Dissertations / Theses on the topic '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.
Full textYang, 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.
Full textKong, 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/.
Full textDahlstedt, 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/.
Full textWang, 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.
Full textTitle 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
Willems, Laura E., and 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.
Full textWillems, Laura E. "Adenosine and Ischaemia in Young To Aged Hearts." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365196.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Full Text
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.
Full textThe 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.
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.
Full textShah, 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.
Full textRaslan, Zaher. "Characterisation of cyclic adenosine monophosphate/protein kinase A signalling networks in blood platelets." Thesis, University of Hull, 2012. http://hydra.hull.ac.uk/resources/hull:6431.
Full textNadal, Magriñà Laura. "Muscarinic, adenosine and tropomyosin-related kinase B receptors modulate the neuromuscular developmental synapse elimination process." Doctoral thesis, Universitat Rovira i Virgili, 2017. http://hdl.handle.net/10803/441749.
Full textEl desarrollo del sistema nervioso periférico implica una inicial exuberante producción de neuronas y, una posterior reducción dependiente de actividad del número de sinapsis en las uniones neuromusculares (NMJ). Este proceso se denomina eliminación sináptica. Al final de la segunda semana postnatal, cada fibra muscular esta inervadas por una solo motoneurona. Los receptores muscarínicos de acetilcolina (mAChR), los receptores de adenosina (AR) y el receptor quinasa de tropomiosina B (TrkB) podrían permitir la competición entre los terminales nerviosos durante el proceso de eliminación sináptica mediante la modulación en la liberación de acetilcolina. En esta tesis se ha investigado, mediante microscopía confocal y un análisis morfológico cuantitativo, el papel de los receptores mAChRs (M1, M2 y M4), de los receptores de adenosina (A1 y A2A) y del receptor TrkB en el del proceso de eliminación en el desarrollo de la NMJ. Los resultados muestran que los receptores mAChRs, AR y el receptor TrkB promueven una desconexión axonal al inicio de la segunda semana postnatal independientemente de la maduración de los receptores de acetilcolina postsinápticos. En resumen, los receptores mAChRs, AR y el receptor TrkB retrasan el proceso de eliminación sináptica en P7 pero lo aceleran en P9. En la cooperación de estos receptores, se ha demostrado que M4 produce un efecto oclusivo sobre M1 y aditivo sobre A1 en P7. La cooperación entre M1, A1 y A2A promueve la pérdida axonal en P9, mientras que M2 es independiente de los otros receptores. M1 y TrkB cooperan para incrementar la pérdida axonal en P9 independientemente de M2 y TrkB. En conclusión, la eliminación sináptica postnatal está regulada por un mecanismo que depende de varios receptores, involucrando la cooperación de diferentes subtipos de receptores muscarínicos, de adenosina y el receptor TrkB, los cuales garantizan la monoinnervación de las sinapsis neuromusculares al final del proceso. saludable.
The development of the peripheral nervous system involves an initially exuberant production of neurons and a subsequent activity-dependent reduction in the number of synapses at the neuromuscular junctions (NMJ). This process is called synaptic elimination. At the end of the first postnatal week, each muscle fiber is innervated by a single motoneuron. Muscarinic acetylcholine receptors (mAChR), adenosine receptors (AR) and the tropomyosin-related kinase B (TrkB) receptor may allow the direct competition between nerve endings during synapse elimination through the modulation of acetylcholine release. Here, it has been investigated by confocal microscopy and quantitative morphological analysis the involvement of the individual and synergic or oclusive effect of M1-, M2- and M4-subtypes of mAChRs, A1 and A2A of ARs and TrkB in the control of the axonal elimination in developing NMJ. The results show that mAChRs, ARs and TrkB promote axonal disconnection at the beginning of the second postnatal week without affecting the postsynaptic maturation of the nicotinic receptor cluster. In summary, mAChRs, ARs and TrkB delay axonal loss at P7 but accelerate it at P9. In terms of receptor cooperation, M4 produces some occlusion of the M1 pathway and some addition to the A1 pathway at P7. The cooperation between M1, A1 and A2A receptors promotes axonal loss at P9, whereas the effect of M2 is independent of the other receptors. M1 and TrkB receptors work together to increase axonal loss rate at P9 but the effect of M2 is largely independent of the TrkB receptor. In conclusion, postnatal synapse elimination is a regulated multireceptor mechanism involving the cooperation of several muscarinic, adenosine and TrkB receptor subtypes that guarantees the monoinnervation of the neuromuscular synapses in the end of the process.
Qiu, Jiehua [Verfasser], and Ulrich [Akademischer Betreuer] Pohl. "5’-adenosine monophosphate-activated protein kinase (AMPK) modulates myoendothelial junctions / Jiehua Qiu ; Betreuer: Ulrich Pohl." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1155097319/34.
Full textMurphy, Cody. "Transregulation of Cardiac Ischaemic Tolerance and Stress Kinase Signalling by A1 Adenosine and ¿-Opioid Receptors." Thesis, Griffith University, 2018. http://hdl.handle.net/10072/382690.
Full textThesis (Masters)
Master of Medical Research (MMedRes)
School of Medical Science
Griffith Health
Full Text
Ng, Fung-kei, and 吳鋒奇. "The influence of a protein kinase A inhibitor on interstitial adenosine of muscle at rest and during contraction." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B45830708.
Full textGoto, Ayumi. "Effects of acute heat stress on glucose metabolism and 5' adenosine monophosphate-activated protein kinase in skeletal muscle." Kyoto University, 2016. http://hdl.handle.net/2433/215632.
Full text0048
新制・課程博士
博士(人間・環境学)
甲第19806号
人博第777号
新制||人||187(附属図書館)
27||人博||777(吉田南総合図書館)
32842
京都大学大学院人間・環境学研究科共生人間学専攻
(主査)教授 林 達也, 教授 森谷 敏夫, 教授 石原 昭彦
学位規則第4条第1項該当
Qamar, Raheel. "Dependence of the Kinetic Mechanism of Adenosine 3',5'-Monophosphate Dependent Protein Kinase Catalytic Subunit in the Direction of Magnesium Adenosine 5'-Diphosphate Phosphorylation on pH and the Concentration of Free Magnesium Ions." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc277956/.
Full textBarnes, Brian R. "AMP-activated protein kinase : the connection between exercise and type II diabetes /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-165-2/.
Full textRodrigues, Fábio Henrique dos Santos 1986. "Derivados de quinazolinas na inibição da adenosina quinase." [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/248424.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Química
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Resumo: A Adenosina Quinase (ADK) é uma enzima importante (EC 2.7.1.20), cuja ação pode estar relacionada a diversas doenças, tais como inflamações, derrame, infarto, entre outras. Desse modo, a inibição de sua atividade é de grande importância, e desperta interesse científico. Na tentativa de inibir a ação da ADK, houve busca por compostos orgânicos cuja capacidade inibitória seja superior comparando-se com inibidores da ADK existentes. Desse modo, derivados de 4-anilinoquinazolinas mostraram-se alvos interessantes. Foi sintetizada uma série de 22 derivados de 8-metóxi-4-anilinoquinazolinas, substituídas nas posições 3'e 4'do anel anilínico. Os compostos sintetizados foram caracterizados e testados frente à ADK, de forma a verificar seu potencial inibitório, principalmente através da técnica de fluorescência de emissão. Da série de compostos, seis apresentaram-se promissores na inibição da ADK. Ensaios in silico também foram realizados, buscando-se uma melhor compreensão do mecanismo de inibição do sistema compostos/ADK
Abstract: The Adenosine Kinase (ADK) is an important enzyme (EC 2.7.1.20) that might be related to several diseases, such as inflammation, stroke and infarct, and many others. Therefore, its activity inhibition is of great importance, arising significant scientific interest. Aiming ADKs inhibition, a search for suitable organic species was realized, in such way that 4-anilinoquinazoline derivatives showed themselves interesting targets. A serie of 22 8-methoxy-4-anilinequinazoline derivatives, substituted on the aniline ring at 3'and 4'positions, was synthesized. The compounds were characterized and tested in in vitro ADKs inhibition, in order to verify their inhibitory potentials, mainly applying emission fluorescence technique. Six compounds of this serie presented promising properties in ADKs inhibition. In silico assays were also conducted, in order to better explain the inhibitory mechanism of the system compounds/ADK
Mestrado
Quimica Organica
Mestre em Química
Long, Yun Chau. "Skeletal muscle metabolic flexibility: the roles of AMP-activated protein kinase and calcineurin /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-152-4/.
Full textMelemedjian, Ohannes, Marina Asiedu, Dipti Tillu, Raul Sanoja, Jin Yan, Arianna Lark, Arkady Khoutorsky, et al. "Targeting adenosine monophosphate-activated protein kinase (AMPK) in preclinical models reveals a potential mechanism for the treatment of neuropathic pain." BioMed Central, 2011. http://hdl.handle.net/10150/610214.
Full textFattori, Ana Carolina Maragno. "Efeitos da imunização com Adenosina Quinase (AK) e Hipoxantina-Guanina Fosforibosiltransferase (HGPRT) recombinantes de Schistosoma mansoni : controle da infecção murina." Universidade Federal de São Carlos, 2016. https://repositorio.ufscar.br/handle/ufscar/7924.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
The mansoni schistosomiasis is the most important of human helminthiasis. Despite advances in its control this disease continues to spread to new geographical areas. It currently affects more than 250 million people. However, limited options are available for and Praziquantel is the drug of choice. Various authors have been searching new drugs and vaccines to control schistosomiasis. This study aimed to evaluate the effects of a prior immunization with recombinant enzymes of Schistosoma mansoni: Adenosine Kinase (AK) and Hypoxanthine-guanine Phosphoribosyltransferase (HGPRT), which are important for parasite purine metabolism, as well as a MIX of these enzymes, and subsequent challenge with cercariae of the parasite in the control of murine infection. Female Balb/c mice were divided into 5 groups. The groups were enzyme-immunized in three doses and 15 days after the last immunization, animals were infected with S. mansoni. After infection in the 47º day egg count were carried in mice faeces and in the 48º day mice were sacrificed for evaluation of leukocyte numbers (blood and peritoneal cavity), worm burden, antibodies production, cytokines quantification and histopathological analysis of the liver of these animals. Our results strongly suggest that, immunization with a MIX originated in these animals reduction in the number of eggs in faeces by 46% when compared with the animals of the infected group. Animals of the groups immunized with AK, HGPRT and/or MIX seem to induce a reduction in the number of eosinophils in the peritoneal cavity when compared to the animals of the infected group. Concerning worm burden, the animals of the MIX group presented greater reduction (31.27%) when compared to the animals of the infected group. The animals of the immunized groups, AK, HGPRT and/or MIX were capable of producing IgG1 antibodies and IgE anti the enzymes and anti the parasite proteins. The animals of the immunized group MIX showed a slight increase in IL-4 production and observed reduction of IL-10, and in the HGPRT group induced a slight increase on IFN-γ production when in compared with the infected group. In addition, the animals of the AK group showed a decrease in the number of hepatic granulomas in tissue (44,55%) and the eggs present in liver (42,31%). Therefore, it suggests that immunization with these enzymes can contributes to schistosomiasis control, as well as it might helps to modulate experimental infection inducing reduction of physiopathology of this parasitosis.
A esquistossomose mansônica é a mais importante das helmintíases humanas. Apesar dos avanços no seu controle continua se espalhando para novas áreas geográficas. Atualmente afeta mais de 250 milhões de pessoas. Entretanto, opções limitadas estão disponíveis para o tratamento da doença e o único fármaco de escolha é o Praziquantel. Assim, vários estudos têm sido propostos para encontrar novos fármacos e vacinas para combater a esquistossomose. Dessa forma, o presente estudo teve como proposta avaliar os efeitos da imunização prévia com as enzimas recombinantes de Schistosoma mansoni Adenosina Quinase (AK) e Hipoxantina-Guanina Fosforibosiltransferase (HGPRT), que participam do metabolismo de purinas do parasito, bem como com o MIX das duas enzimas, e posterior desafio com cercárias do parasito, para o controle da infecção murina. Camundongos fêmea Balb/c foram divididos em 5 grupos. Os grupos imunizados receberam três doses das enzimas e após 15 dias da última imunização, os animais foram infectados com S. mansoni. Após a infecção, no 47° dia foi realizada a contagem de ovos nas fezes e no 48° dia foi realizada a eutanásia dos animais para avaliação de resposta leucocitária (sangue e lavado da cavidade peritoneal), carga parasitária, produção de anticorpos, quantificação de citocinas e análise histopatológica do fígado desses animais. Os resultados demonstraram que, a imunização com o MIX promoveu nesses animais redução do número de ovos nas fezes de 46% quando comparado com os animais do grupo somente infectado. Os animais dos grupos imunizados com AK, HGPRT e/ou MIX apresentaram diminuição na quantidade de eosinófilos na cavidade peritoneal quando comparados com os animais do grupo somente infectado. Em relação à carga parasitária, os animais do grupo imunizado com o MIX apresentaram maior redução (31,27%) quando comparados aos animais do grupo somente infectado. Os animais dos grupos imunizados com AK, HGPRT e/ou MIX foram capazes de produzir anticorpos IgG1 e IgE anti as enzimas e anti as proteínas do parasito. Os animais do grupo imunizado com o MIX apresentaram aumento discreto de IL-4 e foi observada redução de IL-10, e no grupo imunizado com HGPRT houve aumento discreto de IFN-γ, quando comparados com os animais do grupo somente infectado. Além disso, os animais do grupo imunizado com AK apresentaram redução do número de granulomas hepáticos (44,55%) e de ovos no fígado (42,31%), quando comparados com o grupo somente infectado. Assim, sugere-se que a imunização com essas enzimas pode contribuir para o controle da esquistossomose, bem como auxiliar na modulação da infecção experimental, induzindo redução da fisiopatologia desta parasitose.
Robinson, Alexander John. "Stimulation of the mitogen-activated protein kinase (MAPK) pathway in DDTâ‚MF-2 cells by adenosine Aâ‚ receptors and histamine Hâ‚ receptors." Thesis, Nottingham Trent University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252331.
Full textSanders, Charles Ray. "Examination of the relationship of substrate dynamics to enzymic structure, binding energy, and catalysis: NMR studies of adenosine 5'-triphosphate and adenylate kinase /." The Ohio State University, 1988. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487597424137198.
Full textAhmed, Ishtiaq. "Structural studies of Vps4 protein complexes." Thesis, Griffith University, 2022. http://hdl.handle.net/10072/412412.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Pharmacy & Med Sci
Griffith Health
Full Text
Marais, Erna. "Role of cyclic adenosine monophosphate (cAMP), cyclic guanosine monophosphate (cGMP) and p38 mitogen activated protein kinase (p38 MAPK) in preconditioning of the ischaemic myocardium." Thesis, Stellenbosch : Stellenbosch University, 2002. http://hdl.handle.net/10019.1/53039.
Full textENGLISH ABSTRACT: Ischaemic preconditioning (PC) is the phenomenon whereby a short episode of coronary occlusion followed by reperfusion protects the myocardium against a subsequent period of prolonged (also called index or sustained) ischaemia. Even though the exact mechanism of PC remains to be established, it implies that the heart has an endogenous protective mechanism against ischaemia which, if identified, may have important clinical implications. The importance of establishing the mechanism of PC lies in the potential to convert this biological phenomenon into a therapeutic modality to be used clinically. If mediated by certain components of a signal transduction pathway, such a goal will be achievable. Several triggers and signal transduction pathways have been implicated in the mechanism of protection induced by PC: for example, receptor-dependent endogenous triggers (such as adenosine and opioids) and receptor-independent endogenous triggers (such as free radicals and calcium). However, the involvement of both the ~-adrenergic signalling pathway as well as nitric oxide (NO) in PC has not been defined. It has been suggested that all triggers are linked to a common final pathway, for example, activation of protein kinase C (PKC) and/or the mitogen-activated kinases (MAPKs), in particular p38 MAPK. However, the role of the latter is still controversial. The aim of this study was to: (A) characterize changes in the cyclic nucleotides, cAMP and cGMP, and p38 MAPK occurring during the entire experimental procedure in an attempt to gain insights into the possible mechanisms involved in ischaemie PC (Chapter 3); (8) establish the significance of the changes observed in cAMP and cGMP by pharmacological manipulation of their respective pathways (Chapters 4 and 5); (C) establish the role of p38 MAPK in ischaemie PC: trigger or mediator involvement (Chapter 6). Isolated perfused working rat hearts were preconditioned by 3 x 5 min global ischaemia, interspersed by 5 min reperfusion, followed by 25 min global ischaemia and 30 min reperfusion. Functional recovery during reperfusion was used as end-point. Hearts were freeze-clamped at different times during the PC protocol, sustained ischaemia, as well as during reperfusion. Tissue cyclic nucleotides (cAMP and cGMP), cyclic nucleotide phosphodiesterase (cAMP- and cGMP-PDE) activities, adenylyl cyclase and protein kinase A activities and p-adrenergic receptor characteristics were determined. p38 MAPK activation was also assessed by Western blotting, using dual phospho-p38 MAPK (Thr180ITyr182) antibody as well as activating transcription factor 2 (ATF2) activation. In addition, to evaluate the role of p38 MAPK in PC protection, the effect of inhibition of p38 MAPK activation, by 8B203580, was determined in adult isolated rat cardiomyocytes as well as in isolated perfused rat hearts. Based on the results obtained, it is proposed that during a multi-cycle ischaemie PC protocol triggers (presumably endogenous catecholamines and NO) are released which induce cyclic changes in cyclic nucleotides, cAMP and cGMP. Both these cyclic nucleotides transiently activate the downstream stress kinase, p38 MAPK, which may trigger further downstream adaptive processes. Furthermore, the sustained ischaemic period of PC hearts was characterized by attenuated cAMP and elevated cGMP levels, as well as attenuated activation of p38 MAPK, which was associated with cardioprotection. In addition, pharmacological attenuation of p38 MAPK activation during sustained ischaemia led to functional recovery. It is concluded that the cardioprotection of PC is due to attenuation of ischaemia-induced p38 MAPK activation. Pharmacological manipulation of this kinase should be considered as a therapeutic modality in the future.
AFRIKAANSE OPSOMMING: Isgemiese prekondisionering (PK) verwys na die verskynsel waardeur 'n kort, verbygaande episode van isgemie gevolg deur herperfusie, die miokardium teen 'n daaropvolgende langdurige periode van isgemie beskerm. Die presiese meganisme van beskerming van PK moet nog opgeklaar word, maar dit impliseer dat die hart oor 'n endogene beskermingsmeganisme beskik wat, indien geïdentifiseer, belangrike kliniese implikasies mag hê. Die belang van opklaring van die meganisme van PK lê daarin dat 'n biologiese verskynsel in 'n terapeutiese modaliteit vir kliniese gebruik, omgeskakel kan word. Sou dit deur bepaalde komponente van 'n seintransduksiepad gemedieër word, is so 'n doel bereikbaar. Verskeie stimuli en seintransduksiepaaie is in PK betrokke: byvoorbeeld, reseptorafhanklike endogene stimuli (soos adenosien en opioïde), asook reseptor-onafhanklike endogene stimuli (soos vrye radikale en kalsium). Die betrokkenheid van die padrenerge seintransduksiepad asook stikstofoksied (NO) in PK egter nog nie behoorlik evalueer nie. Dit is voorgestel dat alle stimuli op 'n finale algemene pad uitloop, soos byvoorbeeld die aktivering van protein kinase C (PKC) en/of die mitogeen-geaktiveerde kinases (MAPKs), spesifiek die p38 MAPKs. Laasgenoemde se rol in PK is steeds kontroversieël. Die doel van die studie was dus: (A) karakterisering van die veranderinge in die sikliese nukleotiede, cAMP en cGMP, en p38 MAPK wat tydens die hele eksperimentele prosedure plaasvind, in 'n poging om meer insig te verkry aangaande moontlike meganismes betrokke in isgemiese PK (Hoofstuk 3); (8) bepaling van die belang van die waargenome veranderinge in cAMP en cGMP deur hulonderskeie paaie farmakologies te manipuleer (Hoofstukke 4 en 5); (C) bepaling van die rol van p38 MAPK in PK: betrokkenheid as stimulus of mediator (Hoofstuk 6). Geïsoleerde, geperfuseerde werkende rotharte is geprekondisioneer deur blootstelling aan 3 x 5 min globale isgemie, afgewissel met 5 min herperfusie, gevolg deur 25 min globale isgemie en 30 min herperfusie. Funksionele herstel tydens herperfusie is as eindpunt gebruik. Harte is op verskillende tye tydens die PK protokol, volgehoue isgemie, asook herperfusie gevriesklamp. Weefsel sikliese nukleotiede (cAMP en cGMP), die aktiwiteit van sikliese nukleotied fosfodiesterases (cAMP- en cGMP-PDE), adeniel siklase en protein kinase A (PKA) asook die eienskappe van die p-adrenerge reseptor is gemeet. p38 MAPK aktivering is met Westerse oordragtegnieke bepaal, deur van dubbel gefosforileerde p38 MAPK (Thr180fTyr182) antiliggame asook geaktiveerde transkripsie faktor 2 (ATF2) gebruik te maak. Die rol van p38 MAPK in PK beskerming is evalueer deur die effek van inhibisie van p38 MAPK aktivering met SB 203580, in volwasse geïsoleerde rot kardiomiosiete asook in geïsoleerde geperfuseerde rotharte, te bepaal. Na aanleiding van die resultate, is voorgestel dat, tydens 'n multi-siklus isgemie PK protokol, stimuli (moontlik endogene katekolamiene en NO) vrygestel word wat die sikliese veranderinge in sikliese nukleotiede, cAMP en cGMP, veroorsaak. Beide hierdie sikliese nukleotiede aktiveer die distale stres kinase, p38 MAPK, op 'n betekenisvolle, maar verbygaande manier. Hierdie kinase mag verdere distale aanpassingsprosesse stimuleer. Die volgehoue isgemiese periode van PK harte is gekenmerk deur verminderde cAMP en verhoogde cGMP vlakke, asook verminderde aktivering van p38 MAPK. Hierdie veranderinge is met beskerming van die hart teen isgemie geassosieer. Daarbenewens, farmakologiese vermindering van p38 MAPK aktivering tydens volgehoue isgemie het tot verbeterde funksionele herstel gelei. Die gevolgtrekking is gemaak dat die beskermende effek van PK die gevolg is van verminderde aktivering van isgemies-geïnduseerde p38 MAPK. Farmakologiese manipulasie van hierdie kinase moet in die toekoms as terapeutiese modaliteit oorweeg word.
Goaillard, Jean-Marc. "Étude de la modulation de conductances intrinsèques par la voie de l'adenosine monophosphate cyclique dans deux types de cellules excitables : action du récepteur beta2-adrénergique dans les cardiomyocytes ventriculaires de grenouille et du récepteur 5-HT7 dans les neurones intralaminaires thalamiques de rat." Paris 6, 2002. http://www.theses.fr/2002PA066159.
Full textSantos, Stephanie Cristine Carvalho dos. "Efeitos da 5-iodotubercidina em linhagens de melanoma humano parentais e resistentes ao inibidor de BRAF." Universidade de São Paulo, 2019. http://www.teses.usp.br/teses/disponiveis/9/9142/tde-18032019-150858/.
Full textMelanoma accounts for less than 5% of skin cancers, but 95% of deaths occur due to metastases. Metastatic melanoma is refractory to conventional therapies and rapidly acquires resistance to therapies such as oncogene-directed, such as the BRAF inhibitor, of the MAPK pathway. Previous studies of screening in silico of our group, using the databases TCGA and GEO, identified the adenosine kinase gene (ADK) as differentially expressed between invasive melanoma and nevus. 5-iodotubercidin (5-ITu) is a potent pharmacological inhibitor of ADK that among the several effects reported in the literature stands out for the genotoxic potential. DNA damage is the main activator of the cell cycle checkpoint, which leads to transient or permanent cell cycle arrest, in addition to inducing cell death, leading to the hypothesis that ADK may be a potential anti-melanoma agent. This work aimed to evaluate the expression of the ADK gene in human melanomas and chemoresistants to the BRAF inhibitor (iBRAF), evaluated the impacts of 5-ITu on proliferation, cell cycle progression and cell death and finally we evaluated its ability to increase the sensitivity of cells. Real-time PCR was performed to assess the levels of ADK mRNA expression in melanoma lines and primary melanocyte culture; in order to evaluate the cytotoxicity of 5-ITu, the trypan blue and apoptosis - Annexin V and PI exclusion and blue spheroid models were performed using live / dead; the influence of 5-ITu on the clonogenic capacity and its effects on cell proliferation, from the cell cycle assays and the evaluation of proliferation markers by immunofluorescence; the cell lines were submitted to different treatment regimens with 5-ITu and iBRAF in order to evaluate the growth curve and the sensitivity to iBRAF by MTT levels of mRNA expression of ADK higher in the tumor lines in relation to the melanocytes. 5-ITu was able to inhibit the proliferation (IC 50) of melanoma lines at concentrations of 1.9 to 3.5 181;M. 5-ITu was not able to induce cell non-viability, although it reduced the amount of viable cells in all treatment conditions, nor was it able to induce a significant increase in apoptotic or even necrotic cells. However, treatment with 5-ITu reduced the clonogenic capacity of melanoma cells and promoted cell cycle arrest in the G1 and G2 / M phases, leading to an increase in the subG1 population. Treatment with 5-ITu promotes the reduction of expression of proliferation markers, such as ki67, and the combination of 5-ITu and iBRAF treatments was able to increase the doubling time of melanoma cells, although it has been shown to be unable to sensitize melanoma cells to treatment with iBRAF. Thus, it can be concluded that 5-ITu induces the cytostatic effect and shows a potent antiproliferative agent for parental and resistant melanoma.
Matsumoto, João Paulo de Pontes. "Receptor A2a de adenosina: estudo da modulação da liberação de neurotransmissores em modelo in vitro." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-03042013-115748/.
Full textSynaptic transmission is a sine qua non process for nervous system physiology. Such precise process is accomplished in part due to modulation of neurotransmitter release. Adenosine is a putative synaptic transmission modulator. Moreover, adenosine A2a receptor facilitates neurotransmitter release in the Central Nervous System. The present study focuses on the modulation of neurotransmission by adenosine A2a receptor and its intracellular signaling pathway in in vitro model. Here, we provided evidence that adenosine A2a receptor agonist increases an optical biosynthetic sensor of synaptic vesicle release (supereclipct synapto-pHluorin), as well as glutamate and noradrenaline. Furthermore, it was demonstrated that cAMP-dependent protein kinase inhibitor abolished glutamate and norepinephrin increase, as well as synapsin I phosphorylation evoked by adenosine A2a receptor agonist. Therefore, our data suggest that adenosine A2a receptor activation modulates neurotransmitter release and synapsin I phosphorylation in cultured cells from medulla oblongata of Wistar rats, as well as cAMP-dependent protein kinase might be the modus operandi of this modulatory phenomenon
Choe, Jungwoo. "Structural and biochemical studies of trypanosomatid drug target proteins /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/9197.
Full textVodnala, Munender. "Targeting the nucleotide metabolism of the mammalian pathogen Trypanosoma brucei." Doctoral thesis, Umeå universitet, Institutionen för medicinsk kemi och biofysik, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-80904.
Full textTargeting the nucleotide metabolism of the mammalian pathogen Trypanosoma brucei.
Thomas, Julia Dominique Janine. "The characterisation of growth hormone-related cardiac disease with magnetic resonance imaging & The effects of growth hormone dysregulation on adenosine monophosphate-activated protein kinase in cardiac tissue." Thesis, Queen Mary, University of London, 2012. http://qmro.qmul.ac.uk/xmlui/handle/123456789/5391.
Full textRofougaran, Reza. "DNA precursor biosynthesis-allosteric regulation and medical applications." Doctoral thesis, Umeå : Univ, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1678.
Full textFijolek, Artur. "Salvage and de novo synthesis of nucleotides in Trypanosoma brucei and mammalian cells." Doctoral thesis, Umeå : Umeå University, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1850.
Full textShi, Yun. "KATP Channel Phosphorylation: Mechanisms and Contribution to Vascular Tone Regulation by Vasodilating and Vasoconstricting Hormones and Neurotransmitters." unrestricted, 2007. http://etd.gsu.edu/theses/available/etd-11302007-150810/.
Full textTitle from file title page. Chun Jiang, committee chair; Teryl Frey, Deborah Baro, Delon Barfuss, committee members. Electronic text (168 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed Jan. 30, 2008. Includes bibliographical references (p. 146-151).
Bertran-Gonzalez, Jesus. "Study of segregated signaling responses of striatonigral and striatopallidal neurons in BAC transgenic mice." Paris 6, 2009. http://www.theses.fr/2009PA066348.
Full textNakano, Masako. "α2 isoform-specific activation of 5' adenosine monophosphate-activated protein kinase by 5-aminoimidazole-4-carboxamide-1-β-D-ribonucleoside at a physiological level activates glucose transport and increases glucose transporter 4 in mouse skeletal muscle." Kyoto University, 2008. http://hdl.handle.net/2433/135919.
Full textLiu, Huaize [Verfasser], Thorsten Gutachter] Pfirrmann, Regine [Gutachter] [Heller, and Rüdiger [Gutachter] Horstkorte. "The GID-complex is a novel ubiquitin ligase involved in the regulation of adenosine monophosphate-activated protein kinase (AMPK) and the function of the primary cilium : [kumulative Dissertation] / Huaize Liu ; Gutachter: Thorsten Pfirrmann, Regine Heller, Rüdiger Horstkorte." Halle (Saale) : Universitäts- und Landesbibliothek Sachsen-Anhalt, 2020. http://d-nb.info/1218530421/34.
Full textCroset, Amélie. "Identification et caractérisation des mécanismes d'action des molécules appats, les SiDNA, dans l'inhibition des voies de réparation des cassures simple-brin." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T018.
Full textMost conventional cancer treatments, such as chemotherapy or radiotherapy, are cytotoxic and cause DNA damages in the tumoral treated cells, which ultimately lead to their death. However, several intrinsic and acquired resistances of tumors to these treatments are due to the tumor efficient DNA repair activities. One of the major early steps of DNA repair is the recruitment of repair proteins at the damage site and this is coordinated by a cascade of modifications controlled by sensor proteins such as DNA-dependent protein kinase (DNA-PK) and/or poly (ADP-ribose) polymerase (PARP). In this manuscript, we identify and characterize the mechanism of action of short interfering DNA molecules (siDNA), mimicking double-strand breaks (called Dbait) or single-strand breaks (called Pbait) in Single Strand Break Repair pathway (SSBR/BER) inhibition. We demonstrate that Dbait bound and induced both PARP and DNA-PK activities, whereas Pbait acts only on PARP. The comparative study of the two molecules allows analysis of the respective roles of the two signaling pathways: both molecules recruit proteins involved in single-strand break repair (such as PARP, XRCC1 and PCNA) and prevent their recruitment at chromosomal damage. Dbait, but not Pbait, also inhibits recruitment of proteins involved in double-strand break (DSB) repair. By these ways, Pbait and Dbait disorganized DNA repair, thereby sensitizing cells to treatments. SSB repair inhibition depends upon a direct trapping of the main proteins on both molecules and an indirect trapping in PAR polymers. DSB repair inhibition may be indirect, resulting from the phosphorylation of DSB repair proteins by activated DNA-PK. The DNA repair inhibition by both molecules is confirmed by their synthetic lethality with BRCA mutations tumoral cell lines. However, BRCA mutation could be sufficient but not necessary to induce breast cancer cell lines and tumors sensitivity to Dbait treatment. In fact, we demonstrate that Dbait molecules could also have a stand-alone effect in BRCA wild type cells with a high genetic instability. We found a correlation between DNA repair proteins basal level (ɣH2AX, PARP and PAR), DNA break basal level, presence of micronucleus (MN) and tumoral cell lines sensitivity to Dbait treatment. We hypothesis that this genetic instability, determined by MN in tumor biopsies, could be a predictive biomarker of Dbait stand-alone effect, not only in breast cancer treatment, but also in glioblastoma, melanoma, uveal melanoma and colon cancer treatment
Welshhans, Kristy. "Neuronal growth cone dynamics are regulated by a nitric oxide-initiated second messenger pathway." unrestricted, 2007. http://etd.gsu.edu/theses/available/etd-09282007-114034/.
Full textVincent Rehder, committee chair; Sarah Pallas, Walter William Walthall, committee members. Electronic text (248 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed Jan. 28, 2008; title from file title page. Includes bibliographical references (p. 218-248).
Romanello, Larissa. "Estudos das enzimas adenosina kinase e hipoxantinaguanina fosforibosiltransferase de Schistosoma mansoni." Universidade Federal de São Carlos, 2011. https://repositorio.ufscar.br/handle/ufscar/6981.
Full textUniversidade Federal de Minas Gerais
Schistosoma mansoni is the parasite responsible for schistosomiasis mansonica, a disease that affects about 207 million people worldwide, and does not have the purine de novo sinthetic pathway, depending entirely on the purine salvage pathway to supply its demands on purines. Adenosine kinase (AK) and Hypoxanthine-guanine phosphoribosyltransferase (HGPRT) are important enzymes of the purine salvage, the AK directly phosphorylates adenosine into adenosine monophosphate (AMP) and HGPRT is responsible for the reversible phosphorybosylation of hypoxanthine or guanine into IMP or GMP. The purine salvage pathway has been reported as a potential target for developing new drugs against schistosomiasis. The nucleotide coding region of the isoform 2 of AK enzyme was amplified and cloned into pGEM vector and pET28a, the recombinant protein was expressed in E.coli BL21 (DE3), purified in a his-tag nickel-affinity resin and AMP-agarose resin, tested for its activity and crystallized. Two data sets were obtained by X-ray diffraction: a ternary complex of AK2-AMP-adenosine in the MX2 light line of the Synchrotron Light National Laboratory and a binary complex AK2-tubercidin in the rotatory anode X-ray source of the Institute of Physics at Sao Carlos - USP, both at 2.3A of resolution. The nucleotide coding region of the enzyme HGPRT was also amplified, cloned into pGEM and pET28a, which heterologous expression was done in E.coli BL21 (DE3) cells at 18°C and purified on a cobalt his-tag affinitiy resin.
Schistosoma mansoni e o parasita responsavel pela esquistossomose mansonica, doenca que afeta cerca de 207 milhoes de pessoas em todo mundo, e nao possui a via de sintese de novo de purinas, dependendo integralmente da via de salvacao para seu suprimento de purinas. A adenosina kinase (AK) e a Hipoxantina-guanina fosforibosiltransferase (HGPRT) sao importantes enzimas desta via, sendo a AK responsavel pela fosforilacao direta de adenosina para adenosina monofosfato (AMP) e a HGPRT pela fosforibosilacao reversivel de hipoxantina ou guanina para IMP ou GMP respectivamente. Essa via tem sido citada como alvo potencial para o desenvolvimento de novos farmacos contra a esquistossomose. A regiao nucleotidica codificadora da enzima AK, isoforma 2, foi amplificada e clonada em vetor pGEM e pET28a, a proteina recombinante foi expressa em E.coli BL21 (DE3), purificada em coluna de niquel e AMP-agarose, submetida a ensaios de atividade e cristalizada. Dois conjuntos de dados foram obtidos por difracao de raio-X: um complexo ternario de AK2- AMP-adenosina na linha de luz MX2 do Laboratorio Nacional de Luz Sincrotron e um complexo binario de AK2-tubercidina no raio-X do Instituto de Fisica de Sao Carlos USP anodo rotatorio, ambos a 2.3A de resolucao. A regiao nucleotidica codificadora da enzima HGPRT tambem foi amplificada, clonada em pGEM e pET28a, sendo a proteina recombinante expressa em E.coli BL21 (DE3) a 18°C e purificada em coluna de cobalto.
Schulte, Gunnar. "Adenosine receptor signaling and the activation of mitogen-activated protein kinases /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-299-x/.
Full textJackel, Jamie Nicole. "GEMINIVIRUSES AS MODELS TO STUDY THE ESTABLISHMENT AND MAINTENANCE OF DNA METHYLATION." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1367494030.
Full textMundell, Stuart James. "Role of G protein-coupled receptor kinases in the desensitization of Aâ†2 adenosine receptor responses." Thesis, University of Bristol, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262810.
Full textBordes, Pastor Isabel. "Theoretical Studies of the Catalytic Mechanism of the Dihydroxyacetone Kinase." Doctoral thesis, Universitat Jaume I, 2017. http://hdl.handle.net/10803/436901.
Full textLas dihidroxiacetona quinasas (DHAKs) catalizan la transferencia del grupo fosfato desde el adenosin trifosfato (ATP) a la dihidroxiacetona (Dha), generando Dha fosfato (Dha-P), una especie importante para la formación de enlaces C-C en la naturaleza. Las quinasas están presentes en el cuerpo humano e involucradas en el cáncer, la inflamación y los desórdenes autoinmunes. En esta Tesis Doctoral, se ha estudiado el mecanismo de reacción de transferencia de fosfato desde el ATP a la Dha en disolución acuosa y en la DHAK de Escherichia coli empleando la metodología híbrida mecánica cuántica/mecánica molecular (QM/MM). Además, en colaboración con un grupo experimental de Madrid, se ha estudiado la modificación de la especificidad en la DHAK de Citrobacter freundii, desde el ATP al polifosfato inorgánico como dador de fosfatos, un compuesto con grandes ventajas. Se han analizado los efectos de unión de este compuesto con dicha enzima, además de estudiar la reacción química con la Dha.
Noriega, Esteban Núria. "The Rtg1 and Rtg3 proteins are novel transcription factors regulated by the yeast hog1 mapk upon osmotic stress." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7158.
Full textIn Saccharomyces cerevisiae the adaptation to high osmolarity is mediated by the HOG (high-osmolarity glycerol) pathway, which elicits different cellular responses required for cell survival upon osmostress. Regulation of gene expression is a major adaptative response required for cell survival in response to osmotic stress. At least five transcription factors have been reported to be controlled by the Hog1 MAPK. However, they cannot account for the regulation of all of the genes under the control of the Hog1 MAPK. Here we show that the Rtg1/3 transcriptional complex regulates the expression of specific genes upon osmostress in a Hog1-dependent manner. Hog1 phosphorylates both Rtg1 and Rtg3 proteins. However, none of these phosphorylations are essential for the transcriptional regulation upon osmostress. Here we also show that the deletion of RTG proteins leads to osmosensitivity at high osmolarity, suggesting that the RTG-pathway integrity is essential for cell survival upon stress.
Fernandes, Maria Fernanda de Andrade. "Modulação da AMP-activated protein kinase (AMPK) em hipotalamo de ratos wistar submetidos ao exercicio." [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309954.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: As proteínas AMPK e mTOR são as principais moduladoras do balanço energético intracelular, e exercem influência decisiva sobre a ação hipotalâmica da leptina. O exercício agudo, através da produção de IL-6, está associado ao aumento da sensibilidade à ação anorexigênica da leptina. Visando investigar a possível influência das vias AMPK e mTOR, neste aumento da sensibilidade hipotalâmica à leptina induzido pelo exercício agudo, ratos Wistar foram submetidos à natação e posteriormente receberam injeção intracerebroventricular de IL-6, ativadores e/ou inibidores da AMPK e mTOR. A IL-6 reduziu a ingestão alimentar dos animais não exercitados; no entanto, o pré-tratamento com ativador da AMPK ou inibidor da mTOR bloqueou esta ação da IL-6. Ativadores da AMPK aumentaram a ingestão alimentar de forma mais significativa nos animais não exercitados. Inibidores da AMPK reduziram a ingestão mais expressivamente nos animais exercitados. A injeção central de leptina reduziu a ingestão de ratos exercitados mais expressivamente do que foi observado nos animais controle. Tanto o pré-tratamento com inibidor da IL-6, como com ativador da AMPK ou inibidor da mTOR, reverteram esta ação da leptina. O exercício também está associado à redução da fosforilação da via da AMPK e à maior fosforilação da via da mTOR, no hipotálamo. A da resposta das vias em questão ao estímulo com leptina provavelmente seja um dos principais determinantes da modulação do set point hipotalâmico pelo exercício agudo
Abstract: AMP-activated protein kinase (AMPK) and mammalian Target of Rapamycin (mTOR) are key regulators of cellular energy balance and of the effects of leptin on food intake. Acute exerci se is associated with increased sensitivity to the effects of leptin on food intake in an IL-6-dependent manner. To determine whether exerci se ameliorates the AMPK and mTOR response to leptin in the hypothalamus in an IL-6-dependent manner, rats performed two 3-h exercise bouts, separated by one 45-min rest períod. Intracerebroventrícular IL-6 infusion reduced food intake and pretreatment with AMPK activators and mTOR inhibitors prevented IL-6-induced anorexia. Activators of AMPK increased food intake in control rats to a greater extent than that observed in exercised ones, whereas inhibitors of AMPK had the opposite effect. Exercise was associated with both reduced phosphorylation of the AMPK/ ACC signaling pathway and increased phosphorylation of proteins involved in mTOR signal transduction Ín the hypothalamus. The regulatory role of IL-6 in mediating the modulation in AMPK and mTOR pathways in the hypothalamus was also investigated. Treatment with leptin reduced food intake in exercised rats that were pretreated with vehicle, although no increase in sensitivity to leptin-induced anorexia after pretreatment with anti-IL6 antibody, AICAR or Rapamycin was detected. Improved responses of AMPK and mTOR to leptin may contribute to the appetite suppressive actions of exercise
Mestrado
Ciencias Basicas
Mestre em Clinica Medica
Romanello, Larissa. "Estudos das enzimas adenosina kinase isoforma 1, hipoxantina-guanina fosforibosiltransferase isoformas 1, 2 e 3, adenilsuccinato liase, adenilsuccinato sintetase de Schistosoma mansoni." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/76/76132/tde-27102016-102455/.
Full textSchistosoma mansoni is the parasite responsible for schistosomiasis, disease that affects about 300 million people worldwide, and does not have the purine de novo pathway, depending entirely on the purine salvage pathway to supply its demands on purines. Currently, both direct treatment and most disease control initiatives, rely on chemotherapy using a single drug, praziquantel. Concerns over the possibility of resistance developing to praziquantel, has stimulated efforts to develop new drugs for the treatment of schistosomiasis. The purine salvage pathway has been reported as a potential target for developing new drugs against schistosomiasis. Adenosine kinase (AK), hypoxanthine-guanine phosphoribosyltransferase (HGPRT), adenylosuccinate lyase (ADSL), adenylosuccinate synthetase (ADSS) are key enzymes in this pathway. This work is part of a larger project aimed at obtaining all the structures of enzymes involved in purine salvage pathway of Schistosoma mansoni. The cDNA corresponding to the enzymes was amplified and cloned in vector pOPIN, AK isoform 1, HGPRT isoform 1 and ADSL were expressed in E. coli Lemo 21 (DE3) and HGPRT isoform 3 in E. coli B834(DE3); purified in cobalt agarose column, concentrated and crystallized in several conditions of the Morpheus (Molecular Dimensions) crystallization kit at the Oxford Protein Production Facility (OPPF) in Harwell UK. The data collection by xray diffraction were performed at Diamond Light Source UK. Two ADSL structures were obtained, ADSL in complex with AMP at 2.36Å resolution and ADSL Apo form at 2.14Å The analysis revealed a tetrameric structure highly conserved between ADSLs, and this oligomerization state is required since residues three of the four subunits comprise the active site. Despite the active site being highly conserved between human ADSL and SmADSL, the dimeric interface of these enzymes it has been shown sufficiently distinct, which may represent a potential target for the development of an inhibitor. The ADSL enzymatic activity assay showed an endothermic reaction, indicating the contribution of the entropy related to the large quantity of water molecules present in the active site is important for the reaction kinetics. After several optimization experiments of HGPRT1 crystals and about 200 crystals tested was obtained a structure in complex with IMP at 2.8Å resolution. The structure analysis revealed a tetrameric structure. Despite the subunits do not share the active site, this oligomerization state is required, since residues that make up the active site are also involved in interactions in dimeric interface, guiding the invariable residue Arg206 toward the active site. Four mutations were identified in the region of the active site between SmHGPRT and human HGPRT: Ile149Met, Pro176Arg, Val189Ile e Arg192Lys. These structures increase the important structural information available about the Schistosoma mansoni purine salvage pathway and how it can be selectively private resources.
FANG, YING. "SIGNALING PATHWAY FROM THE A2B ADENOSINE RECEPTOR TO EXTRACELLULAR SIGNAL REGULATED KINASES (ERK1/2) IN HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS (HUVEC) AND ITS ROLE IN HUVEC PROLIFERATION." University of Cincinnati / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1148392082.
Full textPursell, Natalie W. "Hsp90-Mediated Maturation of Kinases and Nuclear Steroid Hormone Receptors: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/535.
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