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Adams, Deanna Grace. "Characterization of the stress-activated protein kinase, MEKK3". Diss., The University of Arizona, 2002. http://hdl.handle.net/10150/279970.
Pełny tekst źródłaBrancho, Deborah Marie. "Regulation and Function of Stress-Activated Protein Kinase Signal Transduction Pathways: A Dissertation". eScholarship@UMMS, 2005. https://escholarship.umassmed.edu/gsbs_diss/101.
Pełny tekst źródłaFerreiro, Neira Isabel. "Transcriptional regulation by the mammalian stress-activated protein kinase p38". Doctoral thesis, Universitat Pompeu Fabra, 2011. http://hdl.handle.net/10803/80661.
Pełny tekst źródłaLa regulación de la transcripción por las Proteínas Quinasas activadas por Estrés (SAPKs) es un aspecto esencial para la adaptación a los estímulos extracelulares. En mamíferos, la activación de la SAPK p38 da lugar a la regulación de la expresión génica a través de la fosforilación de varios factores de transcripción. Sin embargo, cómo p38 SAPK regula el programa de expresión génica de adaptación al estrés así como los mecanismos utilizados por la SAPK permanece sin caracterizar. Los resultados presentados en este manuscrito muestran que p38 SAPK juega un rol central en la regulación de la expresión génica en respuesta a estrés, ya que hasta el 80% de los genes inducidos son dependientes de p38 SAPK. También observamos que en respuesta a cada tipo de estrés se induce un grupo de genes específicos, y sólo hay una pequeña respuesta de genes comunes a los diferentes tipos de estrés la cual engloba principalmente factores de transcripción. Además, hemos observado que para regular la transcripción, p38 se recluta a los promotores de respuesta a estrés a través de su interacción con factores de transcripción. Asimismo, la actividad de p38 permite el reclutamiento de la RNA Polimerasa II y de la MAPKK MKK6 a los promotores inducidos por estrés. La presencia de p38 activa en las regiones codificantes sugiere su participación durante la elongación. En conjunto, los resultados mostrados en este manuscrito establecen a p38 como un regulador esencial de la transcripción en respuesta a estrés, así como definen nuevas funciones de p38 en la regulación de la transcripción en respuesta a estrés.
Auciello, Francesca Romana. "Canonical and non-canonical regulation of AMP-activated protein kinase". Thesis, University of Dundee, 2015. https://discovery.dundee.ac.uk/en/studentTheses/2720a2b7-3f1e-445c-b008-c5c235f35395.
Pełny tekst źródłaFoltz, Ian Nevin. "Regulation of the stress-activated protein kinase pathways in hematopoietic cells". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ38887.pdf.
Pełny tekst źródłaO'Ferrall, Erin K. "Phosphorylation of the neurofilament heavy subunit by stress-activated protein kinase". Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33433.
Pełny tekst źródłaDe, Zutter Gerard S. "Stress Activated Protein Kinase Regulation of Gene Expression in Apoptotic Neurons: A Dissertation". eScholarship@UMMS, 2001. https://escholarship.umassmed.edu/gsbs_diss/168.
Pełny tekst źródłaCheetham, Jill. "The Regulation of the Hog1 Stress Activated Protein Kinase in Candida albicans". Thesis, University of Newcastle Upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.489302.
Pełny tekst źródłaYates, Alexandra Caroline. "Stress-activated protein kinases and neurodegenerative disease". Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287325.
Pełny tekst źródłaSchroder, Wayne Ashley. "Cloning and Characterisation of the Human SinRIP Proteins". Thesis, Griffith University, 2003. http://hdl.handle.net/10072/366190.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
Faculty of Science
Full Text
Thornton, Elizabeth Claire. "Identification and characterisation of a novel β subunit of AMP-activated protein kinase". Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312986.
Pełny tekst źródłaSchroder, Wayne Ashley, i n/a. "Cloning and Characterisation of the Human SinRIP Proteins". Griffith University. School of Biomolecular and Biomedical Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20030829.140754.
Pełny tekst źródłaKanke, Toru. "Regulation of stress-activated protein kinases (SAPKs) mediated by proteinase-activated receptor-2 (PAR-2)". Thesis, University of Strathclyde, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248779.
Pełny tekst źródłaCourt, Naomi Wynne. "The subcellular localisation, tissue expression, substrate specificity and binding partners of stress-activated protein kinase-3". University of Western Australia. School of Biomedical and Chemical Sciences, 2004. http://theses.library.uwa.edu.au/adt-WU2004.0084.
Pełny tekst źródłaAu-Yeung, Ka-wai. "Role of Chinese medicinal compounds in the regulation of stress-activated protein kinase in ischaemic/reperfused rat heart". Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22505441.
Pełny tekst źródłaXing, Yu. "Mitogen activated protein kinase cascades mediate the regulation of antioxidant enzymes under abiotic stresses in arabidopsis". HKBU Institutional Repository, 2007. http://repository.hkbu.edu.hk/etd_ra/834.
Pełny tekst źródłaGoto, 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.
Pełny tekst źródła0048
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
Boppart, Marni D. "Regulation of stress-activated protein kinases by exercise and contraction in skeletal muscle". Thesis, Boston University, 2000. https://hdl.handle.net/2144/36769.
Pełny tekst źródłaPLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
The c-Jun NH2-terminal kinase (JNK) and p38 intracellular signaling cascades are mitogen-activated protein kinase (MAPK) signaling pathways that are activated in mammalian cells by a variety of stressors, including proinflammatory cytokines, osmotic shock, and shear stress. The purpose of this dissertation research was to examine the effect of injury-producing exercise on JNK and p38 activities in human skeletal muscle and to determine whether mechanical stress is a primary stimulator of JNK and p38 activities with contraction. Twelve healthy subjects (7M/5F) completed maximal concentric or eccentric knee extensions on an isokinetic dynamometer (10 sets, 10 reps). Needle biopsies were obtained from the vastus lateralis muscle 24 h before exercise, immediately post-exercise, and 6 h post-exercise. While both forms of exercise increased JNK activity immediately post-exercise, eccentric contractions resulted in a much higher activation (15-fold vs. 4-fold increase above basal for eccentric and concentric, respectively). By 6 h post-exercise, JNK activity decreased back to baseline values. In a separate study, 14 male subjects completed a 42.2 km marathon. Biopsies were obtained from the vastus lateralis muscle 10 days prior to the marathon, immediately following the race, and 1, 3, and 5 days after the race. JNK activity increased 7-fold over basal immediately postexercise, but decreased back to basal 1, 3, and 5 days after the exercise. The activity of p38y also was increased and decreased in a similar pattern. However, no regulation was observed for p38α. In a third study, the effects of contraction and static stretch on JNK activity and p38 phosphorylation were determined in the rat soleus muscle in vitro. Static stretch dramatically increased JNK activity and p38 phosphorylation, whereas isometric contraction resulted in much smaller increases in JNK activity and p38 phosphorylation. The regulation of focal adhesion proteins also was examined following both exercise and contraction. The work presented in this thesis demonstrates that injury-producing exercise results in the marked activation of the JNK and p38 stress-activated protein kinases and provides evidence that mechanical stress may be a major contributor to increases in JNK and p38 activities observed following contraction in rat and human skeletal muscle.
2031-01-01
歐楊嘉慧 i Ka-wai Au-Yeung. "Role of Chinese medicinal compounds in the regulation of stress-activated protein kinase in ischaemic/reperfused rat heart". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31223916.
Pełny tekst źródłaAu-Yeung, Ka Wai, i 歐陽嘉慧. "A mechanistic study of the inhibitory effect of magnesium tanshinoate B on stress-activated protein kinase in ischaemia/reperfusion". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B2994188X.
Pełny tekst źródłaPagano, Daniel J. (Daniel Joseph). "Genetic analysis of p38 mitogen-activated protein kinase signaling in innate immunity and stress physiology of Caenorhabditis elegans". Thesis, Massachusetts Institute of Technology, 2014. http://hdl.handle.net/1721.1/106725.
Pełny tekst źródłaCataloged from PDF version of thesis.
Includes bibliographical references.
Host-microbe interactions play an important role in the physiology and evolution of animals. Interactions with microbes can generally be considered beneficial or pathogenic to the host. The ability of an organism to mount an immune response to infection by pathogenic microbes is critical to its survival, and basic mechanisms of innate immunity are conserved in evolutionarily diverse species. A pivotal signaling pathway in the evolutionarily conserved innate immune responses of multicellular organisms is the stress-activated p38 mitogen-activated protein kinase (MAPK) pathway. This thesis focuses on the physiological role of p38 MAPK signaling in the host defense of Caenorhabditis elegans. In Chapter Two, I report the identification and characterization of the conserved ATF/CREB bZIP protein ATF-7 as the key transcriptional regulator of the PMK- 1 p38 MAPK-dependent immune response to pathogens. These data suggest a model in which the PMK- 1 p3 8 MAPK phosphorylates ATF-7 and switches it from a transcriptional repressor to a transcriptional activator of effector genes of the innate immune response of C. elegans. In Chapter Three, I characterize the roles of PMK- 1 and a second p38 MAPK ortholog, PMK-2, which are encoded in an operon, in tissue-specific signaling mechanisms involved in host defense. I show that PMK-2 functions redundantly with PMK- 1 in the nervous system to mediate neurobehavioral responses to pathogens. Furthermore, I demonstrate a role for the miR-58/80-82 family of microRNAs in regulating the tissue expression of pmk-2, which suggests a role for microRNAs in the establishment of tissue-specific expression of co-operonic genes. The work described in this thesis establishes the ancient evolutionary origins of the p38 MAPKCREB/ ATF pathway in innate immunity, and establishes a role for microRNAs in defining the tissue-expression pattern of co-operonic p38 MAPK genes. New directions for further understanding the ancient evolutionary mechanisms of p38 MAPK signaling and their tissue-specific regulation are discussed in Chapter Four.
by Daniel J. Pagano.
Ph. D.
Lepez, Anouk. "Régulation du stress oxydant et contrôle de la prolifération homéostatique des lymphocytes T par l’AMP-activated protein kinase". Doctoral thesis, Universite Libre de Bruxelles, 2020. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/313133.
Pełny tekst źródłaDoctorat en Sciences
info:eu-repo/semantics/nonPublished
Shahidullah, Mohammad, Amritlal Mandal i Nicholas A. Delamere. "A Role for Calcium-Activated Adenylate Cyclase and Protein Kinase A in the Lens Src Family Kinase and Na,K-ATPase Response to Hyposmotic Stress". ASSOC RESEARCH VISION OPHTHALMOLOGY INC, 2017. http://hdl.handle.net/10150/625814.
Pełny tekst źródłaHaberstroh, Katharine Michelle Wendy. "Cadmium-induced cell toxicity and stress-activated protein kinase induction in the midbrain cells of two strains of mice". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ40474.pdf.
Pełny tekst źródłaChang, Malcolm Elliott. "Role of the stress activated protein kinases (sapk's) in mediating resistance to the antineoplastic agent adriamycin (ADR)". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0014/MQ40835.pdf.
Pełny tekst źródłaCombes, Adrien. "Influence des perturbations métaboliques sur des voies de signalisation impliquées dans la biogenèse mitochondriale". Thesis, Lille 2, 2015. http://www.theses.fr/2015LIL2S045/document.
Pełny tekst źródłaWestern life evolution is associated with an increase in sedentary behaviours and metabolic diseases leading to health alteration. This evolution affects the skeletal muscle, which is characterized by a decrease in its ability to produce aerobic energy. However, skeletal muscle is a highly malleable tissue, capable of considerable metabolic adaptations in response to physical activity. Mitochondria produce the aerobic energy within the skeletal muscle. Understanding the molecular mechanisms that regulate mitochondrial biogenesis and its function is necessary to improve physical activity prescription.The intermittent exercise is currently used in rehabilitation programs. Several arguments are put forward to utilizing this method: 1) the time spent at high oxygen consumption, 2) the high intensity of exercise and 3) the metabolic disturbances induced by variations of intensity during exercise. However, the influence of metabolic disturbances on muscle oxidative capacity has not been clearly demonstrated. The purpose of my thesis work has therefore focused on these metabolic perturbations and their effects on signalling pathways involved in mitochondrial biogenesis. In order to characterize the influence of metabolic disturbances on the signalling pathways involved in mitochondrial biogenesis, we compared the influence of acute exercises. We realized two protocols to investigate the influence of metabolic disturbances. The first study compared three intermittent exercises in order to identify the optimal duty-cycle duration to induce the biggest metabolic disturbances and to compare metabolic responses of intermittent and continuous exercise performed at 70%WRpic. The second protocol evaluated the influence of the repetition of metabolic disturbances on signalling pathways involved in mitochondrial biogenesis.In order to identify the duty-cycle duration producing more metabolic fluctuations, we analysed the changes of oxygen consumption and quantified metabolic variations. We used three parameters: 1) a quantitative parameter, 2) a qualitative parameter, and 3) an index combining quantitative and qualitative parameters. Comparison of three different duty-cycle durations (30s work:30s passive recovery; 60s:60s, and 120s:120s) revealed that the 60s:60s modality induces more metabolic fluctuations for a same energy expenditure.Our second study compared 30 minutes of pedalling at 70%WRpic realized by two different modalities: continuous (30min 1 block) and intermittent (30 1min block interspersed by 1min of passive recovery). Repetition of transitions from rest to exercise during the intermittent exercise creates higher metabolic disturbances and leads to a higher phosphorylation of AMPK, p38 MAPK and CaMKII. These kinases are upstream of PGC-1α, an important regulator of mitochondrial biogenesis in skeletal muscle. All together, these results demonstrate that metabolic disturbances are involved in mitochondrial signalling pathways activation.This work opens up new perspectives on exercise training prescription for sedentary or chronic pathology people. Future work will aim to confirm our results in chronic interventions and explore these effects in different populations
Launay, Nathalie. "Voies de signalisation et rôle de l'αB-cristalline suite à la désorganisation du cytosquelette". Paris 6, 2006. http://www.theses.fr/2006PA066375.
Pełny tekst źródłaThe first aim of this research was to identify the pathways involved in the signal transduction induced by specific cytoskeletal stresses in the muscular system. Cytoskeletal network disruption trigger the specific B-crystallin phosphorylation which may protect or stabilize the actin microfilaments and interfere with formation of IF aggregates during stresses exerted at the cytoskeleton. The second aim of this project was to study the role of phosphorylation in the regulation of the αB-crystallin anti-apoptotic function in chemotherapy resistance phenomenon in breast epithelial adenocarcinoma cells. We demonstrate that Ser59 phosphorylation of B-crystallin plays a crucial role in vinblastine-induced apoptosis in MCF7 cells, by down-regulating the anti-apoptotic function of B-crystallin. These results introduce the possibility of regulating the protective status of sHsp in cancer through modifying their state of phosphorylation
Sama, Reddy Ranjith Kumar. "FUS/TLS in Stress Response - Implications for Amyotrophic Lateral Sclerosis: A Dissertation". eScholarship@UMMS, 2014. http://escholarship.umassmed.edu/gsbs_diss/704.
Pełny tekst źródłaLu, Dan. "ATF3, a stress-inducible gene function and regulation /". Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1155740569.
Pełny tekst źródłaGuillonneau, Maëva. "Étude de la nucléophosmine, nouvelle protéine associée à p38 MAPK, dans la réponse des cellules endothéliales à un stress oxydant aigu". Nantes, 2015. https://archive.bu.univ-nantes.fr/pollux/show/show?id=288675a2-942d-436d-b15a-59ae37d33154.
Pełny tekst źródłaThe microvascular compartment is a significant target of oxidative stress that is a major factor in endothelial dysfunction, especially during exposure to ionizing radiation. The alteration of endothelium induced by oxidative stress is involved in radiation-induced toxicity of normal tissues. Limiting endothelial dysfunction is therefore an important issue of current radiotherapeutic treatments. This objective requires a better characterization of oxidative stress signaling in endothelial cells. P38 MAPK pathway is essential in oxidative stress response but still insufficiently characterized. By using a proteomic approach, we identified nucleophosmin (NPM) as a new partner of p38 in the cytoplasm of endothelial cells. PP2a phosphatase is also associated with the NPM/p38 complex. Our work shows that oxidative stress (H2O2, 500μM) regulates the NPM dephosphorylation via PP2a, causes rapid dissociation of the complex, and promotes its translocation to the nucleus. In addition, we show that the presence of NPM dephosphorylated at T199 in the nucleus alters the cellular response to DNA damage induced by oxidative stress. The membrane sphingolipid ceramide is also an important factor in stress pathways, particularly in endothelial cells. Our study describes the involvement of this sphingolipid in the regulation of NPM/p38 pathway. A better characterization of the p38 pathway and its actors provided by our study will identify potential targets in order to limit endothelial dysfunction and its deleterious effect on surrounding tissues
Schaeffer, Céline. "Effets protecteurs d'un neuropeptide, le CGRP, sur des cellules du système cardiovasculaire soumises à un stress oxydant". Dijon, 2003. http://www.theses.fr/2003DIJOMU14.
Pełny tekst źródłaCameron, Pamela. "The cytotoxic and inflammatory effects of E. coli 0157:H7 : the role of stress-activated protein kinases and nuclear factor kappa B". Thesis, University of Strathclyde, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366792.
Pełny tekst źródłaBertran-Gonzalez, Jesus. "Study of segregated signaling responses of striatonigral and striatopallidal neurons in BAC transgenic mice". Paris 6, 2009. http://www.theses.fr/2009PA066348.
Pełny tekst źródłaDe, Silva Matharage Shenali. "Involvement of AMPK and AP-1 Biochemical Pathways in IL-6 Regulation of Steroidogenic Enzymes in the Adrenal Cortex". BYU ScholarsArchive, 2013. https://scholarsarchive.byu.edu/etd/4301.
Pełny tekst źródłaJacob, Claire. "Régulation du stress oxydant par les phosphodiestérases de type 4 : implication des MAP kinases". Rennes 1, 2003. http://www.theses.fr/2003REN1B069.
Pełny tekst źródłaNoriega, 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.
Pełny tekst źródłaIn 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.
Streicher, John Michael. "The role of mitogen activated protein kinase activated protein kinase-2 in regulating p38 mitogen activated protein kinase induced cyclooxygenase-2 induction and heart failure". Diss., Restricted to subscribing institutions, 2009. http://proquest.umi.com/pqdweb?did=1872200951&sid=6&Fmt=2&clientId=1564&RQT=309&VName=PQD.
Pełny tekst źródłaUnderwood, E. A. "Nucleotide regulation of AMP-activated protein kinase". Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1382013/.
Pełny tekst źródłaDavies, Gareth. "Folding of p38 mitogen-activated protein kinase". Thesis, University of Warwick, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412847.
Pełny tekst źródłaScheffler, Tracy Leigh. "AMP-activated protein kinase and muscle metabolism". Diss., Virginia Tech, 2012. http://hdl.handle.net/10919/38829.
Pełny tekst źródłaPh. D.
Hurst, Denise. "AMP-activated protein kinase kinase activity and phosphorylation of AMP-activated protein kinase in contracting muscle of sedentary and endurance trained rats". Diss., CLICK HERE for online access, 2007. http://contentdm.lib.byu.edu/ETD/image/etd2014.pdf.
Pełny tekst źródłaBrown, Jacob D. "Liver Kinase B1/AMP-Activated Protein Kinase Signaling in the Diaphragm". BYU ScholarsArchive, 2010. https://scholarsarchive.byu.edu/etd/2543.
Pełny tekst źródłaSvensson, Nilsson Caroline. "Post-translational modification of protein kinase RNA-activated". Thesis, Uppsala universitet, Institutionen för kemi - BMC, 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-355076.
Pełny tekst źródłaRojnuckarin, Ponlapat. "Mitogen-activated protein kinase pathways in megakaryocyte development /". Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/9200.
Pełny tekst źródłaJulien, Mathéau A. "Mechanical Strain-Mediated Syndecan Regulation and Its Effects on Adhesion of Vascular Smooth Muscle Cells". Diss., Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/7007.
Pełny tekst źródłaMaitra, Sushmit. "The AU-rich element mRNA decay-promoting activity of BRF1 is regulated by mitogen-activated protein kinase activated protein kinase 2". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008r/maitra.pdf.
Pełny tekst źródłaPenfold, Lucy. "Investigating the roles of AMP-activated protein kinase and calcium/calmodulin-dependent protein kinase kinase β in prostate cancer". Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/54390.
Pełny tekst źródłaNadal, Ribelles Mariona 1984. "Control of transcription by the stress activated Hog1 kinase". Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/293257.
Pełny tekst źródłaUna propietat cel·lular fonamental és l’habilitat de detectar i respondre de forma robusta a les fluctuacions en el seu entorn. En cèl·lules de llevat (Saccharomyces cerevisiae), els canvis en l’ osmolaritat extracel·lular són detectats per la via de senyalització de HOG, que coordina el procés d’adaptació cel·lular imprescindible per sobreviure a un estrès osmòtic. L’objectiu d’aquest estudi és identificar i caracteritzar els mecanismes moleculars utilitzats per Hog1 per regular l’expressió gènica en resposta a estrès osmòtic. Fent servir un crivatge genètic a gran escala dissenyat per identificar activitats necessàries per la regulació de l’expressió gènica en resposta a estrès osmòtic, hem identificat un nou substrat de Hog1, l’activitat del qual és requereix tan per la iniciació com l’ elongació de la transcripció. En aquest treball també ens hem centrat en caracteritzar el paper global de Hog1 en la reorganització del transcriptoma de S. cerevisae en condicions d’ estrès osmòtic. Mitjançant la combinació de tècniques moleculars amb tècniques de seqüenciació (ChIP-seq, MNase-seq, Tiling arrays) hem definit el posicionament en el genoma dels components claus que regulen la transcripció, oferint per primera vegada una visió general del procés de transcripció en resposta a estrès osmòtic L’alta resolució d’aquestes tècniques ens ha permès identificar noves dianes transcripcionals de Hog1, com és la regulació d’una altra maquinària transcripcional (RNA Pol III) i la regulació de la transcripció de una nova classe de RNAs no codificants (lncRNAs). En conjunt, els resultats presentats en aquesta tesi proporcionen una nova visió dels mecanismes per els quals Hog1 modula l’expressió gènica
Türk, Roland Daniel. "Expanding the signaling network around AMP-activated protein kinase /". Zürich : ETH, 2007. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17222.
Pełny tekst źródłaZeng, Qingning. "Dissecting mitogen-activated protein kinase cascades involving arabidopsis MKK6". Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/31941.
Pełny tekst źródła