanisms of skeletal muscle fatigue : role of creatine kinase /". Stockholm : [A. Dahlstedt], 2001. http://diss.kib.ki.se/2001/91-631-1673-1/.

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Wang, Hui. "Geminivirus AL2 and L2 proteins interact with and inactivate adenosine kinase". Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1078773653.

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Thesis (Ph. D.)--Ohio State University, 2004.
Title from first page of PDF file. Document formatted into pages; contains xvii, 201 p.; also includes graphics (some col.) Includes bibliographical references (p. 171-201). Available online via OhioLINK's ETD Center
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Willems, Laura E., i n/a. "Adenosine and Ischaemia in Young To Aged Hearts". Griffith University. School of Medical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20061011.163451.

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Ischaemic heart disease is a major contributor to premature death and heart failure in the Westernised world. Ischaemic injury within the heart may be beneficially modulated by the nucleoside adenosine. Derived from catabolism of ATP, adenosine was initially known as a potent bradycardic and hypotensive agent. However, more recently the protective function of adenosine has been investigated. The protective effects of adenosine are mediated via activation of adenosine receptors: A1, A2A, A2B, and A3 receptors. Activation of these potentially protective (or retaliatory) adenosine receptors hinges upon accumulation of adenosine during ischaemia-reperfusion. This Thesis examines the role and mechanisms of adenosine mediated cardioprotection in young and aged hearts, exploring endogenous and exogenous adenosine receptor activation, genetic manipulation of A1 receptors and adenosine deaminase and pharmacological manipulation of adenosine metabolism. The effects of age on ischaemic responses and adenosine handling and protection are also assessed. The core approach to assess each of the above issues involved the Langendorff isolated mouse heart preparation. Experiments within Chapter 3 focuses on the contractile effects of adenosine receptors in normoxic hearts. This study indicates A2A receptors have no direct effect on contractility, while adenosine exerts positive inotropy independently of coronary flow and perfusion pressure (i.e. Independent of the Gregg phenomenon). In addition, investigations in genetically modified hearts hint at positive inotropy in response to A1 receptors. Since the latter is only evidenced in modified lines, it is possible A1-mediated inotropy may be abnormal or supraphysiological. In Chapter 4 the impact of genetic 'deletion' of A1ARs and/or adenosine deaminase (ADA) on intrinsic tolerance to ischaemia were studied. Data demonstrate that genetic deletion of A1 receptors significantly limits the ability of the mouse myocardium to withstand injury during ischaemic insult. Thus, providing strong support for a role of A1ARs in determining intrinsic tolerance to ischaemia-reperfusion. ADA KO mice confirm protection afforded by endogenous adenosine and the notion of adenosine metabolism modification as a protective strategy. Interestingly, effects of A1AR KO differ from A1AR overexpression or A1AR agonism in that the latter decrease contractile diastolic dysfunction while A1AR KO selectively increase systolic dysfunction and increase oncosis without altering diastolic injury. This challenges current dogma regarding the action of A1 adenosine receptors on ischaemic injury. In Chapter 5 the effects of adenosine metabolism inhibition (via adenosine deaminase (ADA) and adenosine kinase (AK) inhibitors) were studied. Inhibition of adenosine deaminase with the drug EHNA, and adenosine phosphorylation with iodotubercidin significantly protected mouse hearts from ischaemia-reperfusion, reducing contractile dysfunction and cardiac enzyme efflux. However, inhibitors failed to improve the outcome of the aged myocardium. 8-SPT and 5-HD reduced the protective effects of EHNA and iodotubercidin demonstrating thus; cardioprotection via ADA and AK appears to rely on adenosine receptor activation and involves a mitoK ATP dependent mechanism. Since aging is of considerable importance with regard to outcomes of ischaemic heart disease, experiments in Chapter 6 focused on effects of aging (and gender) on cardiovascular function and injury during ischaemia-reperfusion. In assessing post ischaemic outcomes in hearts from young adult (2-4 months), mature adult (8 months), middle aged (12 months), aged (18 months) and senescent (24-28 months) C57/BL/6J mice, data reveal a substantial age-related decline in ischaemic tolerance (which appears selective for myocardial vs. vascular injury). The decline in ischaemic tolerance is expressed primarily within the initial 12 months in both males and females with relatively little further decline with continued aging. There is evidence of a modest improvement in tolerance in senescence vs. aged hearts possibly reflecting selection of a protected phenotype in senescent populations. In addition, mature and middle-aged female hearts showed improved tolerance to ischaemia-reperfusion compared to males, supporting a role for hormonal changes. Effects of aging and purine metabolism were studied in Chapter 7. Data suggest impaired tolerance to ischaemia-reperfusion in older hearts may stem in part from shifts in myocardial purine catabolism. Data reveal reduced accumulation of salvageable and cardioprotective adenosine and enhanced accumulation of poorly salvaged (and potentially injurious) hypoxanthine and xanthine. These changes may potentially predispose the aged myocardium to ischaemic injury and radical generation via the xanthine oxidase reaction. The final data Chapter of this Thesis describes preliminary data regarding aging, signalling and adenosine mediated protection. It was found that protein kinase C (PKC) and A1 receptors mediate protection in young hearts and also that A1 receptors appear to mediate protection via a PKC LindependentLi signalling cascade. In addition, experiments in aged hearts (attempting to elucidate mechanisms behind impaired adenosinergic protection with age) suggest a PKC-independent A1-mediated protection path may be preserved with aging, since A1 receptors continue to offer some protection while PKC activation does not. It is possible the failure of exogenous adenosine to offer protection in aged hearts may result from a lesion at or downstream of PKC.
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Willems, Laura E. "Adenosine and Ischaemia in Young To Aged Hearts". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365196.

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Ischaemic heart disease is a major contributor to premature death and heart failure in the Westernised world. Ischaemic injury within the heart may be beneficially modulated by the nucleoside adenosine. Derived from catabolism of ATP, adenosine was initially known as a potent bradycardic and hypotensive agent. However, more recently the protective function of adenosine has been investigated. The protective effects of adenosine are mediated via activation of adenosine receptors: A1, A2A, A2B, and A3 receptors. Activation of these potentially protective (or retaliatory) adenosine receptors hinges upon accumulation of adenosine during ischaemia-reperfusion. This Thesis examines the role and mechanisms of adenosine mediated cardioprotection in young and aged hearts, exploring endogenous and exogenous adenosine receptor activation, genetic manipulation of A1 receptors and adenosine deaminase and pharmacological manipulation of adenosine metabolism. The effects of age on ischaemic responses and adenosine handling and protection are also assessed. The core approach to assess each of the above issues involved the Langendorff isolated mouse heart preparation. Experiments within Chapter 3 focuses on the contractile effects of adenosine receptors in normoxic hearts. This study indicates A2A receptors have no direct effect on contractility, while adenosine exerts positive inotropy independently of coronary flow and perfusion pressure (i.e. Independent of the Gregg phenomenon). In addition, investigations in genetically modified hearts hint at positive inotropy in response to A1 receptors. Since the latter is only evidenced in modified lines, it is possible A1-mediated inotropy may be abnormal or supraphysiological. In Chapter 4 the impact of genetic 'deletion' of A1ARs and/or adenosine deaminase (ADA) on intrinsic tolerance to ischaemia were studied. Data demonstrate that genetic deletion of A1 receptors significantly limits the ability of the mouse myocardium to withstand injury during ischaemic insult. Thus, providing strong support for a role of A1ARs in determining intrinsic tolerance to ischaemia-reperfusion. ADA KO mice confirm protection afforded by endogenous adenosine and the notion of adenosine metabolism modification as a protective strategy. Interestingly, effects of A1AR KO differ from A1AR overexpression or A1AR agonism in that the latter decrease contractile diastolic dysfunction while A1AR KO selectively increase systolic dysfunction and increase oncosis without altering diastolic injury. This challenges current dogma regarding the action of A1 adenosine receptors on ischaemic injury. In Chapter 5 the effects of adenosine metabolism inhibition (via adenosine deaminase (ADA) and adenosine kinase (AK) inhibitors) were studied. Inhibition of adenosine deaminase with the drug EHNA, and adenosine phosphorylation with iodotubercidin significantly protected mouse hearts from ischaemia-reperfusion, reducing contractile dysfunction and cardiac enzyme efflux. However, inhibitors failed to improve the outcome of the aged myocardium. 8-SPT and 5-HD reduced the protective effects of EHNA and iodotubercidin demonstrating thus; cardioprotection via ADA and AK appears to rely on adenosine receptor activation and involves a mitoK ATP dependent mechanism. Since aging is of considerable importance with regard to outcomes of ischaemic heart disease, experiments in Chapter 6 focused on effects of aging (and gender) on cardiovascular function and injury during ischaemia-reperfusion. In assessing post ischaemic outcomes in hearts from young adult (2-4 months), mature adult (8 months), middle aged (12 months), aged (18 months) and senescent (24-28 months) C57/BL/6J mice, data reveal a substantial age-related decline in ischaemic tolerance (which appears selective for myocardial vs. vascular injury). The decline in ischaemic tolerance is expressed primarily within the initial 12 months in both males and females with relatively little further decline with continued aging. There is evidence of a modest improvement in tolerance in senescence vs. aged hearts possibly reflecting selection of a protected phenotype in senescent populations. In addition, mature and middle-aged female hearts showed improved tolerance to ischaemia-reperfusion compared to males, supporting a role for hormonal changes. Effects of aging and purine metabolism were studied in Chapter 7. Data suggest impaired tolerance to ischaemia-reperfusion in older hearts may stem in part from shifts in myocardial purine catabolism. Data reveal reduced accumulation of salvageable and cardioprotective adenosine and enhanced accumulation of poorly salvaged (and potentially injurious) hypoxanthine and xanthine. These changes may potentially predispose the aged myocardium to ischaemic injury and radical generation via the xanthine oxidase reaction. The final data Chapter of this Thesis describes preliminary data regarding aging, signalling and adenosine mediated protection. It was found that protein kinase C (PKC) and A1 receptors mediate protection in young hearts and also that A1 receptors appear to mediate protection via a PKC LindependentLi signalling cascade. In addition, experiments in aged hearts (attempting to elucidate mechanisms behind impaired adenosinergic protection with age) suggest a PKC-independent A1-mediated protection path may be preserved with aging, since A1 receptors continue to offer some protection while PKC activation does not. It is possible the failure of exogenous adenosine to offer protection in aged hearts may result from a lesion at or downstream of PKC.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Full Text
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Gaskin, F. Spencer. "Mechanisms of adenosine monophosphate-activated protein kinase-induced preconditioning in ischemia/reperfusion". Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/4805.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2007.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "August 2007" Includes bibliographical references.
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Fedele, Denise E. "Adenosine Kinase: a key regulator of hippocampal inhibition, seizure susceptibility, and neuronal development /". Zürich : ETH, 2006. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=16609.

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Shah, Mittal. "The role of 5' adenosine monophosphate-activated protein kinase (AMPK) in bone physiology". Thesis, Royal Veterinary College (University of London), 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.559073.

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Książki na temat "Adenosine kinase"

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Lai, Patrick F. H. Enterocytic differentiation and cyclic adenosine monophosphate-dependent protein kinase activity in the human colonic carcinoma cell line, Caco-2. Ottawa: National Library of Canada, 1995.

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Alaimo, Darrick James. Hepatic insulin receptor tyrosine kinase activity in diabetes: Modulation by assorted adenosine triphosphatases/phosphatases which copurify in partially purified preparations of the insulin receptor. [s.l: s.n.], 1992.

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Juranka, Peter Frank. Genetic and biochemical analysis of adenosine kinase in mammalian cells. 1986.

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Therapeutic Kinase Inhibitors. Springer, 2012.

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Neuber, Evelyn I. The effect of steroid hormones, dibutyryl cAMP, and a protein kinase C inhibitor on mouse oocyte maturation in vitro. 1990.

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Schmidt, Ulrike. Secondary Messenger Systems in PTSD. Redaktorzy Israel Liberzon i Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0014.

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Second messengers such as cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP), inositoltriphosphate, and diacylglycerol (DAG) are a prerequisite for the signal transduction of extracellular receptors. The latter are central for cellular function and thus are implicated in the pathobiology of a variety of disorders, such as schizophrenia, bipolar disorder, major depression, and post-traumatic stress disorder (PTSD). This chapter focuses on the involvement of second messenger molecules and their regulators as direct targets in human and animal PTSD and aims to stimulate the underdeveloped research in this field. The synthesis of literature reveals that second messengers clearly play a central role in PTSD-associated brain regions and processes. In particular, pituitary adenylate cyclase-activating polypeptide (PACAP), an important regulator of intracellular cAMP levels, as well as protein kinase c, the major target of DAG, belong to the hitherto most promising PTSD candidate molecules directly involved in second messenger signaling.
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Części książek na temat "Adenosine kinase"

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Schomburg, Dietmar, i Dörte Stephan. "Adenosine kinase". W Enzyme Handbook 13, 663–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-59176-1_131.

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Park, Jaoek, i Radhey S. Gupta. "Adenosine Metabolism, Adenosine Kinase, and Evolution". W Adenosine, 23–54. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_2.

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Böning, Dieter, Michael I. Lindinger, Damian M. Bailey, Istvan Berczi, Kameljit Kalsi, José González-Alonso, David J. Dyck i in. "Adenosine 5′-Monophosphate-Activated Protein Kinase". W Encyclopedia of Exercise Medicine in Health and Disease, 18. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4023.

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Mimouni, Mohsine, Françoise Bontemps i Georges Van den Berghe. "Production of Adenosine and Nucleoside Analogues by an Exchange Reaction Catalyzed by Adenosine Kinase". W Purine and Pyrimidine Metabolism in Man VIII, 613–16. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2584-4_127.

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Smolenski, Ryszard T., Kameljit Kalsi, Marek Zych, Zdzislaw Kochan i Magdi H. Yacoub. "Effects of Adenine/Ribose Supply on Adenosine Production and ATP Concentration in Adenosine Kinase Inhibited Cardiac Cells". W Advances in Experimental Medicine and Biology, 385–88. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5381-6_77.

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Hurley, Mary C., Bertha Lin i Irving H. Fox. "Regulation of Deoxyadenosine and Nucleoside Analog Phosphorylation by Human Placental Adenosine Kinase". W Purine and Pyrimidine Metabolism in Man V, 141–49. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1248-2_22.

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Leung, Susanna C. S., Diantha Smith, Ronan Chen, John A. McCallum, Marian McKenzie i Michael T. McManus. "Characterization of Adenosine 5′-Phospho-Sulfate Kinase (APSK) Genes from Higher Plants". W Sulfur Metabolism in Plants, 67–70. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4450-9_8.

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Marala, Ravi B., i S. Jamal Mustafa. "Modulation of protein kinase C by adenosine: Involvement of adenosine A1 receptor-pertussis toxin sensitive nucleotide binding protein system". W Signal Transduction Mechanisms, 51–58. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2015-3_6.

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Fredholm, Bertil B., Pär Gerwins, Jean W. Assender i Eva Irenius. "Regulation of Phospholipases C and D, Calcium, and Protein Kinase C by Adenosine A1 Receptors". W Adenosine and Adenine Nucleotides: From Molecular Biology to Integrative Physiology, 103–12. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2011-5_13.

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Fu, Nai-Wu, Shu-Yong Yeh, Chin Chang, Xiu-Hua Zhao i Li-Sung Chang. "Photosensitization of Mitochondrial Adenosine-Triphosphatase and Adenylate Kinase by Hematoporphyrin Derivative in Vitro". W Methods in Porphyrin Photosensitization, 161–67. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2165-1_19.

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Streszczenia konferencji na temat "Adenosine kinase"

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Guerreiro Souzedo, Gabriela, LJUBICA TASIC i Caio Henrique Nasi De Barros. "Synthesis of Quinazoline Derivatives for Adenosine Kinase Inhibition". W XXV Congresso de Iniciação Cientifica da Unicamp. Campinas - SP, Brazil: Galoa, 2017. http://dx.doi.org/10.19146/pibic-2017-78452.

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Creighton, Judy R., Sarah L. Sayner, Mikhail F. Alexeyev i Paul Insel. "Adenosine Monophosphate Kinase (AMPK) Promotes Lung Endothelial Barrier Repair". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3434.

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Creighton, Judy. "Adenosine Monophosphate-Activated Kinase (AMPK) Contributes To A Vascular Protective Hypoxic Response Mechanism". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5495.

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Maciaszek, J. L., B. Andemariam i G. Lykotrafitis. "Red Blood Cell Surface Receptor Expression of BCAM/Lu is Regulated by Protein Kinase A Activity". W ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14311.

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Irregular sickle red blood cells (RBCs) can contribute to the pathogenesis of vasoocclusion and other complications of sickle cell disease (SCD) via abnormal adherence to the vascular endothelium. It has previously been demonstrated that epinephrine enhances SCD RBC adhesion by activating the BCAM/Lu and ICAM-4 surface receptors [1–2]. Epinephrine acts on the RBC β2-adrenergic receptor, thereby activating Gas proteins that stimulate adenylyl cyclase (AC). This enzyme catalyzes the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP), leading to protein kinase A (PKA) activation, an intermediate step in the upregulation of BCAM/Lu and ICAM-4 mediated adhesion. The interaction of BCAM/Lu with the α5 chain of laminin may contribute to vaso-occlusive events in SCD due to overexpression of BCAM on SCD RBCs.
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Fox, M., K. Phoenix, F. Vumbaca, K. Vernier i K. Claffey. "The Role of Adenosine Monophosphate-Activated Kinase α2 as a Putative Tumor Suppressor in Breast Cancer." W Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-3153.

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Lopez, Roxanne L., Dorothy Dean i Sushmita Nandy. "Abstract PS17-59: Comparative study of breast tumors with differential expression of intracellular energy sensor adenosine monophosphate kinase". W Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-ps17-59.

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Stinson, R., S. Atkinson, A. H. Morice i L. Sadofsky. "Calcium/Calmodulin-Dependent Protein Kinase II (CaMKII) Mediates Adenosine Triphosphate (ATP) Release Following Hypotonic Stimulation of Airway Epithelial Cells". W American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3255.

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Hopple, Sara, Mark Bushfield, Fiona Murdoch i D. Euan MacIntyre. "REGULATION OF PLATELET cAMP FORMATION BY PROTEIN KINASE C". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644512.

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Exogenous synthetic 1,2-diacylglycerols (e.g. 1,2-dioctanoylglycerol, DiC8) and 4β Phorbol esters (e.g. phorbol myristate acetate, PMA) routinely are used to probe the effects of protein Kinase C (PKC) on cellular responsiveness. Such agents act either independently or synergistically with elevated [Ca2+]i to induce platelet activation, but also inhibit agonist-induced inositol lipid metabolism and Ca2+ flux. These findings led to the concept that activated PKC can function as a bi-directional regulator of platelet reactivity. Therefore, DiCg and PMA were utilized to examine the effects of activated PKC on receptor-mediated stimulation and inhibition of adenylate cyclase, as monitored by cAMP accumulation. All studies were performed using intact human platelets in a modified Tyrodes solution, and cAMP was quantified by radioimmunoassay. Pretreatment (2 min.; 37°C) of platelets with PMA (≤ 300 nM) but not DiCg (200 μM) attenuated the elevation of platelet cAMP content evoked by PGD2 300 nM) but not by PGE1 (≤300 nM), PGI2 (≤100 nM) or adenosine (≤ 100 μM).These effects of PMA were unaffected by ADP scavengers, by Flurbiprofen (10 μM) or by cAMP phosphodiesterase inhibitors (IBMX, 1 mM) but were abolished by the PKC inhibitor Staurosporine (STP, 100 nM). In contrast, DiC8 (200 μM), but not PMA ( ≤ 300 nM), reduced the inhibitory effect of adrenaline (5 μM) on PGE1 (300 nM)-induced cAMP formation. This effect of DiCg was unaltered by STP (100 nM). Selective inhibition of PGD2-induced cAMP formation by PMA most probably can be attributed to PKC catalysed phosphorylation of the DP receptor. Reduction of the inhibitory effect of adrenaline by DiC8 could occur via an action at the α2 adrenoreceptor or Ni. These differential effects of PMA and DiC8 may result from differences in their distribution or efficacy, or to heterogeneity of platelet PKC.
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Ibe, Joyce Christina F., Guofei Zhou, Qiyuan Zhou, Tianji Chen i J. Usha Raj. "Adenosine Monophosphate-Activated Protein Kinase ±2 Is Critical For The Survival Of Human Pulmonary Artery Smooth Muscle Cells During Hypoxia". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2612.

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Torres Acosta, M. A., S. Weinberg, L. Morales-Nebreda, K. Helmin, A. M. Joudi i B. D. Singer. "Regulatory TCell-Specific Loss of Adenosine Monophosphate Protein Kinase (AMPK) Impairs Suppressive Function and Potentiates Immune Response to B16 Melanoma Tumors". W American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1270.

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