Dissertations / Theses on the topic 'Potassium channels, pancreatic cancer'
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Li, Fangfang. "Regulation of pancreatic β-cell death and cancer cell migration by TPRM2 channels." Thesis, University of Leeds, 2016. http://etheses.whiterose.ac.uk/13374/.
Full textNewton, Hannah S. "Potassium channels and adenosine signaling in T cells of head and neck cancer patients." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1603713656776019.
Full textKondratska-Klymenko, Kateryna. "Role of calcium-permeable channels in pancreatic ductal adenocarcinoma resistance to chemotherapy." Thesis, Lille 1, 2015. http://www.theses.fr/2015LIL10099/document.
Full textPancreatic ductal adenocarcinoma (PDAC) representing the most prevalent pancreatic neoplasm accounting for about 90% of all pancreatic tumors, is one of the leading causes of cancer death in men and women. The current five-year relative survival rate is about 6% . One of the reasons of this is that early stage pancreatic cancer usually has no symptoms and thus the majority of cases are diagnosed at the late metastatic or invasive stages which are not suitable for surgery. Pancreatic cancer cells have been shown to exhibit a number of genetic mutations leading to uncontrolled cell proliferation, as well as evasion of programmed cell death (apoptosis). Changes in the cytosolic free Ca2+ concentration, play a central role in many fundamental cellular processes and disturbance of the Ca2+ homeostasis regulatory mechanisms leads to a vast variety of severe pathologies, including cancer. Among these, store-operated calcium channels (SOCs) have been shown to regulate a variety of calcium dependent cellular processes altered in different cancers. However, although the role of Ca2+ and calcium-permeable channels is well established in many signaling pathways in a variety of cell types, the information of the role of calcium-permeable channels in PDAC cells is limited. Therefore, identification of the molecular nature as well as functions of calcium-permeable channels in these cells is of great importance as it can reveal novel approaches for treating pancreatic cancer through targeting calcium-dependent processes
Asher, Viren. "The expression of EAG and HERG potassium channels in ovarian cancer and their role in cell proliferation." Thesis, University of Nottingham, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.594215.
Full textInnamaa, Anni. "Expression and function of the two pore potassium (K2P) channels TREK-1, TREK-2 and TASK-3 in ovarian cancer." Thesis, University of Nottingham, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.606812.
Full textVallejo, Gracia Albert. "Kv1.3 and Kv1.5 channels in leukocytes." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/397797.
Full textAhmed, Meftun. "Oscillatory Ca2+ signaling in glucose-stimulated murine pancreatic β-cells : Modulation by amino acids, glucagon, caffeine and ryanodine." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1408.
Full textAhmed, Meftun. "Oscillatory Ca2+ signaling in glucose-stimulated murine pancreatic β-cells : Modulation by amino acids, glucagon, caffeine and ryanodine." Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1408.
Full textOscillations in cytoplasmic Ca2+ concentration ([Ca2+]i) is the key signal in glucose-stimulated β-cells governing pulsatile insulin release. The glucose response of mouse β-cells is often manifested as slow oscillations and rapid transients of [Ca2+] i. In the present study, microfluorometric technique was used to evaluate the role of amino acids, glucagon, ryanodine and caffeine on the generation and maintenance of [Ca2+] i oscillations and transients in individual murine β-cells and isolated mouse pancreatic islets. The amino acids glycine, alanine and arginine, at around their physiological concentrations, transformed the glucose-induced slow oscillations of [Ca2+] i in isolated mouse β-cells into sustained elevation. Increased Ca2+ entry promoted the reappearance of the slow [Ca2+] i oscillations. The [Ca2+] i oscillations were more resistant to amino acid transformation in intact islets, supporting the idea that cellular interactions are important for maintaining the oscillatory activity. Individual rat β-cells responded to glucose stimulation with slow [Ca2+] i oscillations due to periodic entry of Ca2+ as well as with transients evoked by mobilization of intracellular stores. The [Ca2+] i oscillations in rat β-cells had a slightly lower frequency than those in mouse β-cells and were more easily transformed into sustained elevation in the presence of glucagon or caffeine. The transients of [Ca2+] i were more common in rat than in mouse β-cells and often appeared in synchrony also in cells lacking physical contact. Depolarization enhanced the generation of [Ca2+] i transients. In accordance with the idea that β-cells have functionally active ryanodine receptors, it was found that ryanodine sometimes restored oscillatory activity abolished by caffeine. However, the IP3 receptors are the major Ca2+ release channels both in β-cells from rats and mice. Single β-cells from ob/ob mice did not differ from those of lean controls with regard to frequency, amplitudes and half-widths of the slow [Ca2+] i oscillations. Nevertheless, there was an excessive firing of [Ca2+] i transients in the β-cells from the ob/ob mice, which was suppressed by leptin at close to physiological concentrations. The enhanced firing of [Ca2+] i transients in ob/ob mouse β-cells may be due to the absence of leptin and mediated by activation of the phospholipase C signaling pathway.
Serrano, Novillo Clara. "Biology of the cardiovascular Kv7.1 functional complex." Doctoral thesis, Universitat de Barcelona, 2020. http://hdl.handle.net/10803/668686.
Full textEls canals de potassi dependents (Kv) regulen processos fisiològics molt importants, com la proliferació, la migració o el volum cel·lular. La seva rellevància es posa de manifest amb les diferents patologies associades a alteracions en la expressió dels canals, incloent malalties cardiovasculars, cerebrals, autoimmunes o càncer. Es tracta de proteïnes transmembrana formades per l’associació de 4 subunitats α que s’uneixen per formar el por. La gran varietat de diversitat funcional és deguda a la capacitat de heterotetramerització dels canals, variants d’splicing, modificacions post-traduccionals o la associació a subunitats reguladores KCNE, entre d’altres. En cardiomiòcits, Kv7.1 s’associa a KCNE1 per generar les corrents IKs, encarregades de la repolarització del potencial cardíac. La seva associació i tràfic són tema de debat des de fa anys, amb dues escoles defensant idees oposades. La primera, que les dues proteïnes s’associen en les fases inicials de la biogènesi; la segona, que trafiquen independent cap a la membrana, on difondran per trobar-se. Els Kv també s’han detectat a musculatura vascular llisa, on mantenen el potencial de repòs i controlen així el to vascular. Kv7.1, Kv7.4 i Kv7.5 es troben en diferents venes i arteries, on una expressió aberrant provoca alteracions fisiològiques. Tot i així, el seu paper concret encara es desconeix. En la present tesi doctoral hem comprovat que Kv7.1 i KCNE1 utilitzen vies diferents per arribar a la membrana plasmàtica. KCNE1 viatja per la via convencional, mentre que Kv7.1 utilitza una ruta no convencional que escapa del Golgi. Quan co-expressats, Kv7.1 redirigeix KCNE1 cap aquesta via alternativa. Hem demostrat que aquesta via són les ER-PM junctions, que també són el compartiment on la seva associació té lloc. Els interactors moleculars del canal durant el seu tràfic cap a ER-PM junctions també s’ha estudiat durant aquest treball. A més a més, hem descrit per primer cop l’expressió de Kv1.3, Kv1.5, Kv7.1 i Kv7.5 en l’endoteli de venes i artèries humanes. Hem vist un remodelatge en aquesta expressió en diferents càncers vasculars, en alguns casos relacionat amb la malignitat del tumor.
Kaizik, Stephan Martin. "Analysis of mouse models of insulin secretion disorders." Thesis, University of Oxford, 2010. http://ora.ox.ac.uk/objects/uuid:4d44b68a-a0a0-4c92-8809-00ddbfe3e636.
Full textSAGAR, SHASHIDHAR MANOLI SAGAR SHASHIDHAR MANOLI. "Voltage gated K+ channels (Kv) and integrin receptors in Pancreatic ductal adenocarcinoma (PDAC)." Doctoral thesis, 2016. http://hdl.handle.net/2158/1045918.
Full text[Verfasser], Jiraporn Ousingsawat. "Potassium channels in prostate and colonic cancer / vorgelegt von Jiraporn Ousingsawat." 2007. http://d-nb.info/986198102/34.
Full textSpitzner, Melanie [Verfasser]. "Role of potassium ion channels (K+ channels) on proliferation and development of colonic cancer / vorgelegt von Melanie Spitzner." 2008. http://d-nb.info/987515292/34.
Full textEl-Kholy, Wasim. "The role of hyperpolarization activated cyclic nucleotide modulated and voltage gated potassium channels in pancreatic beta-cell function." 2007. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=478866&T=F.
Full textRoy, Jeremy. "THE CONTRIBUTION OF K+ ION CHANNELS AND THE Ca2+-PERMEABLE TRPM8 CHANNEL TO BREAST CANCER CELL PROLIFERATION." 2010. http://hdl.handle.net/10222/13118.
Full textHance, Michael W. "The Effects of 17- Beta Estradiol on G-Protein Inwardly Rectifying Potassium Channels (GIRKs) in Breast Cancer." 2009. http://trace.tennessee.edu/utk_graddiss/41.
Full textGomes, Fernanda Ramos. "Analysis of ether-à-go-go potassium channel (Eag1) splice variants in melanoma cells." Doctoral thesis, 2010. http://hdl.handle.net/11858/00-1735-0000-0006-ADAF-4.
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