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Dissertations / Theses on the topic 'C-Jun N-terminal kinase (JNK)'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 September 2023

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1

Arnold, Richard Graham. "The role of c-Jun-N-Terminal Kinase (JNK) in hindlimb ischaemia-reperfusion injury." Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.579569.

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In spite of improvements in the care of the critically ill patient, both elective and emergency vascular surgical interventions are associated with significant morbidity and mortality. Successful reperfusion of the ischaemic limb often initiates a systemic inflammatory response syndrome (SIRS), which may be complicated by multiple organ failure, including Acute Lung Injury (All) and the Acute Respiratory Distress Syndrome (ARDS). An exaggerated inflammatory response has been shown to play an integral role in the development of ARDS following lower torso or limb ischaemia-reperfusion injury. JN
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2

Kyula, Joan Nduku. "HSV-1 induced activation of C-JUN-N-Terminal Kinase (JNK) and P38 MAPK." Thesis, Glasgow Caledonian University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413914.

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3

Lanuza, Masdeu Jordi. "Regulation and actions mediated by C-jun N-terminal kinase pathaway." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/110348.

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Es va generar un ratolí transgènic amb la capacitat d'activar JNK específicament al pàncrees. Tot i que aquests ratolins no tenen cap afectació morfoestructural en els seus illots pancreàtics ni diferències en el contingut total d'insulina però presenten intolerància a la glucosa i no secreten insulina en resposta a hiperglucèmia. A nivell molecular, les cèl•lules β pancreàtiques amb JNK activa, tenen un bloqueig a la via de senyalització d'insulina que fa que es redueixi la secreció d'insulina i l'expressió de gens diana de la insulina. El tractament amb rossiglitazona, un fàrmac del grup de
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4

Gourmaud, Sarah. "Expression de c-Jun N-terminal kinase (JNK) dans la maladie d'Alzheimer : intérêts diagnostiques et thérapeutiques." Paris 7, 2014. http://www.theses.fr/2014PA077106.

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La maladie d'Alzheimer (MA) se caractérise par l'accumulation de peptides d'amyloïde-β42 (Aß₄₂), de protéine tau hyperphosphorylée (ptau) et une perte neuronale. Les niveaux d'Aß₄₂ et de tau au niveau du liquide céphalo-rachidien (LCR) des patients sont utilisés comme biomarqueurs diagnostique. Les protéines PKR et JNK sont des kinases impliquées dans la production d'AE342, la phosphorylation de tau et la mort neuronale. L'accumulation de leur forme active a été mise en évidence dans le cerveau de patients MA. Il existe trois isoformes de JNK. JNK1 et JNK2 sont ubiquitaires et JNK3 est presque
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5

Smith, Abigail O. "Defining the Role of c-Jun N-terminal Kinase (JNK) Signaling in Autosomal Dominant Polycystic Kidney Disease." eScholarship@UMMS, 2021. https://escholarship.umassmed.edu/gsbs_diss/1141.

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Polycystic kidney disease is an inherited degenerative disease in which the uriniferous tubules are replaced by expanding fluid-filled cysts that ultimately destroy organ function. Autosomal dominant polycystic kidney disease (ADPKD) is the most common form, afflicting approximately 1 in 1,000 people. It primarily is caused by mutations in the transmembrane proteins Polycystin-1 (PKD1) and Polycystin-2 (PKD2). The most proximal effects of polycystin mutations leading to cyst formation are not known, but pro-proliferative signaling must be involved for the tubule epithelial cells to increase in
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6

Santos, Fernando Reyes, Maggie K. Diamond-Stanic, Mujalin Prasannarong, and Erik J. Henriksen. "The Serine Kinase C-Jun N-Terminal Kinase (JNK) Contributes to Oxidant-Induced Insulin Resistance in Isolated Rat Skeletal Muscle." Thesis, The University of Arizona, 2012. http://hdl.handle.net/10150/244754.

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Insulin resistance of the mammalian skeletal muscle glucose transport system, one cause of which is oxidative stress, leads to the development of type 2 diabetes. While the direct contributions to insulin resistance of certain stress-activated serine kinases have been described previously, the specific contribution of c-Jun N-terminal kinase (JNK) is not fully understood. Therefore, we assessed the role of JNK in insulin resistance caused by in vitro exposure to the oxidant hydrogen peroxide (H₂O₂). Soleus muscles from lean Zucker rats were incubated in low levels (~30 μM) of H₂O₂ in the absen
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7

Wang, Fang St George Clinical school UNSW. "Oxidative stress induced C-Jun N-terminal Kinase (JNK) activation in tendon cells upregulates MMP1 mRNA and protein expression." Awarded by:University of New South Wales. St George Clinical school, 2006. http://handle.unsw.edu.au/1959.4/28815.

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To explore the potential mechanisms of tendon degeneration, we investigated the role of c-Jun N-terminal Kinase (JNK) activation and the regulation of matrix metalloproteinase 1 (MMP1) in tendon matrix degradation under oxidative stress. JNK and MMP1 activity in samples from normal and ruptured human supraspinatus tendons were evaluated by immunohistochemistry. Real-time quantitative PCR was utilized to evaluate MMP1 mRNA expression and western blotting for MMP1 and JNK protein detection. JNK activation and increased MMP1 activity were found in the torn human supraspinatus tendon tissue, as we
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8

Yu, Lola. "Investigating the role of the c-Jun NH2-terminal kinase pathway in ErbB2-driven breast cancer and macrophage polarization." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1094.

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Breast cancer is the second most common malignancy in the world, accounting for over 1.7 million new diagnoses and an estimated 500,000 deaths per year (1). Overexpression of the receptor tyrosine kinase ErbB2, also known as Her2 or Neu, occurs in over 30% of breast cancers and correlates with metastasis, poor prognosis, and decreased survival (1, 2). Although therapeutics targeting ErbB2 show clinical efficacy, many patients display no initial response or develop drug resistance over time (2). A deeper understanding of the molecular basis of ErbB2-driven tumorigenesis is thus required for the
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9

Joy, Jery 1992. "Chromosomal instability : interplay between proteotoxic and metabolic stress." Doctoral thesis, Universitat Pompeu Fabra, 2020. http://hdl.handle.net/10803/668516.

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Chromosomal Instability (CIN) and associated aneuploidy are salient features of the majority of human solid tumors. In the Drosophila epithelial model of CIN, the generation of highly aneuploid karyotypes drive cell delamination and c-Jun N-terminal Kinase (JNK) dependent cell death. Aneuploidy associated generation of Reactive Oxygen Species (ROS) plays a key role in the activation of JNK. When delaminating cells are maintained in the tissue by apoptosis inhibition, aberrant karyotypes promote a cell-autonomous malignant behavior. Here we have dissected the molecular mechanisms under
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10

Le, Aurore. "Deciphering the role of c-Jun N-Terminal Kinase (JNK1) in an in vivo model of skin inflammation." Doctoral thesis, Universite Libre de Bruxelles, 2020. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/314810.

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JNK1 (c-Jun N-terminal kinase 1) has been studied in numerous biological phenomena, but its role in skin inflammation diseases has not been fully defined yet. We therefore evaluated the role of JNK1 in imiquimod-induced dermatitis, a classical model that shares many features with human psoriasis. We showed that JNK1 was necessary for the expression of inflammatory markers and for acanthosis induced by imiquimod. We demonstrated that the loss of JNK1 in dendritic cells or myeloid cells reduced inflammatory markers but did not affect acanthosis induced by imiquimod. In vitro experiments in bone
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11

Sluss, Hayla Karen. "The c-Jun NH₂-Terminal Kinase Regulates Jun in vitro and in vivo during the Process of Dorsal Closure: A Dissertation." eScholarship@UMMS, 1997. https://escholarship.umassmed.edu/gsbs_diss/264.

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Tyrosine phosphorylation of proteins by protein tyrosine kinases is an important step in initiating mitogenic signal transduction pathways. The receptor tyrosine kinases represent a class of protein kinases that employ phosphorylation cascades to transmit a signal generated at the cell surface. The AP-1 transcription factor is a common target of receptor tyrosine kinase activation, transformation by Ras-like proteins and activation of the MAP kinase pathway. The AP-1 complex contains a dimer of Jun proteins or a heterodimer of Jun and Fos or other bZip proteins. The transcriptional activation
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12

Kenney, Justin Ward. "Nicotine and learning interact to alter transcription factor activity at the c-jun N-terminal kinase 1 gene promoter in the hippocampus." Diss., Temple University Libraries, 2010. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/112533.

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Psychology<br>Ph.D.<br>Approximately 1 in 5 Americans smoke despite the widely known negative health consequences of the habit. One factor that contributes to the high rates of nicotine addiction and its continued use is the ability of the drug to alter long-term memory. Learning in the presence of nicotine results in changes to the cellular and molecular processes that support the formation and storage of long-term memories. The consolidation of long-term memory requires a number of mechanisms, such as gene transcription. Previous work has found that learning a contextual fear conditioning ta
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13

Pang, Wei Wei. "The role of mitochondria in regulating MAPK signalling pathways during oxidative stress." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2006. http://theses.library.uwa.edu.au/adt-WU2007.0026.

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[Truncated abstract] Reactive oxygen species (ROS) have been implicated to play a major role in many pathological conditions including heart attack and stroke. Their ability to modulate the extracellular signal-regulated protein kinase (ERK) and c-Jun Nterminal kinase (JNK) signalling pathways, thereby influencing cellular response has been well-documented. Recent studies implicate a central role for mitochondria in ERK and JNK activation by ROS although the mechanisms remained unresolved. Using Jurkat T-lymphocyte as a cell model, this study demonstrated increased mitochondrial ROS production
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14

Henrie, Hélène. "Régulation de la dynamique des microtubules par la kinase de stress JNK dans les cellules épithéliales : caractérisation de CLIP-170 comme un nouveau substrat." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS461/document.

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Les microtubules sont des éléments dynamiques du cytosquelette qui contrôlent à la fois l’organisation du cytoplasme, la polarité, la migration et la division cellulaire. Notre laboratoire a précédemment montré que la kinase de stress JNK (c-Jun NH2-terminal Kinase) régule la dynamique des microtubules dans les cellules épithéliales de mammifères, en augmentant les vitesses de polymérisation, ainsi que les fréquences de sauvetage (transition vers une phase de repolymérisation). Alors que certaines protéines neuronales capables de réguler la dynamique des microtubules ont été identifiées comme
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15

Manganaro, Lara. "Concerted action of cellular JNK and Pin-1 restricts HIV-1 genome integration to activated CD4+T lymphocytes." Doctoral thesis, Scuola Normale Superiore, 2009. http://hdl.handle.net/11384/85950.

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16

Prunier, Céline. "Étude de mécanismes de répression de l'activité des protéines Smad." Paris 6, 2002. http://www.theses.fr/2002PA066303.

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17

Zamani, Marzieh. "The role of the JNK/AP-1 pathway in the induction of iNOS and CATs in vascular cells." Thesis, University of Hertfordshire, 2013. http://hdl.handle.net/2299/10626.

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Nitric oxide (NO) is an important biological molecule within the body, which over production of this molecule in response to different stimulations can cause various inflammatory diseases. Over production of this molecule is caused by the induction of the inducible nitric oxide synthase (iNOS) enzyme. This enzyme uses L-arginine as a substrate and therefore the presence and transport of this amino acid into the cells can be a key factor in regulating NO over production. Different signalling mechanisms have been implicated in the regulation of this pathway and one of which involves the Mitogen
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18

Tonner, Juliane [Verfasser]. "Spezifische Expression von c-Jun N-terminalen Kinasen (JNK) im Nervensystem : eine immunhistochemische Analyse / Juliane Tonner." Kiel : Universitätsbibliothek Kiel, 2009. http://d-nb.info/1019871245/34.

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19

Chaudhury, Hera Ashraf. "c-Jun N-terminal kinase primes endothelial cells at atheroprone sites for apoptosis." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/6136.

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Atherosclerosis can be initiated by pro-inflammatory activation of endothelial cells (EC) which leads to the recruitment of leukocytes to the vessel wall, and also by endothelial apoptosis which elevates the permeability of arteries to lipoproteins. The greater curvature of the aorta is exposed to high shear and is protected from EC apoptosis, inflammation and atherosclerosis, whereas the lesser curvature is exposed to low shear and is susceptible to atherosclerosis. Pro-inflammatory mediators (e.g. TNFα, LPS) trigger phosphorylation of c-Jun N-terminal kinase (JNK) and p38 MAP kinases to posi
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20

Helbig, Lars [Verfasser]. "Aktivierung von c-Jun-N-terminalen Kinasen (SAPK,JNK) als Teil der späten Cisplatin abhängigen DNA-Schadensantwort / Lars Helbig." Mainz : Universitätsbibliothek Mainz, 2013. http://d-nb.info/1034965247/34.

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21

Sclip, Alessandra. "C-Jun-N-terminal kinase regulates Aβ oligomers production, synapthopathy and cognitive deficits in Alzheimer's disease". Thesis, Open University, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.594746.

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Alzheimer's disease (AD) is a debilitating neurodegenerative disorder characterized by Amyloid-B CAP) and tau deposition in the brain. The number of patients suffering AD is estimated at 36 million worldwide, making AD the most common fonn of dementia. There is no efficient therapy for AD, thus efforts to develop new pharmacological strategies to treat AD need to be intensified. Increasing evidence establishes a central role of soluble and oligomeric form of AP peptide in the pathogenesis of AD. AP accumulates in the synaptic compartment and disrupts the synaptic functionality, leading at leas
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22

Camardo, Andrew T. "C-JUN N-TERMINAL KINASE INHIBITORY NANOTHERAPEUTICS FOR REGENERATIVE ELASTIC MATRIX REPAIR IN ABDOMINAL AORTIC ANEURYSMS." Cleveland State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=csu1499868307678719.

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23

He, Hua, and 何華. "Anti-tumor mechanisms of cyclooxygenase inhibitors and a c-Jun-N-terminal kinase inhibitor in gastrointestinal cancers." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30075245.

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24

Orton, Christopher R. "Analysis of Protein Adduction Kinetics and the Effects of Protein Adduction on C-Jun N-Terminal Kinase Signaling." Diss., The University of Arizona, 2006. http://hdl.handle.net/10150/194247.

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Defining the mechanics and consequences of protein adduction is crucial to understanding the toxicity of reactive electrophiles. Application of tandem mass spectrometry and data analysis algorithms enables detection and mapping of chemical adducts at the level of amino acid sequence. Nevertheless, detection of adducts does not indicate relative reactivity of different sites. In this dissertation I describe a method to measure the kinetics of competing adduction reactions at different sites on the same protein using quantitative mass spectrometry. Adducts are formed by electrophiles at Cys-
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25

Garcia, Marta. "Rôle des voies de transduction intracellulaire c-Jun N-terminal Kinase dans la neurodégénérescence striatale : application à la maladie de Huntington." Paris 11, 2003. http://www.theses.fr/2003PA112066.

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La maladie de Huntington (MH) est une affection génétique neurodégénérative héréditaire, létale causée par l'expansion d'un motif polyglutamine dans la huntingtine. Cette maladie résulte d'une mort neuronale dans une région cérébrale, le striatum. Une approche expérimentale utilisée pour étudier ce point, consiste à reproduire chez l'animal, les caractéristiques phénotypiques de la maladie par administration systémique d'une neurotoxine: l'acide 3-Nitropropionique (3-NP). Notre travail de recherche a concerné l'élucidation des mécanismes intracellulaires qui gouverne la mort des neurones stria
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26

Chan, Anthony Siu Lung. "Activation of c-jun N-terminal kinase by G protein-coupled receptors and the cross-communication with epidermal growth factor signaling /." View Abstract or Full-Text, 2002. http://library.ust.hk/cgi/db/thesis.pl?BICH%202002%20CHAN.

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Thesis (Ph. D.)--Hong Kong University of Science and Technology, 2002.<br>Includes bibliographical references (leaves 201-236). Also available in electronic version. Access restricted to campus users.
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Tavares, Macedo Joana [Verfasser], and Bärbel [Akademischer Betreuer] Blaum. "Production and glycan binding characterization of human properdin and structural elucidation of c-Jun N-terminal kinase 3 inhibitors / Joana Tavares Macedo ; Betreuer: Bärbel Blaum." Tübingen : Universitätsbibliothek Tübingen, 2019. http://d-nb.info/1201644925/34.

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28

Amin, Shahreen. "Regulation of the tyrosine phosphatase SHP-1 expression by C-jun-N-terminal kinase and RFX-1 and AP-4 transcription factors in insulin-like growth factor-1 (IGF-1) stimulated breast adenocarcinoma MCF-7 cells." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/26837.

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This thesis is devoted to reveal the negative regulators in IGF-1 (Insulin like growth factor 1) stimulated growth of a human breast adenocarcinoma cell line. It is a well established fact that increased circulating levels of IGF-1 correlate with increased risk of breast cancer. IGF-1 activation of its receptor, IGF-1R, is implicated in the progression of breast cancer, where IGF-1 stimulation leads to proliferative and anti-apoptotic responses by stimulating MAPK Erk and PI3K, respectively. In this study, IGF-1 stimulated MCF-7 cells proliferated more in the absence of MAPK JNK, implicating t
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29

He, Tiantian. "Studying the Role of Peroxiredoxin 1 in ROS Modulation and Drug Resistance." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112139.

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Les peroxyrédoxines sont des enzymes essentielles de la cellule. Outre leur rôle d’antioxydant, elles sont aussi des régulateurs de la signalisation cellulaire et des suppresseurs de tumeurs. La péroxiredoxine 1 (Prx1) est la plus abondante parmi les six isoformes de peroxyrédoxines humaines. Elle est fréquemment surexprimée dans plusieurs types de cellules cancéreuses, et on a pu associer Prx1 aux processus de carcinogenèse et de métastase, ainsi qu’à la résistance à la radiothérapie ou la chimiothérapie. Ainsi, Prx1 pourrait donc être une cible anticancéreuse intéressante. Au cours de ce tra
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30

Chan, Yushin, and 詹育欣. "The role of c-Jun N-terminal kinase (JNK)." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/60142941903169660454.

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碩士<br>長庚大學<br>基礎醫學研究所<br>92<br>Paclitaxel is one of the microtubule-active agents. It interacts with β-tubulin, stabilzes the microtubule structure and thus alters the microtubule dynamics, resulting in the G2/M phase arrest. After a prolonged G2/M arrest, cells undergo apoptosis. Paclitaxel also activates JNK/SAPK (c-Jun N-terminal kinases/stress-activated protein kinases) and the activated JNK further phosphorylates c-Jun, a transcription factor, regulating downstream genes expression. JNK activation is required for the early phase of paclitaxel-induced apoptosis. However, the exact role
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31

Melino, Michelle. "The role of c-jun N-terminal kinase (JNK) in human T cell function." 2009. http://hdl.handle.net/2440/56209.

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T cells are involved in cellular pathways which enable the immune system to protect us against infection and cancer. However, the same mechanisms also allow T cells to generate chronic inflammatory conditions, including autoimmunity and allergy. Thus a concerted effort has been made to try to understand how the immune system functions in order to inhibit responses which may have harmful effects on tissues and organs. There is a continued search for new immunosuppressants which can only be accomplished through a better understanding of the pathways that regulate T cell function. This includes t
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Melino, Michelle. "The role of c-jun N-terminal kinase (JNK) in human T cell function." Thesis, 2009. http://hdl.handle.net/2440/56209.

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T cells are involved in cellular pathways which enable the immune system to protect us against infection and cancer. However, the same mechanisms also allow T cells to generate chronic inflammatory conditions, including autoimmunity and allergy. Thus a concerted effort has been made to try to understand how the immune system functions in order to inhibit responses which may have harmful effects on tissues and organs. There is a continued search for new immunosuppressants which can only be accomplished through a better understanding of the pathways that regulate T cell function. This includes
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33

Mitra, Shreya. "Role of c-Jun N-terminal kinase (JNK) in mediating mammary cancer cell migration and metastasis." 2009. http://hdl.handle.net/2152/18422.

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The c-Jun N-terminal kinases (JNKs) are MAPK family members and are activated by stress, growth factors and cytokines. They are encoded by three separate genes (jnk 1, 2, and 3), spliced alternately creating 10 isoforms. JNK signaling promotes both cell death and cell survival in a stimuli and tissue specic manner and is also implicated in tumorigenesis. Using the Polyoma Virus Middle T Antigen (PyVMT) transgenic mouse model where jnk2 was either expressed or deleted, we found that the PyVMTjnk2-/- tumors expressed higher Epidermal Growth Factor Receptor Substrate 8 (EPS8) mRNA and protein. E
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Kaschwich, Mark. "Die Rolle der C-jun N-terminalen Kinase (JNK) im neuronalen Zelltod nach Schädigung des Cytoskeletts." 2006. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=015430602&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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35

Shine-Gwo, Shiah, and 夏興國. "Mechanism of c-Jun NH2-terminal Kinase (JNK) Signal Transduction Pathway in Anticancer Drugs-induced Apoptosis." Thesis, 1999. http://ndltd.ncl.edu.tw/handle/17640492931482607622.

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博士<br>國立臺灣大學<br>毒理學研究所<br>87<br>ABSTRACT B-Lapachone (B-Lap) has been found to inhibit DNA topoisomerases (Topo) by a mechanism distinct from that of other commonly known Topo inhibitors. In the present study, we demonstrated a pronounced elevation of H2O2 and O2- in human leukemia HL-60 cells treated with b-Lap. Treatment with other Topo poisons, such as camptothecin (CPT), VP-16, and GL331, did not have the same effect. On the other hand, antioxidant vitamin C (Vit. C) treatment effectively antagonized b-Lap-induced apoptosis. This suggested that a reactive oxygen species (ROS)-re
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Huang, Yi-Feng, and 黃怡鳳. "The Role of c-Jun N-terminal kinase 1 (JNK1) in BMP2 induced osteoblastic differentiation." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/25726381910909510774.

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博士<br>國立陽明大學<br>生物藥學研究所<br>100<br>Runx2 plays a crucial role in osteoblastic differentiation, which can be upregulated by bone morphogenetic protein 2 (BMP2). Mitogen-activated protein kinase (MAPK) cascades, such as extracellular signal-regulated kinase (ERK) and p38, have been reported to be activated by BMP2 to increase Runx2 activity. The role of cjun-N-terminal kinase (JNK), the other member of MAPK, in osteoblastic differentiation has not been well elucidated. In this study, we first demonstrated that JNK1 is activated by BMP2 in multipotent C2C12 and preosteoblastic MC3T3-E1 cell lines.
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Ganduri, Ramesh. "Cocrystallization Studies Extending from Small Molecules to Proteins: a) Cocrystals, Salts and Eutectics, b) Chemical, Structural and Biological Evaluation of Anthrapyrazolones as Inhibitors of JNK proteins." Thesis, 2018. https://etd.iisc.ac.in/handle/2005/5363.

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In summary, we have designed and synthesized three halogenated derivatives of 1,9- pyrazoloanthrone. The involvement of halogen bonding provides highly directional interactions in the binding pocket and hence demonstrates improved inhibitory activity. Among the three halogenated derivatives of 1,9-pyrazoloanthrone, R3 exhibits the most specific inhibition of JNKs activity at significantly lower concentrations (1M) compared to R1, R2 and SP600125 with no off-target effects on other kinases such as p38 and ERK1/2. Further, R3 being a potent and specific inhibitor of JNKs, regulates LPStri
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Chen, Ya-Hui, and 陳雅惠. "The Roles of FasL/Fas Apoptotic System and C-Jun N-terminal Kinase (JNK) Activation in the Outgrowth of Cultured Trophoblast Spheroids on Monolayers of Endometrial Epithelial Cells." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/45106666235537619033.

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碩士<br>國立陽明大學<br>解剖暨細胞生物學研究所<br>92<br>During embryo implantation in mammals, trophoblast cells of the attached blastocyst penetrate the endometrial epithelium of the uterus before invasion into the endometrial stroma. Signaling of apoptosis was demonstrated in endometrial epithelial cells (EEC) surrounding the trophoblast cells; however, the signaling mechanisms leading to apoptosis in EEC remain unclear. Since mitogen-activated protein kinases (MAPKs) were shown to mediate apoptosis in several model systems and found to be activated in the uterus during decidualization, and then evidenced the
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Prasad, Karothu Durga. "Exploration of 1,9-Pyrazoloanthrones as a Copious Reserve for Multifarious Chemical and Biological Applications." Thesis, 2014. http://etd.iisc.ac.in/handle/2005/2980.

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Pyrazoloanthrone and its analogues form the central core of the thesis and the work is focused on the evaluation of chemical and biological applications of pyrazoloanthrones. Selective and sensitive detection of biologically, environmentally and industrially important molecular species such as fluoride, cyanide and picric acid by using pyrazoloanthrones as sensors form the first part while the second part deals with selective and specific kinase inhibition by pyrazoloanthrones to moderate inflammation associated disorders like septic shock. All the investigations are based on extensive crystal
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Prasad, Karothu Durga. "Exploration of 1,9-Pyrazoloanthrones as a Copious Reserve for Multifarious Chemical and Biological Applications." Thesis, 2014. http://etd.iisc.ernet.in/handle/2005/2980.

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Pyrazoloanthrone and its analogues form the central core of the thesis and the work is focused on the evaluation of chemical and biological applications of pyrazoloanthrones. Selective and sensitive detection of biologically, environmentally and industrially important molecular species such as fluoride, cyanide and picric acid by using pyrazoloanthrones as sensors form the first part while the second part deals with selective and specific kinase inhibition by pyrazoloanthrones to moderate inflammation associated disorders like septic shock. All the investigations are based on extensive crystal
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41

Λαγκαδινού, Ελένη. "Διερεύνηση μηχανισμών χημειοαντίστασης στην οξεία μυελογενή λευχαιμία με έμφαση στο ρόλο ενδοκυττάριων μονοπατιών μεταγωγής σήματος". Thesis, 2008. http://nemertes.lis.upatras.gr/jspui/handle/10889/2208.

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Η θεραπεία της Οξείας Μυελογενούς Λευχαιμίας (ΟΜΛ) είναι συχνά ανεπιτυχής λόγω ανάπτυξης κυτταρικής αντίστασης στα αντιλευχαιμικά φάρμακα. Εκτός από την έκφραση Ρ-γλυκοπρωτείνης στα λευχαιμικά κύτταρα, άλλοι κυτταρικοί παράγοντες μπορούν επίσης να συμβάλλουν στην χημειοαντίσταση. Η c- Jun N-terminal Kinase (JNK) είναι μία πρωτεινική κινάση που ενεργοποιείται όταν τα κύτταρα εκτεθούν σε χημειοθεραπευτικά φάρμακα (ΧΜΘ). Πρόσφατες μελέτες σε συμπαγείς όγκους συσχετίζουν την χημειοαντίσταση με αδυναμία των καρκινικών κυττάρων να ενεργοποιήσουν τη JNK κατόπιν επίδρασης ΧΜΘ. Σκοπός της εργασίας είνα
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42

Hidding, Ute Maria Antonia. "Die Rolle von c-Jun N-terminalen Kinasen (JNK) in mikrogliären Zellkulturen." 2005. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=014906349&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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43

Staak, Nils Holger [Verfasser]. "Einfluss von c-Jun und den c-Jun N-terminalen Kinasen, JNK1, JNK2 und JNK3, auf die Regeneration des Nervus facialis / vorgelegt von Nils Holger Staak." 2009. http://nbn-resolving.de/urn:nbn:de:gbv:8-diss-53957.

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44

Gopalan, Archana. "Targeting breast cancer with natural forms of vitamin E and simvastatin." Thesis, 2012. http://hdl.handle.net/2152/ETD-UT-2012-05-5520.

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Breast cancer is the second leading cause of death due to cancer in women. A number of effective therapeutic strategies have been implemented in clinics to cope with the disease yet recurrent disease and toxicity reduce their effectiveness. Hence, there is a need to identify and develop more effective therapies with reduced toxic side effects to improve overall survival rates. This dissertation investigates the mechanisms of action of two natural forms of vitamin E and a cholesterol lowering drug, simvastatin, as a therapeutic strategy in human breast cancer cells. Vitamin E in nature consists
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45

Körner, Julia [Verfasser]. "Die Rolle der c-Jun N-terminalen Kinasen (JNK) in der DSS-Colitis / vorgelegt von Julia Körner." 2008. http://d-nb.info/993003273/34.

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46

Frick, Elisabeth [Verfasser]. "Die Rolle der c-Jun N-terminalen Kinasen (JNK1 und JNK2) im niedrig dosierten DSS-Colitis-Modell / vorgelegt von Elisabeth Frick." 2009. http://d-nb.info/999997157/34.

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Li, Li-Fu, and 李立夫. "Apoptosis Signal-Regulated Kinase 1 and c-Jun N-terminal Kinase Regulated Ventilation-Induced Inflammatory Cytokine and Lung Apoptosis." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/98554179740295415443.

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博士<br>長庚大學<br>臨床醫學研究所<br>93<br>Positive pressure ventilation with large tidal volumes has been shown to cause release of cytokines, including macrophage inflammatory protein-2 (MIP-2), a functional equivalent of human Interleukin (IL)-8. The mechanisms regulating ventilation-induced cytokine production are unclear. We designed three experiments to explore the mechanisms underlying ventilator-induced lung injury. We hypothesized that high tidal volume ventilation-induced IL-8 or MIP-2 production and lung apoptosis are dependent on the activation of apoptosis signal-regulated kinase 1 (ASK1)
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Betigeri, Seema S. "Jun N-terminal kinase 1 (JNK1) as a molecular target to limit cellular mortality under hypoxia." 2009. http://hdl.rutgers.edu/1782.2/rucore10001600001.ETD.000050494.

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Hsiao, Ya-Hsin, та 蕭雅心. "Anti-inflammatory effects of Physalin A via regulation nuclear factor κB and c-Jun N-terminal kinase activation". Thesis, 2014. http://ndltd.ncl.edu.tw/handle/79fya5.

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碩士<br>中國醫藥大學<br>基礎醫學研究所碩士班<br>102<br>Physalis angulata L. has been traditionally used in the supportive treatment of diabetes, hepatitis, and asthma. Physalin A is a major component of chalcones from Physalis angulata. The anti-inflammatory effects of Physalin A were studied by using lipopolysaccharide (LPS)-stimulated mouse macrophage RAW 264.7 cells and λ-carrageenan (Carr)-induced hind mouse paw edema model. Physalin A was tested for its ability to reduce nitric oxide (NO) and prostaglandin E2 (PGE2) production, and the inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) exp
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Lin, Bor-tyng, and 林伯庭. "The Role of c-Jun N-terminal Kinase in Angiotensin II-induced Cellular Senescence of Vascular Smooth Muscle Cells." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/10684685523838938535.

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碩士<br>國立成功大學<br>細胞生物及解剖學研究所<br>96<br>Abdominal aortic aneurysm (AAA) is present in 8% of the population over 60 years of age and exhibits a high mortality rate when rupture. AAA is characterized by extracellular matrix destruction and depletion of vascular smooth muscle cells (VSMC) in the tunica media. Angiotensin II (Ang II) was shown to induce AAA formation in animal models and c-Jun N-terminal kinase (JNK) was shown to play a critical role. A previous study suggested that Ang II induces premature senescence of VSMCs via a p53/p21-dependent pathway. We hypothesized that JNK activation media
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